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8/20/2019 01 Dadang How to Detect and Treat ATrial Fibrilasi_dr. Dadang (1) - Copy
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How to detect and
treat
ATRIAL
FIBRILLATION
Dr Dadang Hendrawan SpJP(K)
Bagian Kardio logi & Kedokteran Vaskuler
FK. Unibraw –RSU Dr. Sai fu l Anw ar M A L A N G
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Atrial Fibrillation
AF is a supraventricular tachyarrhythmiacharacterized by uncoordinated atrial activationwith consequent deterioration of atrialmechanical function ( ACC / AHA / ESC Guideline 2006 )
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Characteristics of an ECG recording
for a patient with AFNormal sinus rhythm
Atrial fibrillationT
P
R
• An ECG of a patient with AF is characterized by disorganized electrical
activity:
1. Consistent P waves are replaced by rapid irregular waves
2. Irregular R–R intervals
12
Fuster et al , Circulation 2011; Camm et al, Eur Heart J 2010
SQ
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Background
• Atrial fibrillation is the most commonsustained arrhythmia
• Affects 2 million Americans
• 6% over the a e of 65 ex erience it
• Responsible for 15% strokes
Benjamin E: Epidemiology of Atrial Fibrillation. In Falk RH, Podrida PJ, eds:Atrial Fibrillation: Mechanisms and Management.2nd Ed, Lippincott-Raven Press, New York 1997, pp.1-22.
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Atrial Fibrillation Demographics by Age
U.S. population
Population with
atrial fibrillation
U.S. population
x 1000
Population with AF
x 1000
30,000 500
400
Adapted from Feinberg WM. Arch Intern Med. 1995;155:469-473.
Age, yr
95
20,000
10,000
0
300
200
100
0
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Atrial fibrillation accounts
18%
Unspecified
6%
PSVT6%
PVCs
4%
Atrial
Flutter
for 1/3 of all patient
dischargeswith arrhythmia as
principal diagnosis.
2%VF
Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.
34%
Atrial
Fibrillation
9%
SSS
8%Conduction
Disease
3% SCD
10% VT
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Classification
• After 2 or more episodes, AF is considered recurrent AF .• If the arrhythmia terminates spontaneously, recurrent AF is
designated paroxysmal AF
• When sustained beyond 7 d, it is termed persistent AF .
• -standing AF (e.g., longer than 1 y), usually leading to
permanent AF
• Lone AF applies to individuals younger than 60 y without
clinical or echocardiographic evidence of cardiopulmonarydisease, including hypertension.
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AF can be symptomatic
and asymptomatic• Typical symptoms of AF include palpitations, fatigue, chest pain, light
headedness, dyspnoea, syncope1
• However, AF may be asymptomatic2
– Patients (n=110) with history of AF underwent ECG monitoring with implantable
pacemaker
for 19±11 months2
• 50 patients had AF episodes lasting >48 hours
• 19 (38%) of these were asymptomatic, with no AF detected by serial ECG recordings
1. Fuster et al , Circulation 2011; 2. Israel et al , J Am Coll Cardiol 2004
Baseline FU1 FU2 FU3 FU4 FU5 FU6 FU7 FU8 FU9 FU10 FU11 FU12 FU13
N o o
f p a t i e n t s
110
20
15
10
5
Cumulative incidence of asymptomatic AF recurrence >48 hours not detected by serialECG recordings during follow-up (FU)
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Pathophysiology
• “Focal” triggering mechanism involving automaticity
• Multiple reentrant wavelets
• These mechanisms are not mutually exclusive and may coexist
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Presentation
• History
• Physical Examination
• ECG
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• Endocrine disordes
• Changes in autonomic tone
• Primary or metastatic disease in or adjacent to
Etiologies and Factors Predisposing
Patients to AF
• Postoperative
• Congenital heart disease
• Neurogenic
• Idiopathic (lone AF)
• Familial AF
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Minimun evaluation
1. History and physical examination. to define
2. Electrocardiogram. to identify
. rans orac c ec ocar ogram. o en y
4. Blood test of thyroid, renal and hepatic
function
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Additional Testing
One or several tests may be necessary :
1. Six-minute walk test
2. Exercise testing
3. Holter monitorin or event recordin 4. Transesophageal echocardiograpy
5. Electrophysiological study
6. Chest radiograph. to evaluate
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Objectives
• Rate Control
• Prevention of thromboembolism
• rhythm
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Rate control VS Rhythm control
• Two landmark studies published (AFFIRM) and (RACE)
trials, found that treating atrial fibrillation (AF) with a rhythm
control strategy offers no survival or clinical advantages
over simpler rate control therapy using medications
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Rate Control
• Rate control may be reasonable initial therapy in older
patients with persistent AF who have hypertension or
heart disease
• The definition of ade uate rate control has been
based primarily on short-term hemodynamic benefits
and not well studied with respect to regularity or
irregularity of the ventricular response to AF, quality of
life, symptoms,or development of cardiomyopathy.
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• Criteria for rate control vary with patient age but
usually
– ventricular rates 60 - 80 beats/m at rest – between 90 and 115 beats/m during moderate exercise
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• Rate Control
• Prevention of thromboembolism
rhythm
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20
15
Risk
Factor Points
Congestive 1
Key Risk Factors: CHADS2 Score Helps
Predict Stroke Risk in Patients With AF
10
5
00 1 2 3 4 5
6
CHADS2 score
ear a ure
Hypertension 1
Age > 75 1
Diabetes 1
Prior stroke/
TIA 2
ACC / AHA / ESC Guideline 2006
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ACCF/AHA/HRS 2011 and ACCP
2008 guidelines: based on CHADS2CHADS2 scoring
1
• CHF +1
• Hypertension +1
• Age ≥75 years +1
• Diabetes mellitus +1
•
1. Gage et al , JAMA 2001; 2. Singer et al , Chest 2008; 3. Fuster et al , Circulation 2011
Recommended therapy
CHADS2score
ACCP
20082ACCF/AHA/HRS
20113
0 ASA
75–325 mg/day
ASA
81–325 mg/day
1 VKA (INR 2–3) or
ASA 75–325 mg/day
VKA (INR 2–3) or
ASA 81–325 mg/day
≥2 VKA (INR 2–3) VKA (INR 2–3)
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ESC 2010 guidelines: based on
CHADS2 and CHA2DS2-VASc• CHF/LV dysfunction +1
• Hypertension +1
• Age ≥75 years +2
• Diabetes mellitus
+1
• Prior Stroke/TIA/TE +2
• Vascular disease +1
• –
• Initial evaluation: CHADS2
• If CHADS2 ≥2 oral anticoagulation
• If CHADS2
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VKA limitations
• Significant inter- and intra-patient variability in doseresponse1 due to:
– Co-morbidities
– Genetic polymorphisms
– Interactions with food and concomitant drugs
– npre c a e p armaco ogy
• Narrow therapeutic window1
– Regular coagulation monitoring and dose adjustments
required
– Increased risk of stroke or bleeding outside the INR range2
1. Ansell et al , Chest 2008; 2. Nieuwlaat et al , Am Heart J 2007
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Newer oral anticoagulants for stroke
prevention in AF: clinical trial
overviewOral anticoagulant Phase II studies Phase III studies
Direct thrombin inhibitors
Dabigatran PETRO1 RE-LY2,3
RELY-ABLE4
Direct Factor Xa inhibitors
varoxa an J-ROCKET AF6
Apixaban Phase II safety (Japan)7 ARISTOTLE8
AVERROES9
AVERROES-LTOLE10
Edoxaban Phase II dose-finding11
Phase II safety (Asia)
12
ENGAGE AF-TIMI 4813
Studies in yellow are complete, the others are ongoing
1. Ezekowitz et al , Am J Cardiol 2007; 2. Connolly et al , N Engl J Med 2009; 3. Connolly et al , N Engl J Med 2010;
4. clinicaltrials.gov, NCT00808067; 5. Patel et al , N Engl J Med 2011; 6. Hori et al , J Thromb Haemost 2011;
7. Ogawa et al , Circ J 2011; 8. Granger et al , N Engl J Med 2011; 9. Connolly et al , N Engl J Med 2011;
10. clinicaltrials.gov, NCT00496769; 11. Weitz et al , Thromb Haemost 2010; 12. Chung et al , Thromb Haemost 2011;
13. Ruff et al , Am Heart J 2010
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Rivaroxaban
20 mg once daily**
N=14,264
ROCKET AF: rivaroxaban vs
warfarinRandomized, double-blind, double-dummy, non-inferiority,
event-driven trial
Non-valvular AF
History of stroke,TIA or non-CNSSE
- u p
d y
Warfarin target INR 2.5
(2–3 inclusive)
*Enrolment of patients with
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ROCKET AF: primary efficacy
endpoint
Population/
analysis*
No. of
patients
Rivaroxaban
(% per year)
Warfarin
(% per
year)
Hazard
ratio
(95% CI)
p -value
Non-
inferiority Superiority
Per-protocol,
on-treatment
6958 1.7 2.2 0.79
(0.66–0.96)
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