13.Tahiaritmii

R.V. - Tahiaritmii feb 2012

Semnificaţie – manifestări clinice •  Simptome:

–  datorate ↓DC •  cerebral: vertij-lipotimii → sincopa (⊃ sd. Adams-Stokes) •  cardiace: angina pectorala •  renale: respiraţie acidotică → comă •  musculare: astenie fizică / fatigabilitate

–  datorate stazei •  pulmonare •  periferice

•  Semne –  de DC↓ –  de stază

NB!: manifestările clinice depind de mecanismul tahidicardiei şi de substratul pe care apar

NB!: simptomele se pot datora şi bradiaritmiilor induse de tahiaritmii


EGM intracavitare: EPS


Mecanismele TSV sustinute "   Reintrare:

"   in NSA

"   la nivelul caii lente-

cale rapida: TRNAV

"   la nivelul atriului =

FiA, Fl A

"   pe cale accesorie: TRAV

"   Automatice:

"   Aritmii atriale automatice

"   Aritmii jonctionale

automatice:

"   TJNP pura

"   TJNP cu bloc


Tahicardia sinusala

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Aritmia sinusala respiratorie

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Extrasistolia atriala

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Tahicardia atriala multifocala

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Tahicardia jonctionala neparoxistica

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Context clinic sugestiv: regularizarea frecventei

cardiace la pt cu FA cronica tratat cu digitala


Tahicardia prin reintrare in NAV (TRNAV): mecanism

"  Conducere anterograda = pe “calea lenta” in AD posteroseptal

"  Conducere retrograda = pe “calea rapida” in AD anteroseptal


D1

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aVR

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Situatii clinice posibile in prezenta caii accesorii atrio - ventriculare

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asimptomatica

simptomatica


Preexcitatie permanenta


Efectul de �acordeon�: unda delta de durata variabila


Tahicardia reintranta atrioventriculara (TRAV) CFHC8FCA=75�

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TRAV cu conducere antidromica

"  tahiaritmie regulata cu QRS largi prin

prezenta undei delta

"  raspuns ventricular rapid > 180-200/min

"  mecanism:

"  Conducere anterograda pe calea accesorie

"  Conducere retrograda prin NAV

"  dg diferential cu TV monomorfa sustinuta

"  Risc crescut de moarte subita cardiaca in

caz de aparitia FA → FV


TSV in sdr. WPW cu conducere antidromica

! Tahiaritmie regulata cu QRS largi; P ne-evidentiabil; dg dif TV monomorfa


Sdr. WPW cu fibrilatie atriala


Evaluarea riscului vital in WPW

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Tratamentul in sdr. WPW

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•  Tratament:

•  de obicei rezistenta la tratament

•  Stop digitala; fenitoina

•  β-blocante, potasiu, Ca-blocante

•  in BPOC = O2


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Epidemiologia FA

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Etiologia FA

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FA IDIOPATICA: pana la 30% din cazuri !


Clasificare FA depistata prima oara

PAROXISTICA (autolimitata)

PERSISTENTA (ne-autolimitata)

PERMANENTA

ESC Practice Guidelines. EHJ 2010

events.35,36 Leadless implantable loop recorders provide continu-ous AF monitoring over a 2 year period with automatic AF detec-tion based on RR interval analysis. Preliminary clinical data indicategood sensitivity but less specificity for AF detection.40 No dataexist on the implementation of such devices in the clinicalroutine of AF monitoring.

3.5 Types of atrial fibrillationClinically, it is reasonable to distinguish five types of AF based onthe presentation and duration of the arrhythmia: first diagnosed,paroxysmal, persistent, long-standing persistent, and permanentAF (Figure 2).

(1) Every patient who presents with AF for the first time is con-sidered a patient with first diagnosed AF, irrespective ofthe duration of the arrhythmia or the presence and severityof AF-related symptoms.

(2) Paroxysmal AF is self-terminating, usually within 48 h.Although AF paroxysms may continue for up to 7 days, the48 h time point is clinically important—after this the likelihoodof spontaneous conversion is low and anticoagulation must beconsidered (see Section 4.1).

(3) Persistent AF is present when an AF episode either lastslonger than 7 days or requires termination by cardioversion,either with drugs or by direct current cardioversion (DCC).

(4) Long-standing persistent AF has lasted for ≥1 year whenit is decided to adopt a rhythm control strategy.

(5) Permanent AF is said to exist when the presence of thearrhythmia is accepted by the patient (and physician). Hence,rhythm control interventions are, by definition, not pursuedin patients with permanent AF. Should a rhythm control

strategy be adopted, the arrhythmia is redesignated as ‘long-standing persistent AF’.

This classification is useful for clinical management of AF patients(Figure 2), especially when AF-related symptoms are also con-sidered. Many therapeutic decisions require careful considerationof additional individual factors and co-morbidities.

Silent AF (asymptomatic) may manifest as an AF-related com-plication (ischaemic stroke or tachycardiomyopathy) or may bediagnosed by an opportunistic ECG. Silent AF may present asany of the temporal forms of AF.

3.6 Initial managementA thorough medical history should be obtained from the patientwith suspected or known AF (Table 5). The acute managementof AF patients should concentrate on relief of symptoms andassessment of AF-associated risk. Clinical evaluation shouldinclude determination of the EHRA score (Table 63), estimationof stroke risk (see Section 4.1), and search for conditions that pre-dispose to AF (see Section 2.1.2) and for complications of thearrhythmia (see Section 2.1.1). The 12-lead ECG should be

First diagnosed episode of atrial fibrillation

Paroxysmal(usually <48 h)

Persistent(>7 days or requires CV)

Permanent(accepted)

Long-standingPersistent (>1 year)

Figure 2 Different types of AF. AF¼ atrial fibrillation; CV¼cardioversion. The arrhythmia tends to progress from paroxysmal(self-terminating, usually ,48 h) to persistent [non-self-terminatingor requiring cardioversion (CV)], long-standing persistent (lastinglonger than 1 year) and eventually to permanent (accepted) AF.First-onset AF may be the first of recurrent attacks or already bedeemed permanent.

Table 5 Relevant questions to be put to a patient withsuspected or known AF

Does the heart rhythm during the episode feel regular or irregular?

Is there any precipitating factor such as exercise, emotion, or alcohol intake?

Are symptoms during the episodes moderate or severe—the severity may be expressed using the EHRA score,3 which is similar to the CCS-SAF score.41

Are the episodes frequent or infrequent, and are they long or short lasting?

Is there a history of concomitant disease such as hypertension, coronary heart disease, heart failure, peripheral vascular disease, cerebrovascular disease, stroke, diabetes, or chronic pulmonary disease?

Is there an alcohol abuse habit?

Is there a family history of AF?

AF ¼ atrial fibrillation; CCS-SAF ¼ Canadian Cardiovascular Society Severity inAtrial Fibrillation; EHRA ¼ European Heart Rhythm Association.

Table 6 EHRA score of AF-related symptoms

Classification of AF-related symptoms (EHRA score)

EHRA class Explanation

EHRA I ‘No symptoms’

EHRA II ‘Mild symptoms’; normal daily activity not affected

EHRA III ‘Severe symptoms’; normal daily activity affected

EHRA IV ‘Disabling symptoms’; normal daily activity discontinued

AF ¼ atrial fibrillation; EHRA ¼ European Heart Rhythm Association.

ESC GuidelinesPage 10 of 61


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Substrat Trigger

,,Perpetuatori’’

Permanentă

Persistentă

Paroxistică

RR intervals on the 10 s strip (recorded at 25 mm/s) by six. Therisk of AF-related complications is not different between shortAF episodes and sustained forms of the arrhythmia.12 It is there-fore important to detect paroxysmal AF in order to preventAF-related complications (e.g. stroke). However, short ‘atrial high-rate episodes’, e.g. detected by pacemakers, defibrillators, or otherimplanted devices, may not be associated with thrombo-emboliccomplications unless their duration exceeds several hours (seeSection 3.4).

AF may manifest initially as an ischaemic stroke or TIA, and it isreasonable to assume that most patients experience asymptomatic,often self-terminating, arrhythmia episodes before AF is first diag-nosed. The rate of AF recurrence is 10% in the first year after theinitial diagnosis, and !5% per annum thereafter. Co-morbiditiesand age significantly accelerate both the progression of AF andthe development of complications.3,23

3.3 ‘Natural’ time courseAF progresses from short, rare episodes, to longer and more fre-quent attacks. Over time (years), many patients will develop sus-tained forms of AF (Figure 1). Only a small proportion ofpatients without AF-promoting conditions (see Section 2.1.2) willremain in paroxysmal AF over several decades (2–3% of AFpatients).32 The distribution of paroxysmal AF recurrences is notrandom, but clustered.3 ‘AF burden’ can vary markedly overmonths or even years in individual patients.3 Asymptomatic AF iscommon even in symptomatic patients, irrespective of whetherthe initial presentation was persistent or paroxysmal. This hasimportant implications for (dis)continuation of therapies aimed atpreventing AF-related complications.

3.4 Electrocardiogram techniques todiagnose and monitor atrial fibrillationThe intensity and duration of monitoring should be determined bythe clinical need to establish the diagnosis, and should be drivenmainly by the clinical impact of AF detection. More intense AFrecording is usually necessary in clinical trials than in clinicalpractice.3,33

Patients with suspected but undiagnosed atrial fibrillationIn patients with suspected AF, a 12-lead ECG is recommended asthe first step to establish the diagnosis. Clinical symptoms such aspalpitations or dyspnoea should trigger ECG monitoring todemonstrate AF, or to correlate symptoms with the underlyingrhythm. There are only limited data comparing the value of differ-ent monitoring strategies.3,34 –37 More intense and prolongedmonitoring is justified in highly symptomatic patients [EuropeanHeart Rhythm Association IV (EHRA IV)—see Section 3.6],patients with recurrent syncope, and patients with a potential indi-cation for anticoagulation (especially after cryptogenic stroke).34,38

In selected patients, implantation of a leadless AF monitoringdevice may be considered to establish the diagnosis.39

Patients with known atrial fibrillationIndications for AF monitoring in patients with previously diagnosedAF differ compared with undiagnosed patients. When arrhythmia-or therapy-related symptoms are suspected, monitoring using

Holter recordings or external event recorders should be con-sidered. In patients with rhythm or rate control treatment andwithout further arrhythmia- or therapy-related symptoms, a12-lead ECG should be recorded at regular intervals. In patientsreceiving antiarrhythmic drug therapy, the frequency of 12-leadECG recording depends on the type of antiarrhythmic drug treat-ment, the potential side effects, complications, and risks ofproarrhythmia.

Tools for non-continuous ECG monitoringAvailable non-continuous ECG methods include scheduled orsymptom-activated standard ECGs, Holter (24 h to 7 days) moni-toring and transtelephonic recordings, patient- and automaticallyactivated devices, and external loop recorders. If AF is present atthe time of recording, use of the standard 12-lead ECG is sufficientto confirm the diagnosis. In paroxysmal AF, prolonged non-continuous recording will facilitate AF detection. It has been esti-mated that 7 day Holter ECG recording or daily andsymptom-activated event recordings may document the arrhyth-mia in !70% of AF patients, and that their negative predictivevalue for the absence of AF is between 30 and 50%.3 In stroke sur-vivors, a step-wise addition of five daily short-term ECGs, one 24 hHolter ECG, and another 7 day Holter ECG will each increase thedetection rate of AF by a similar extent.34

Tools for continuous ECG monitoringImplantable devices capable of intracardiac atrial electrogramrecording such as dual-chamber pacemakers and defibrillatorscan detect AF appropriately, particularly when an arrhythmia dur-ation ≥5 min is used as a cut-off value. Longer atrial high-rate epi-sodes (e.g. .5.5 h) may be associated with thrombo-embolic

‘Upstream’ therapy of concomitant conditions

Anticoagulation

Rate control

Antiarrhythmic drugs

Ablation

Cardioversion

silent paroxysmal persistent long-standingpersistent

permanent

first

docu

men

ted

AF

Figure 1 ‘Natural’ time course of AF. AF ¼ atrial fibrillation.The dark blue boxes show a typical sequence of periods in AFagainst a background of sinus rhythm, and illustrate the pro-gression of AF from silent and undiagnosed to paroxysmal andchronic forms, at times symptomatic. The upper bars indicatetherapeutic measures that could be pursued. Light blue boxesindicate therapies that have proven effects on ‘hard outcomes’in AF, such as stroke or acute heart failure. Red boxes indicatetherapies that are currently used for symptom relief, but may inthe future contribute to reduction of AF-related complications.Rate control (grey box) is valuable for symptom relief and mayimprove cardiovascular outcomes.

ESC Guidelines Page 9 of 61


Permanentă Persistentă Paroxistică

Durata


Consecintele FA. Implicatii terapeutice

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arrest, or atrioventricular block. Repeat oral pharmacological car-dioversion (‘pill-in-the-pocket’ therapy)67 may be appropriate forselected ambulatory patients once the safety of such an interven-tion has been established (see page 26). Several agents are availablefor pharmacological cardioversion (Table 12).

Flecainide given i.v. to patients with AF of short duration(especially ,24 h) has an established effect (67–92% at 6 h) onrestoring sinus rhythm. The usual dose is 2 mg/kg over 10 min.The majority of patients convert within the first hour after i.v.administration. It is rarely effective for termination of atrialflutter or persistent AF.

Oral administration of flecainide may be effective forrecent-onset AF. Recommended doses are 200–400 mg (seealso ‘pill-in-the-pocket’ approach). Flecainide should be avoidedin patients with underlying heart disease involving abnormal LVfunction and ischaemia.

Several placebo-controlled randomized studies have demon-strated the efficacy of propafenone in converting recent-onsetAF to sinus rhythm. Within a few hours, the expected conversionrate was between 41 and 91% after i.v. use (2 mg/kg over 10–20 min). The corresponding early conversion rates in placebo-treated patients were 10–29%. Propafenone has only a limitedefficacy for conversion of persistent AF and for atrial flutter.Similar to flecainide, propafenone should be avoided in patients

with underlying heart disease involving abnormal LV functionand ischaemia. In addition, owing to its weak b-blocking proper-ties, propafenone should be avoided in severe obstructive lungdisease. The time to conversion varies from 30 min to 2 h. Pro-pafenone is also effective if administered orally (conversionbetween 2 and 6 h).

Cardioversion with amiodarone occurs several hours laterthan with flecainide or propafenone. The approximate conversionrate at 24 h in placebo-treated patients was 40–60%, with anincrease to 80–90% after amiodarone treatment. In the shortand medium term, amiodarone does not achieve cardioversion.At 24 h the drug has demonstrated better effect compared withcontrol in some but not all randomized studies.

In patients with recent-onset AF, ibutilide in one or twoinfusions of 1 mg over 10 min each, with a wait of 10 minbetween doses, has demonstrated conversion rates within90 min of !50% in several well-designed randomized studies,placebo controlled or with a control group of drugs withknown little effect. The time to conversion is !30 min. Themost important side effect is polymorphic ventricular tachycar-dia, most often non-sustained, but DCC may be needed, andthe QTc interval is expected to increase by !60 ms. Ibutilideis, however, more effective for conversion of atrial flutterthan AF.

Table 12 Drugs and doses for pharmacological conversion of (recent-onset) AF

Drug Dose Follow-up dose Risks

Amiodarone 5 mg/kg i.v. over 1 h 50 mg/h Phlebitis, hypotension. Will slow the ventricular rate. Delayed AF conversion to sinus rhythm.

Flecainide 2 mg/kg i.v. over 10 min, or 200–300 mg p.o.

N/A Not suitable for patients with marked structural heart disease; may prolong QRS duration, and hence the QT interval; and may inadvertently increase the ventricular rate due to conversion to atrial flutter and 1:1 conduction to the ventricles.

Ibutilide 1 mg i.v. over 10 min

1 mg i.v. over 10 min after waiting for 10 min

Can cause prolongation of the QT interval and torsades de pointes; watch for abnormal T-U waves or QT prolongation. Will slow the ventricular rate.

Propafenone 2 mg/kg i.v. over 10 min, or 450–600 mg p.o.

Not suitable for patients with marked structural heart disease; may prolong QRS duration; will slightly slow the ventricular rate, but may inadvertently increase the ventricular rate due to conversion to atrial flutter and 1:1 conduction to the ventricles.

Vernakalant 3 mg/kg i.v. over 10 min

Second infusion of 2 mg/kg i.v. over 10 min after15 min rest

So far only evaluated in clinical trials; recently approved. 68–70 a

aVernakalant has recently been recommended for approval by the European Medicines Agency for rapid cardioversion of recent-onset AF to sinus rhythm in adults (≤7 days fornon-surgical patients; ≤3 days for surgical patients).68,69 A direct comparison with amiodarone in the AVRO trial (Phase III prospective, randomized, double-blind,Active-controlled, multi-center, superiority study of Vernakalant injection versus amiodarone in subjects with Recent Onset atrial fibrillation), vernakalant was more effective thanamiodarone for the rapid conversion of AF to sinus rhythm (51.7% vs. 5.7% at 90 min after the start of treatment; P , 0.0001).70 It is to be given as an initial i.v. infusion (3 mg/kgover 10 min), followed by 15 min of observation and a further i.v. infusion (2 mg/kg over 10 min), if necessary. Vernakalant is contraindicated in patients with systolic bloodpressure ,100 mm Hg, severe aortic stenosis, heart failure (class NYHA III and IV), ACS within the previous 30 days, or QT interval prolongation. Before its use, the patientsshould be adequately hydrated. ECG and haemodynamic monitoring should be used, and the infusion can be followed by DCC if necessary. The drug is not contraindicated inpatients with stable coronary artery disease, hypertensive heart disease, or mild heart failure. The clinical positioning of this drug has not yet been determined, but it is likely to beused for acute termination of recent-onset AF in patients with lone AF or AF associated with hypertension, coronary artery disease, or mild to moderate (NYHA class I– II) heartfailure.ACS ¼ acute coronary syndrome; AF ¼ atrial fibrillation; DCC ¼ direct current cardioversion; i.v. ¼ intravenous; N/A ¼ not applicable; NYHA, New York Heart Association;p.o. ¼ per os; QRS ¼ QRS duration; QT ¼ QT interval; T-U ¼ abnormal repolarization (T-U) waves.



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Riscul de AVC in FA: CHADS2

"   Elemente scorului CHADS2:

"   Insuficienta cardiaca congestiva: 1 pt

"   Hipertensiune: 1 pt

"   Varsta: 1 pt

"   Diabet: 1 pt

"   AVC sau AIT: 2 pt

Rockson SG, Albers GW. JACC 2004;43:929.


Risc AVC in FA: CHA2DS2-VASc

(range, 2.0–3.0), unless contraindicated. Such a practice appears totranslate to better outcomes in AF patients in routine care.10,51

As shown in Table 7, there is a clear relationship betweenCHADS2 score and stroke rate.50 The original validation of thisscheme classified a CHADS2 score of 0 as low risk, 1–2 as mod-erate risk, and .2 as high risk.

The Stroke in AF Working Group performed a comparison of12 published risk-stratification schemes to predict stroke inpatients with non-valvular AF, and concluded that there were sub-stantial, clinically relevant differences among published schemesdesigned to stratify stroke risk in patients with AF. Most hadvery modest predictive value for stroke (c-statistics—as ameasure of the predictive value—of !0.6); also, the proportionof patients assigned to individual risk categories varied widelyacross the schemes. The CHADS2 score categorized most subjectsas ‘moderate risk’ and had a c-statistic of 0.58 to predict stroke inthe whole cohort.

In the present guidelines, we have tried to de-emphasize the useof the ‘low’, ‘moderate’, and ‘high’ risk categorizations, given thepoor predictive value of such artificial categories, and recognizethat risk is a continuum. Thus, we encourage a risk factor-basedapproach for more detailed stroke risk assessment, recommendingthe use of antithrombotic therapy on the basis of the presence (orabsence) of stroke risk factors.

Support for this approach comes from various published ana-lyses, where even patients at ‘moderate risk’ (currently definedas CHADS2 score ¼ 1, i.e. one risk factor) still derive significantbenefit from OAC over aspirin use, often with low rates ofmajor haemorrhage. Importantly, prescription of an antiplateletagent was not associated with a lower risk of adverse events.Also, the CHADS2 score does not include many stroke riskfactors, and other ‘stroke risk modifiers’ need to be consideredin a comprehensive stroke risk assessment (Table 8).

‘Major’ risk factors (previously referred to as ‘high’ riskfactors) are prior stroke or TIA, or thrombo-embolism, andolder age (≥75 years). The presence of some types of valvularheart disease (mitral stenosis or prosthetic heart valves) wouldalso categorize such ‘valvular’ AF patients as ‘high risk’.

‘Clinically relevant non-major’ risk factors (previouslyreferred to as ‘moderate’ risk factors) are heart failure [especiallymoderate to severe systolic LV dysfunction, defined arbitrarily asleft ventricular ejection fraction (LVEF) ≤40%], hypertension, ordiabetes. Other ‘clinically relevant non-major’ risk factors (pre-viously referred to as ‘less validated risk factors’) include femalesex, age 65–74 years, and vascular disease (specifically, myocardialinfarction, complex aortic plaque and PAD). Note that risk factorsare cumulative, and the simultaneous presence of two or more‘clinically relevant non-major’ risk factors would justify a strokerisk that is high enough to require anticoagulation.

This risk factor-based approach for patients with non-valvularAF can also be expressed as an acronym, CHA2DS2-VASc [con-gestive heart failure, hypertension, age ≥75 (doubled), diabetes,stroke (doubled), vascular disease, age 65–74, and sex category(female)].52 This scheme is based on a point system in which 2points are assigned for a history of stroke or TIA, or age ≥75;and 1 point each is assigned for age 65–74 years, a history ofhypertension, diabetes, recent cardiac failure, vascular disease

(myocardial infarction, complex aortic plaque, and PAD, includingprior revascularization, amputation due to PAD, or angiographicevidence of PAD, etc.), and female sex (Table 8). Thus, thisacronym extends the CHADS2 scheme by considering additionalstroke risk factors that may influence a decision whether or notto anticoagulate (see Section 4.1.1).

Table 8 CHA2DS2VASc score and stroke rate

(a) Risk factors for stroke and thrombo-embolism in non-valvular AF

‘Major’ risk factors ‘Clinically relevant non-major’risk factors

Previous stroke, TIA, or systemic embolism

Age > 75 years

Heart failure or moderate to severe LV systolic dysfunction

(e.g. LV EF < 40%)Hypertension - Diabetes mellitus

Female sex - Age 65–74 yearsVascular diseasea

(b) Risk factor-based approach expressed as a point based scoring system, with the acronym CHA2DS2-VASc

(Note: maximum score is 9 since age may contribute 0, 1, or 2 points)

Risk factor Score

Congestive heart failure/LV dysfunction 1

Hypertension 1

Age >75 2

Diabetes mellitus 1

Stroke/TIA/thrombo-embolism 2

Vascular diseasea 1

Age 65–74 1

Sex category (i.e. female sex) 1

Maximum score 9

(c) Adjusted stroke rate according to CHA2DS2-VASc score

CHA2DS2-VAScscore

Patients (n = 7329) Adjusted stroke rate (%/year)b

0 1 0%

1 422 1.3%

2 1230 2.2%

3 1730 3.2%

4 1718 4.0%

5 1159 6.7%

6 679 9.8%

7 294 9.6%

8 82 6.7%

9 14 15.2%

See text for definitions.aPrior myocardial infarction, peripheral artery disease, aortic plaque. Actual ratesof stroke in contemporary cohorts may vary from these estimates.bBased on Lip et al.53

AF ¼ atrial fibrillation; EF ¼ ejection fraction (as documented byechocardiography, radionuclide ventriculography, cardiac catheterization, cardiacmagnetic resonance imaging, etc.); LV ¼ left ventricular;TIA ¼ transient ischaemic attack.


(range, 2.0–3.0), unless contraindicated. Such a practice appears totranslate to better outcomes in AF patients in routine care.10,51

As shown in Table 7, there is a clear relationship betweenCHADS2 score and stroke rate.50 The original validation of thisscheme classified a CHADS2 score of 0 as low risk, 1–2 as mod-erate risk, and .2 as high risk.

The Stroke in AF Working Group performed a comparison of12 published risk-stratification schemes to predict stroke inpatients with non-valvular AF, and concluded that there were sub-stantial, clinically relevant differences among published schemesdesigned to stratify stroke risk in patients with AF. Most hadvery modest predictive value for stroke (c-statistics—as ameasure of the predictive value—of !0.6); also, the proportionof patients assigned to individual risk categories varied widelyacross the schemes. The CHADS2 score categorized most subjectsas ‘moderate risk’ and had a c-statistic of 0.58 to predict stroke inthe whole cohort.

In the present guidelines, we have tried to de-emphasize the useof the ‘low’, ‘moderate’, and ‘high’ risk categorizations, given thepoor predictive value of such artificial categories, and recognizethat risk is a continuum. Thus, we encourage a risk factor-basedapproach for more detailed stroke risk assessment, recommendingthe use of antithrombotic therapy on the basis of the presence (orabsence) of stroke risk factors.

Support for this approach comes from various published ana-lyses, where even patients at ‘moderate risk’ (currently definedas CHADS2 score ¼ 1, i.e. one risk factor) still derive significantbenefit from OAC over aspirin use, often with low rates ofmajor haemorrhage. Importantly, prescription of an antiplateletagent was not associated with a lower risk of adverse events.Also, the CHADS2 score does not include many stroke riskfactors, and other ‘stroke risk modifiers’ need to be consideredin a comprehensive stroke risk assessment (Table 8).

‘Major’ risk factors (previously referred to as ‘high’ riskfactors) are prior stroke or TIA, or thrombo-embolism, andolder age (≥75 years). The presence of some types of valvularheart disease (mitral stenosis or prosthetic heart valves) wouldalso categorize such ‘valvular’ AF patients as ‘high risk’.

‘Clinically relevant non-major’ risk factors (previouslyreferred to as ‘moderate’ risk factors) are heart failure [especiallymoderate to severe systolic LV dysfunction, defined arbitrarily asleft ventricular ejection fraction (LVEF) ≤40%], hypertension, ordiabetes. Other ‘clinically relevant non-major’ risk factors (pre-viously referred to as ‘less validated risk factors’) include femalesex, age 65–74 years, and vascular disease (specifically, myocardialinfarction, complex aortic plaque and PAD). Note that risk factorsare cumulative, and the simultaneous presence of two or more‘clinically relevant non-major’ risk factors would justify a strokerisk that is high enough to require anticoagulation.

This risk factor-based approach for patients with non-valvularAF can also be expressed as an acronym, CHA2DS2-VASc [con-gestive heart failure, hypertension, age ≥75 (doubled), diabetes,stroke (doubled), vascular disease, age 65–74, and sex category(female)].52 This scheme is based on a point system in which 2points are assigned for a history of stroke or TIA, or age ≥75;and 1 point each is assigned for age 65–74 years, a history ofhypertension, diabetes, recent cardiac failure, vascular disease

(myocardial infarction, complex aortic plaque, and PAD, includingprior revascularization, amputation due to PAD, or angiographicevidence of PAD, etc.), and female sex (Table 8). Thus, thisacronym extends the CHADS2 scheme by considering additionalstroke risk factors that may influence a decision whether or notto anticoagulate (see Section 4.1.1).

Table 8 CHA2DS2VASc score and stroke rate

(a) Risk factors for stroke and thrombo-embolism in non-valvular AF

‘Major’ risk factors ‘Clinically relevant non-major’risk factors

Previous stroke, TIA, or systemic embolism

Age > 75 years

Heart failure or moderate to severe LV systolic dysfunction

(e.g. LV EF < 40%)Hypertension - Diabetes mellitus

Female sex - Age 65–74 yearsVascular diseasea

(b) Risk factor-based approach expressed as a point based scoring system, with the acronym CHA2DS2-VASc

(Note: maximum score is 9 since age may contribute 0, 1, or 2 points)

Risk factor Score

Congestive heart failure/LV dysfunction 1

Hypertension 1

Age >75 2

Diabetes mellitus 1

Stroke/TIA/thrombo-embolism 2

Vascular diseasea 1

Age 65–74 1

Sex category (i.e. female sex) 1

Maximum score 9

(c) Adjusted stroke rate according to CHA2DS2-VASc score

CHA2DS2-VAScscore

Patients (n = 7329) Adjusted stroke rate (%/year)b

0 1 0%

1 422 1.3%

2 1230 2.2%

3 1730 3.2%

4 1718 4.0%

5 1159 6.7%

6 679 9.8%

7 294 9.6%

8 82 6.7%

9 14 15.2%

See text for definitions.aPrior myocardial infarction, peripheral artery disease, aortic plaque. Actual ratesof stroke in contemporary cohorts may vary from these estimates.bBased on Lip et al.53

AF ¼ atrial fibrillation; EF ¼ ejection fraction (as documented byechocardiography, radionuclide ventriculography, cardiac catheterization, cardiacmagnetic resonance imaging, etc.); LV ¼ left ventricular;TIA ¼ transient ischaemic attack.


a CHA2DS2-VASc score of 1) may consider aspirin rather thanOAC therapy.

4.1.4. Risk of bleedingAn assessment of bleeding risk should be part of the patient assess-ment before starting anticoagulation. Despite anticoagulation ofmore elderly patients with AF, rates of intracerebral haemorrhageare considerably lower than in the past, typically between 0.1 and0.6% in contemporary reports. This may reflect lower anticoagula-tion intensity, more careful dose regulation, or better control ofhypertension. Intracranial bleeding increases with INR values.3.5–4.0, and there is no increment in bleeding risk with INRvalues between 2.0 and 3.0 compared with lower INR levels.

Various bleeding risk scores have been validated for bleedingrisk in anticoagulated patients, but all have different modalities inevaluating bleeding risks and categorization into low-, moderate-,and high-risk strata, usually for major bleeding risk. It is reasonableto assume that the major bleeding risk with aspirin is similar to thatwith VKA, especially in elderly individuals.56 The fear of falls may beoverstated, as a patient may need to fall !300 times per year forthe risk of intracranial haemorrhage to outweigh the benefit ofOAC in stroke prevention.

Using a ‘real-world’ cohort of 3978 European subjects with AFfrom the EuroHeart Survey, a new simple bleeding risk score,HAS-BLED (hypertension, abnormal renal/liver function, stroke,bleeding history or predisposition, labile INR, elderly (.65),drugs/alcohol concomitantly), has been derived (Table 10).60 Itwould seem reasonable to use the HAS-BLED score to assessbleeding risk in AF patients, whereby a score of ≥3 indicates

‘high risk’, and some caution and regular review of the patient isneeded following the initiation of antithrombotic therapy,whether with VKA or aspirin.

† Congestive heart failure,Hypertension. Age > 75 yearsDiabetes.Stroke/TIA/thrombo-embolism(doubled)

*Other clinically relevantnon-major risk factors:age 65–74, female sex, vascular disease

eA

rorr

llyk

mase

CHADS2 score > 2†

OAC

OAC (or aspirin)

Nothing (or aspirin)

Age >75 years

>2 other risk factors*

1 other risk factor*

Yes

Yes

Yes

Yes

No

No

No

NoConsider other risk factors*

Figure 4 Clinical flowchart for the use of oral anticoagulation for stroke prevention in AF. AF ¼ atrial fibrillation; OAC ¼ oral anticoagulant;TIA ¼ transient ischaemic attack. A full description of the CHADS2 can be found on page 13.

Table 10 Clinical characteristics comprising theHAS-BLED bleeding risk score

Letter Clinical characteristica Points awarded

H Hypertension 1

A Abnormal renal and liver function (1 point each) 1 or 2

S Stroke 1

B Bleeding 1

L Labile INRs 1

E Elderly (e.g. age >65 years) 1

D Drugs or alcohol (1 point each) 1 or 2

Maximum 9 points

aHypertension’ is defined as systolic blood pressure .160 mmHg. ‘Abnormalkidney function’ is defined as the presence of chronic dialysis or renaltransplantation or serum creatinine ≥200 mmol/L. ‘Abnormal liver function’ isdefined as chronic hepatic disease (e.g. cirrhosis) or biochemical evidence ofsignificant hepatic derangement (e.g. bilirubin .2 x upper limit of normal, inassociation with aspartate aminotransferase/alanine aminotransferase/alkalinephosphatase .3 x upper limit normal, etc.). ‘Bleeding’ refers to previous bleedinghistory and/or predisposition to bleeding, e.g. bleeding diathesis, anaemia, etc.‘Labile INRs’ refers to unstable/high INRs or poor time in therapeutic range (e.g.,60%). Drugs/alcohol use refers to concomitant use of drugs, such as antiplateletagents, non-steroidal anti-inflammatory drugs, or alcohol abuse, etc.INR ¼ international normalized ratio. Adapted from Pisters et al.60



Recomandarile de tratament anti-trombotic in functie de profilul de risc in FiA (ACCP/VII)

Nivel de risc Indicatorii riscului Tratament Risc scazut varsta ≤ 65 ani Aspirina 325 mg/zi

fara FR aditionali

Intermediar Varsta 65-75 ani ACO (INR: 2,0-3,0)

DZ sau ASA

B coronara

Inalt Varsta > 75 ani ACO (INR: 2,0-3,0)

Istoric de AVC, AIT sau ES

HTA, DZ

Disfunctie VS sau ICC


TAHIARITMIILE

VENTRICULARE

Tahiaritmii cu QRS larg


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Myerburg et al. Am J Cardiol 1984;54:1355-8.


Clasificare si semnificatie clinica

Morganroth et al. JACC 1986.

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Tratamentul ESV W  �-0��7ID@9H9��.0(-�5G=ADHCA5H=79��β�6@C75BH9��

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Studiul CAST-I: cresterea mortalitatii sub AA clasa I la pacienti cu IM in

antecedente


TV: definitie si caractere ECG

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Mecanismele TV

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TV monomorfa: diagnostic

•  tahiaritmie regulata >

120/�

•  QRS larg > 120 msec

•  Disociatie AV

•  Batai de fuziune

•  Capturi ventriculare

• Criterii morfologice


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Tahicardia ventriculara neparoxistica (RIVA) =

AUTOMATISM CRESCUT


TV polimorfa: torsada varfurilor PDP

•  TV rapida, degenereaza in FV

•  produsa prin PDP

•  cu QT lung sau cu QT normal

•  Cauze:

•  sdr. de QT lung

•  hipo K, hipo Mg

•  AA Ia si III

•  Tratament:

•  MgSO4 IV

•  “Overdrive pacing”

•  isuprel lent

•  xilina, fenitoina

•  QT lung: AICD, beta-blocante,

flecainida, stelectomie.


Dg ≠ TV vs. TSV cu QRS largi

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Tratament TV W  .0�:5F5�897CAD9BG5F9�<9AC8=B5A=75��

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Oprirea TV prin �overdrive pacing�


Tratamentul profilactic al TV

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Fibrilatia ventriculara •  Unde fibrilatorii de amplitudine diferita, in absenta

complexelor QRS •  Asistola mecanica urmata de asistola electrica •  Colaps, stop respirator si deces in 3-5 minute de la

instalare in absenta CPR •  Cauze:

–  Ischemia acuta din IMA aritmii V spontane severe

–  Cardiomiopatii (CMHO !) FA din WPW –  CHT cu HVS hipoxia din BPOC –  Iatrogen: medicamente, diselectrolitemii, cateterism cardiac –  Sdr. de QT lung cu TdP SEE nesincron

•  Precedata sau nu de TV •  Tratament:

–  SEE 200-300 J CPR, IOT –  Bicarbonat EV daca CPR > 60 sec Lidocaina,

bretiliu, amiodaron EV –  Corectarea cauzei

•  Profilactic: DI sau amiodaron


Tratamentul aritmiilor V maligne: defibrilatorul implantabil

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•  CMH

•  CAVD

•  LQT

•  Brugada

•  SQT

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Documents

13.Tahiaritmii