BY-Dr Sarita Choudhary
WHY THINK ABOUT CRT Increasing number of new cases of heart failure being
diagnosed
Recent studies show despite optimal medical drug treatment mortality remains gt 25 at three years
Hospital admissions and office visits are frequent following diagnosis
20-40 of patients with heart failure have conduction
disease and QRSd gt 120 msec
Cardiac resynchronization therapy (CRT) is a
recommended treatment for patients with moderate to severe (drug-refractory) heart failure with left ventricular (LV) systolic dysfunction and evidence of ventricular dyssynchrony defined by a QRS duration gt120 ms
It improves symptoms exercise tolerance quality of life morbidity and mortality
However the problem of non-response to CRT remains crucial with prevalence of 30 of non-responders for clinical response and 45 for echocardiographic response
Notable Recommendation Changes in 2012 ACCFAHAHRS Focused Update
2012 DBT Focused Update Recommendations Comments
Class I1 CRT is indicated for patients who have LVEF less than or equal to 35 sinus rhythm LBBB with a QRS duration greater than or equal to 150 ms and NYHA class II III or ambulatory IV symptoms on GDMT (Level of Evidence A for NYHA class IIIIV Level of Evidence B for NYHA class II)
Modified recommendation (specifying CRT in patients with LBBB of 150 ms expanded to include those with NYHA class II symptoms)
Class IIa1 CRT can be useful for patients who have LVEF less than or equal to 35 sinus rhythm LBBB with a QRS duration 120 to 149 ms and NYHA class II III or ambulatory IV symptoms on GDMT (Level of Evidence B)
New recommendation
2 CRT can be useful for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with a QRS duration greater than or equal to 150 ms and NYHA class IIIambulatory class IV symptoms on GDMT(Level of Evidence A)
New recommendation
3 CRT can be useful in patients with atrial fibrillation and LVEF less than or equal to 35 on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) AV nodal ablation or pharmacologic rate control will allow near 100 ventricular pacing with CRT (Level of Evidence B)
Modified recommendation (wording changed to indicate benefit based on ejection fraction rather than NYHA class level of evidence changed from C to B)
4 CRT can be useful for patients on GDMT who have LVEF less than or equal to 35 and are undergoing new or replacement device placement with anticipated requirement for significant (40) ventricular pacing (Level of Evidence C)
Modified recommendation (wording changed to indicate benefit based on ejection fraction and need for pacing rather than NYHA class class changed from IIb to IIa)
Notable Recommendation Changes in 2012 ACCFAHAHRS Focused Update
2012 DBT Focused Update Recommendations Comments
Class IIb1 CRT may be considered for patients who have LVEF less than or equal to 30 ischemic etiology of heart failure sinus rhythm LBBB with a QRS duration of greater than or equal to 150 ms and NYHA class I symptoms on GDMT (Level of Evidence C)
New recommendation
2 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with QRS duration 120 to 149 ms and NYHA class IIIambulatory class IV on GDMT (Level of Evidence B)
New recommendation
3 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with a QRS duration greater than or equal to 150 ms and NYHA class II symptoms on GDMT (Level of Evidence B)
New recommendation
Class III No Benefit1 CRT is not recommended for patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration less than 150 ms (Level of Evidence B)
New recommendation
2 CRT is not indicated for patients whose comorbidities andor frailty limit survival with good functional capacity to less than 1 year (Level of Evidence C)
Modified recommendation (wording changed to include cardiac as well as noncardiac comorbidities)
Ventricular Dysynchrony and Cardiac Resynchronization
Ventricular Dysynchrony1 Electrical Inter- or
Intraventricular conduction delays typically manifested as left bundle branch block
Structural disruption of myocardial collagen matrix impairing electrical conduction and mechanical efficiency
Mechanical Regional wall motion abnormalities with increased workload and stressmdashcompromising ventricular mechanics
Cardiac Resynchronization
Therapeutic intent of atrial synchronized biventricular pacing Modification of interventricular intraventricular and atrial-
ventricular activation sequences in patients with ventricular dysynchrony
Complement to optimal medical therapy
1 Tavazzi L Eur Heart J 2000211211-1214
Clinical Consequences of Ventricular Dysynchrony
Abnormal interventricular septal wall motion
Reduced dPdt
Reduced pulse pressure
Reduced EF and CO
Reduced diastolic filling time
Prolonged MR duration
Proposed Mechanisms
IntraventricularSynchrony
AtrioventricularSynchrony
InterventricularSynchrony
LAPressure
LV DiastolicFilling
RV StrokeVolume
LVESV LVEDV
Reverse Remodeling
Cardiac Resynchronization
MR dPdt EF CO( Pulse Pressure)
Achieving Cardiac ResynchronizationMechanical Goal Atrial-synchronized bi-ventricular pacing
Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left
ventricular cardiac vein via the coronary sinus
Right AtrialLead
Right VentricularLead
Left VentricularLead
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
WHY THINK ABOUT CRT Increasing number of new cases of heart failure being
diagnosed
Recent studies show despite optimal medical drug treatment mortality remains gt 25 at three years
Hospital admissions and office visits are frequent following diagnosis
20-40 of patients with heart failure have conduction
disease and QRSd gt 120 msec
Cardiac resynchronization therapy (CRT) is a
recommended treatment for patients with moderate to severe (drug-refractory) heart failure with left ventricular (LV) systolic dysfunction and evidence of ventricular dyssynchrony defined by a QRS duration gt120 ms
It improves symptoms exercise tolerance quality of life morbidity and mortality
However the problem of non-response to CRT remains crucial with prevalence of 30 of non-responders for clinical response and 45 for echocardiographic response
Notable Recommendation Changes in 2012 ACCFAHAHRS Focused Update
2012 DBT Focused Update Recommendations Comments
Class I1 CRT is indicated for patients who have LVEF less than or equal to 35 sinus rhythm LBBB with a QRS duration greater than or equal to 150 ms and NYHA class II III or ambulatory IV symptoms on GDMT (Level of Evidence A for NYHA class IIIIV Level of Evidence B for NYHA class II)
Modified recommendation (specifying CRT in patients with LBBB of 150 ms expanded to include those with NYHA class II symptoms)
Class IIa1 CRT can be useful for patients who have LVEF less than or equal to 35 sinus rhythm LBBB with a QRS duration 120 to 149 ms and NYHA class II III or ambulatory IV symptoms on GDMT (Level of Evidence B)
New recommendation
2 CRT can be useful for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with a QRS duration greater than or equal to 150 ms and NYHA class IIIambulatory class IV symptoms on GDMT(Level of Evidence A)
New recommendation
3 CRT can be useful in patients with atrial fibrillation and LVEF less than or equal to 35 on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) AV nodal ablation or pharmacologic rate control will allow near 100 ventricular pacing with CRT (Level of Evidence B)
Modified recommendation (wording changed to indicate benefit based on ejection fraction rather than NYHA class level of evidence changed from C to B)
4 CRT can be useful for patients on GDMT who have LVEF less than or equal to 35 and are undergoing new or replacement device placement with anticipated requirement for significant (40) ventricular pacing (Level of Evidence C)
Modified recommendation (wording changed to indicate benefit based on ejection fraction and need for pacing rather than NYHA class class changed from IIb to IIa)
Notable Recommendation Changes in 2012 ACCFAHAHRS Focused Update
2012 DBT Focused Update Recommendations Comments
Class IIb1 CRT may be considered for patients who have LVEF less than or equal to 30 ischemic etiology of heart failure sinus rhythm LBBB with a QRS duration of greater than or equal to 150 ms and NYHA class I symptoms on GDMT (Level of Evidence C)
New recommendation
2 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with QRS duration 120 to 149 ms and NYHA class IIIambulatory class IV on GDMT (Level of Evidence B)
New recommendation
3 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with a QRS duration greater than or equal to 150 ms and NYHA class II symptoms on GDMT (Level of Evidence B)
New recommendation
Class III No Benefit1 CRT is not recommended for patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration less than 150 ms (Level of Evidence B)
New recommendation
2 CRT is not indicated for patients whose comorbidities andor frailty limit survival with good functional capacity to less than 1 year (Level of Evidence C)
Modified recommendation (wording changed to include cardiac as well as noncardiac comorbidities)
Ventricular Dysynchrony and Cardiac Resynchronization
Ventricular Dysynchrony1 Electrical Inter- or
Intraventricular conduction delays typically manifested as left bundle branch block
Structural disruption of myocardial collagen matrix impairing electrical conduction and mechanical efficiency
Mechanical Regional wall motion abnormalities with increased workload and stressmdashcompromising ventricular mechanics
Cardiac Resynchronization
Therapeutic intent of atrial synchronized biventricular pacing Modification of interventricular intraventricular and atrial-
ventricular activation sequences in patients with ventricular dysynchrony
Complement to optimal medical therapy
1 Tavazzi L Eur Heart J 2000211211-1214
Clinical Consequences of Ventricular Dysynchrony
Abnormal interventricular septal wall motion
Reduced dPdt
Reduced pulse pressure
Reduced EF and CO
Reduced diastolic filling time
Prolonged MR duration
Proposed Mechanisms
IntraventricularSynchrony
AtrioventricularSynchrony
InterventricularSynchrony
LAPressure
LV DiastolicFilling
RV StrokeVolume
LVESV LVEDV
Reverse Remodeling
Cardiac Resynchronization
MR dPdt EF CO( Pulse Pressure)
Achieving Cardiac ResynchronizationMechanical Goal Atrial-synchronized bi-ventricular pacing
Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left
ventricular cardiac vein via the coronary sinus
Right AtrialLead
Right VentricularLead
Left VentricularLead
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Cardiac resynchronization therapy (CRT) is a
recommended treatment for patients with moderate to severe (drug-refractory) heart failure with left ventricular (LV) systolic dysfunction and evidence of ventricular dyssynchrony defined by a QRS duration gt120 ms
It improves symptoms exercise tolerance quality of life morbidity and mortality
However the problem of non-response to CRT remains crucial with prevalence of 30 of non-responders for clinical response and 45 for echocardiographic response
Notable Recommendation Changes in 2012 ACCFAHAHRS Focused Update
2012 DBT Focused Update Recommendations Comments
Class I1 CRT is indicated for patients who have LVEF less than or equal to 35 sinus rhythm LBBB with a QRS duration greater than or equal to 150 ms and NYHA class II III or ambulatory IV symptoms on GDMT (Level of Evidence A for NYHA class IIIIV Level of Evidence B for NYHA class II)
Modified recommendation (specifying CRT in patients with LBBB of 150 ms expanded to include those with NYHA class II symptoms)
Class IIa1 CRT can be useful for patients who have LVEF less than or equal to 35 sinus rhythm LBBB with a QRS duration 120 to 149 ms and NYHA class II III or ambulatory IV symptoms on GDMT (Level of Evidence B)
New recommendation
2 CRT can be useful for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with a QRS duration greater than or equal to 150 ms and NYHA class IIIambulatory class IV symptoms on GDMT(Level of Evidence A)
New recommendation
3 CRT can be useful in patients with atrial fibrillation and LVEF less than or equal to 35 on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) AV nodal ablation or pharmacologic rate control will allow near 100 ventricular pacing with CRT (Level of Evidence B)
Modified recommendation (wording changed to indicate benefit based on ejection fraction rather than NYHA class level of evidence changed from C to B)
4 CRT can be useful for patients on GDMT who have LVEF less than or equal to 35 and are undergoing new or replacement device placement with anticipated requirement for significant (40) ventricular pacing (Level of Evidence C)
Modified recommendation (wording changed to indicate benefit based on ejection fraction and need for pacing rather than NYHA class class changed from IIb to IIa)
Notable Recommendation Changes in 2012 ACCFAHAHRS Focused Update
2012 DBT Focused Update Recommendations Comments
Class IIb1 CRT may be considered for patients who have LVEF less than or equal to 30 ischemic etiology of heart failure sinus rhythm LBBB with a QRS duration of greater than or equal to 150 ms and NYHA class I symptoms on GDMT (Level of Evidence C)
New recommendation
2 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with QRS duration 120 to 149 ms and NYHA class IIIambulatory class IV on GDMT (Level of Evidence B)
New recommendation
3 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with a QRS duration greater than or equal to 150 ms and NYHA class II symptoms on GDMT (Level of Evidence B)
New recommendation
Class III No Benefit1 CRT is not recommended for patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration less than 150 ms (Level of Evidence B)
New recommendation
2 CRT is not indicated for patients whose comorbidities andor frailty limit survival with good functional capacity to less than 1 year (Level of Evidence C)
Modified recommendation (wording changed to include cardiac as well as noncardiac comorbidities)
Ventricular Dysynchrony and Cardiac Resynchronization
Ventricular Dysynchrony1 Electrical Inter- or
Intraventricular conduction delays typically manifested as left bundle branch block
Structural disruption of myocardial collagen matrix impairing electrical conduction and mechanical efficiency
Mechanical Regional wall motion abnormalities with increased workload and stressmdashcompromising ventricular mechanics
Cardiac Resynchronization
Therapeutic intent of atrial synchronized biventricular pacing Modification of interventricular intraventricular and atrial-
ventricular activation sequences in patients with ventricular dysynchrony
Complement to optimal medical therapy
1 Tavazzi L Eur Heart J 2000211211-1214
Clinical Consequences of Ventricular Dysynchrony
Abnormal interventricular septal wall motion
Reduced dPdt
Reduced pulse pressure
Reduced EF and CO
Reduced diastolic filling time
Prolonged MR duration
Proposed Mechanisms
IntraventricularSynchrony
AtrioventricularSynchrony
InterventricularSynchrony
LAPressure
LV DiastolicFilling
RV StrokeVolume
LVESV LVEDV
Reverse Remodeling
Cardiac Resynchronization
MR dPdt EF CO( Pulse Pressure)
Achieving Cardiac ResynchronizationMechanical Goal Atrial-synchronized bi-ventricular pacing
Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left
ventricular cardiac vein via the coronary sinus
Right AtrialLead
Right VentricularLead
Left VentricularLead
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Notable Recommendation Changes in 2012 ACCFAHAHRS Focused Update
2012 DBT Focused Update Recommendations Comments
Class I1 CRT is indicated for patients who have LVEF less than or equal to 35 sinus rhythm LBBB with a QRS duration greater than or equal to 150 ms and NYHA class II III or ambulatory IV symptoms on GDMT (Level of Evidence A for NYHA class IIIIV Level of Evidence B for NYHA class II)
Modified recommendation (specifying CRT in patients with LBBB of 150 ms expanded to include those with NYHA class II symptoms)
Class IIa1 CRT can be useful for patients who have LVEF less than or equal to 35 sinus rhythm LBBB with a QRS duration 120 to 149 ms and NYHA class II III or ambulatory IV symptoms on GDMT (Level of Evidence B)
New recommendation
2 CRT can be useful for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with a QRS duration greater than or equal to 150 ms and NYHA class IIIambulatory class IV symptoms on GDMT(Level of Evidence A)
New recommendation
3 CRT can be useful in patients with atrial fibrillation and LVEF less than or equal to 35 on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) AV nodal ablation or pharmacologic rate control will allow near 100 ventricular pacing with CRT (Level of Evidence B)
Modified recommendation (wording changed to indicate benefit based on ejection fraction rather than NYHA class level of evidence changed from C to B)
4 CRT can be useful for patients on GDMT who have LVEF less than or equal to 35 and are undergoing new or replacement device placement with anticipated requirement for significant (40) ventricular pacing (Level of Evidence C)
Modified recommendation (wording changed to indicate benefit based on ejection fraction and need for pacing rather than NYHA class class changed from IIb to IIa)
Notable Recommendation Changes in 2012 ACCFAHAHRS Focused Update
2012 DBT Focused Update Recommendations Comments
Class IIb1 CRT may be considered for patients who have LVEF less than or equal to 30 ischemic etiology of heart failure sinus rhythm LBBB with a QRS duration of greater than or equal to 150 ms and NYHA class I symptoms on GDMT (Level of Evidence C)
New recommendation
2 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with QRS duration 120 to 149 ms and NYHA class IIIambulatory class IV on GDMT (Level of Evidence B)
New recommendation
3 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with a QRS duration greater than or equal to 150 ms and NYHA class II symptoms on GDMT (Level of Evidence B)
New recommendation
Class III No Benefit1 CRT is not recommended for patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration less than 150 ms (Level of Evidence B)
New recommendation
2 CRT is not indicated for patients whose comorbidities andor frailty limit survival with good functional capacity to less than 1 year (Level of Evidence C)
Modified recommendation (wording changed to include cardiac as well as noncardiac comorbidities)
Ventricular Dysynchrony and Cardiac Resynchronization
Ventricular Dysynchrony1 Electrical Inter- or
Intraventricular conduction delays typically manifested as left bundle branch block
Structural disruption of myocardial collagen matrix impairing electrical conduction and mechanical efficiency
Mechanical Regional wall motion abnormalities with increased workload and stressmdashcompromising ventricular mechanics
Cardiac Resynchronization
Therapeutic intent of atrial synchronized biventricular pacing Modification of interventricular intraventricular and atrial-
ventricular activation sequences in patients with ventricular dysynchrony
Complement to optimal medical therapy
1 Tavazzi L Eur Heart J 2000211211-1214
Clinical Consequences of Ventricular Dysynchrony
Abnormal interventricular septal wall motion
Reduced dPdt
Reduced pulse pressure
Reduced EF and CO
Reduced diastolic filling time
Prolonged MR duration
Proposed Mechanisms
IntraventricularSynchrony
AtrioventricularSynchrony
InterventricularSynchrony
LAPressure
LV DiastolicFilling
RV StrokeVolume
LVESV LVEDV
Reverse Remodeling
Cardiac Resynchronization
MR dPdt EF CO( Pulse Pressure)
Achieving Cardiac ResynchronizationMechanical Goal Atrial-synchronized bi-ventricular pacing
Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left
ventricular cardiac vein via the coronary sinus
Right AtrialLead
Right VentricularLead
Left VentricularLead
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Notable Recommendation Changes in 2012 ACCFAHAHRS Focused Update
2012 DBT Focused Update Recommendations Comments
Class IIb1 CRT may be considered for patients who have LVEF less than or equal to 30 ischemic etiology of heart failure sinus rhythm LBBB with a QRS duration of greater than or equal to 150 ms and NYHA class I symptoms on GDMT (Level of Evidence C)
New recommendation
2 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with QRS duration 120 to 149 ms and NYHA class IIIambulatory class IV on GDMT (Level of Evidence B)
New recommendation
3 CRT may be considered for patients who have LVEF less than or equal to 35 sinus rhythm a non-LBBB pattern with a QRS duration greater than or equal to 150 ms and NYHA class II symptoms on GDMT (Level of Evidence B)
New recommendation
Class III No Benefit1 CRT is not recommended for patients with NYHA class I or II symptoms and non-LBBB pattern with QRS duration less than 150 ms (Level of Evidence B)
New recommendation
2 CRT is not indicated for patients whose comorbidities andor frailty limit survival with good functional capacity to less than 1 year (Level of Evidence C)
Modified recommendation (wording changed to include cardiac as well as noncardiac comorbidities)
Ventricular Dysynchrony and Cardiac Resynchronization
Ventricular Dysynchrony1 Electrical Inter- or
Intraventricular conduction delays typically manifested as left bundle branch block
Structural disruption of myocardial collagen matrix impairing electrical conduction and mechanical efficiency
Mechanical Regional wall motion abnormalities with increased workload and stressmdashcompromising ventricular mechanics
Cardiac Resynchronization
Therapeutic intent of atrial synchronized biventricular pacing Modification of interventricular intraventricular and atrial-
ventricular activation sequences in patients with ventricular dysynchrony
Complement to optimal medical therapy
1 Tavazzi L Eur Heart J 2000211211-1214
Clinical Consequences of Ventricular Dysynchrony
Abnormal interventricular septal wall motion
Reduced dPdt
Reduced pulse pressure
Reduced EF and CO
Reduced diastolic filling time
Prolonged MR duration
Proposed Mechanisms
IntraventricularSynchrony
AtrioventricularSynchrony
InterventricularSynchrony
LAPressure
LV DiastolicFilling
RV StrokeVolume
LVESV LVEDV
Reverse Remodeling
Cardiac Resynchronization
MR dPdt EF CO( Pulse Pressure)
Achieving Cardiac ResynchronizationMechanical Goal Atrial-synchronized bi-ventricular pacing
Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left
ventricular cardiac vein via the coronary sinus
Right AtrialLead
Right VentricularLead
Left VentricularLead
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Ventricular Dysynchrony and Cardiac Resynchronization
Ventricular Dysynchrony1 Electrical Inter- or
Intraventricular conduction delays typically manifested as left bundle branch block
Structural disruption of myocardial collagen matrix impairing electrical conduction and mechanical efficiency
Mechanical Regional wall motion abnormalities with increased workload and stressmdashcompromising ventricular mechanics
Cardiac Resynchronization
Therapeutic intent of atrial synchronized biventricular pacing Modification of interventricular intraventricular and atrial-
ventricular activation sequences in patients with ventricular dysynchrony
Complement to optimal medical therapy
1 Tavazzi L Eur Heart J 2000211211-1214
Clinical Consequences of Ventricular Dysynchrony
Abnormal interventricular septal wall motion
Reduced dPdt
Reduced pulse pressure
Reduced EF and CO
Reduced diastolic filling time
Prolonged MR duration
Proposed Mechanisms
IntraventricularSynchrony
AtrioventricularSynchrony
InterventricularSynchrony
LAPressure
LV DiastolicFilling
RV StrokeVolume
LVESV LVEDV
Reverse Remodeling
Cardiac Resynchronization
MR dPdt EF CO( Pulse Pressure)
Achieving Cardiac ResynchronizationMechanical Goal Atrial-synchronized bi-ventricular pacing
Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left
ventricular cardiac vein via the coronary sinus
Right AtrialLead
Right VentricularLead
Left VentricularLead
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Clinical Consequences of Ventricular Dysynchrony
Abnormal interventricular septal wall motion
Reduced dPdt
Reduced pulse pressure
Reduced EF and CO
Reduced diastolic filling time
Prolonged MR duration
Proposed Mechanisms
IntraventricularSynchrony
AtrioventricularSynchrony
InterventricularSynchrony
LAPressure
LV DiastolicFilling
RV StrokeVolume
LVESV LVEDV
Reverse Remodeling
Cardiac Resynchronization
MR dPdt EF CO( Pulse Pressure)
Achieving Cardiac ResynchronizationMechanical Goal Atrial-synchronized bi-ventricular pacing
Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left
ventricular cardiac vein via the coronary sinus
Right AtrialLead
Right VentricularLead
Left VentricularLead
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Proposed Mechanisms
IntraventricularSynchrony
AtrioventricularSynchrony
InterventricularSynchrony
LAPressure
LV DiastolicFilling
RV StrokeVolume
LVESV LVEDV
Reverse Remodeling
Cardiac Resynchronization
MR dPdt EF CO( Pulse Pressure)
Achieving Cardiac ResynchronizationMechanical Goal Atrial-synchronized bi-ventricular pacing
Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left
ventricular cardiac vein via the coronary sinus
Right AtrialLead
Right VentricularLead
Left VentricularLead
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Achieving Cardiac ResynchronizationMechanical Goal Atrial-synchronized bi-ventricular pacing
Transvenous Approach Standard pacing lead in RA Standard pacing or defibrillation lead in RV Specially designed left heart lead placed in a left
ventricular cardiac vein via the coronary sinus
Right AtrialLead
Right VentricularLead
Left VentricularLead
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Step 1 Cannulate CS
bull Use extreme care when passing the guide catheter through vessels
bull Due to the relative stiffness of the catheter damage to the walls of the vessels may include dissections or perforations
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Step 2 Perform Venograms Varying Patient Anatomy 123
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Cardiac Venous Anatomy
CS Os
Middle Posterior
Postero-lateral
Great
Lateral
Antero-lateral
Anterior
Step 2 Perform Venograms
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Lead in Lateral Cardiac Vein
Step 2 Perform Venograms
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Step 4 Place Leads
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Clinical characteristics of CRT responders and non-responders
Response more likely Response less likely
QRS duration gt150ms lt150ms
Heart disease Non-ischemic Ischemic
Dyssynchrony Present Absent
Bundle branch block Left Right
Scar burden(MRI) Low burden High burden
Non-transmural Transmural
Posterolateral segments spared
Posterolateral segments involved
Severity of mitral regurgitation
Mild-moderate Severe
Lead position Posterior-lateral Anterior or inferior
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
CRT Responders functional improvement -NYHA functional class(1) Quality of life(10 pt) Distance covered in 6mins hall walk test(60 m) Change of peak oxygen uptake VO2 (1-2
mlkgmin) during exercise Reduction in LV diameter LVEDV(10)LVESV(15)
Main reasons for non-response to CRT
Improper patient selection Suboptimal lead placement Inappropriate device programming
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Device interrogation RV and LV capture AV and VV optimization
Capture threshold test-o To assess appropriate capture in both RV and LVo Atrial capture testing is not crucial unless
suspect atrial capture problemso Capture threshold varies Normal daily variation
posture and meal times drugs cardiac ischemia disease progression
o The diagnosis of loss of biventricular capture is documented with analysis of the QRS complexes on the surface ECG
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Threshold tests in the era of CRT devices that had a single ventricular channel with an internal Y-connector to the RV and LV (as opposed to current devices that have separate ventricular channels that allow measurement of RV and LV thresholds individually)
The threshold test is initiated with a high voltage output that results in BV capture with gradual reduction in amplitude until one of the ventricles fails to be entrained resulting in a change in QRS morphology
The algorithm was designed to identify the ventricle which had lost capture by evaluating
changes in QRS axis
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
When to suspect loss of Biventricular capture
1048713The most frequent situation is a hemodynamic deterioration occurring after a period of significant clinical improvement
1048713In some cases can cause acute or sub‐acute pulmonary edema
1048713 The loss of biventricular capture may be asymptomatic and diagnosed during a scheduled follow‐up with the analysis of QRS complexes on surface ECG or it may be suspected from data from the device
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Algorithms to confirm LV capture on a standard ECG
Ammann et al described loss of LV capture as RS ratiolt1 in V1 and gt1 in lead I sensitivity of 94 and specificity of 93 Yong and Duby Loss of LV capture is indicated by increasing
QRS positivity in lead I and loss of RV capture by increasing positivity in lead III
sensitivity of 97ndash100 and a specificity of 92ndash97
In Biventricular pacing loss of q or Q wave in lead 1 is 100 predictive of loss of LV capture
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Geneva algorithmFirst step- evaluates QRS width in the limb
leads whose widening points to a change from BV capture to univentricular (LV or RV) capture
The second step evaluates net QRS amplitude in lead I with greater negativity indicating increasing participation of LV capture (ie RV-BV or BV-LV capture)
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Causes of loss of permanent or temporarybiventricular pacing
Left ventricular lead dislodgement Increase in LV or RV pacing thresholds1048713 Right ventricular lead dislodgement1048713 Non-optimal AV delay1048713 Atrial tachyarrhythmias with rapid ventricular rate1048713 Low maximal tracking rate1048713 Frequent ventricular premature beats1048713 Atrial undersensing1048713 T Wave oversensing1048713 Far-field atrial sensing1048713 Ventricular double counting
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
A-V and V-V delays adjustment
Two major approaches are currently used to guide their adjustment echocardiography and intracardiac electrograms (IEGMs)
Echocardiography-directed adjustment can be by many different methods (eg the Ritters formula the iterative technique) but LV outflow tract velocityndashtime integral (VTI) (a surrogate measure of stroke measure) maximization is the most popular
IEGM-directed adjustment is by proprietary algorithms developed by different CIED manufacturers recommending values for the A-V and V-V delays on the basis of the intracardiac atrial RV and LV signals
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
AV OPTIMIZATION The AV delay is the time between the
atrial beat and the corresponding ventricular paced event Usually programmed empirically at 80ndash120 ms
A long AV delay gives the ventricle a lot of ldquoopportunityrdquo to beat on its own before the ventricular output pulse is delivered
Shorten the AV delay as much as is reasonable Paced AV delay Sensed AV delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
AV delay- significant impact on systolic function
Rule of thumb in AV delay optimization - program AV delay to about 75of the native PR interval(interval from intrinsic atrial contraction to intrinsic ventricular contraction) - for continuous ventricular pacing
Too short AV delay- undermine CRT stimulation and increase symptoms
Too long AV delay- increases MR
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Rate-responsive AV delay (RRAVD) is the automatic shortening of the AV delay as the patientrsquos heart rate increases
Program this ON Sensed AV delay is from AS to VP (the sensed
AV delay starts the timer at the moment the atrial device is sensed)
Paced AV delay is from AP to VP (the paced AV delay starts the time at the moment the atrial output pulse is delivered)
As a result it is generally prudent to program a sensed AV delay that is about 25 ms shorter than the paced AV delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
VV OPTIMIZATION VV optimization- harmonize activities of RV and
LV Optimal VV timing delay is the one that
produces the greatest VTI value using echo Echo remains the gold standard of VV timing
optimization Timing optimization is that proper CRT depends
on precise timing of the ventricular contractions Timing must allow for
Adequate time for the passive filling of the ventricles Proper contraction of the right and left ventricles with
respect to each other
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
In up to 8ndash10 of the patients undergoing biventricular pacemaker implantation LV lead placement is not possible for a variety of reasons namely inability to cannulate the CS absence of suitable branches lack of lead stability phrenic nerve capture etc
Surgical LV epicardial lead placement using left anterior or lateral mini-thoracotomy video-assisted thoracoscopy approach and robotically enhanced systems is an option in these patients
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
FAILURE RESPONSE TO CRT
YES
CORRECT
NO
LOSS OF LV PACING
NO
OPTIMIZE AV
DELAYVV
DELAYNO RESPONSE
DYSSYNCHRONY PRESENT
POOR LEAD POSITION
YES
REPOSITION LV LEAD
YES
CORRECT
ATRIAL
FIBRILLATIO
NVENTRICULA
R DOUB
LE COUNTING
OVERSENSIN
GLOSS OF LV CAPTU
RELOW URL
LONG AV
DELAYPVARP EXTENSION
ATRIAL UNDERSENS
INGFREQU
ENT PVC
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
Pacing strategies can we do better
Typically LBBB is linked with an electrical activation sequence that courses the apex with delayed activation of the lateral and posterolateral portion of the LV
Biventricular pacing improves LV synchrony via stimulation of the late-activated regions of the LV
There is still controversy regarding the best lead positioning strategy and the choice between an optimal anatomical position targeting either the segment with maximal mechanical dyssynchrony or a region with maximal electrical delay is still up for debate
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
The current trend is that the LV lead be placed at an optimal anatomic pacing site (usually defined as the lateral and posterolateral LV wall)
However the lack of a favourable clinical response in nearly a third of the patients receiving CRT suggests limitations in this approach to pacing site selection
Since CRT is a form of electrical therapy for disorderly electrical activation of the heart it makes sense to attempt to target the region with the maximal electrical delay
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