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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