cardiac resynchronization and defibrillation therapies: complementary approaches to the management...

Cardiac Resynchronizationand Defibrillation

Therapies:Complementary Approaches

to the Managementof Heart Failure

Ventricular Resynchronization

Pathophysiology and Identification of Responders

Mechanisms of Dysfunction Dueto Contractile Discoordination

Reduced ejection volume

– Internal sloshing of cavitary blood volume from prematurely activated region to late-activated one

– Increased end-systolic volume (stress) Mechano-energetic inefficiency

– Reduced systolic function despite maintained or increasedenergetic expenditure

Late systolic stretch

– Cross-bridge detachment, reduced contractility

– Delayed relaxation

– After-contraction/arrhythmia Mitral valve dysfunction

– Papillary muscle discoordination

Kass DA. Rev Cardiovasc Med. 2003;4(suppl 2):S3-S13.

A

Impact of Mechanical Dyssynchrony

Adapted from Kass DA. Rev Cardiovasc Med. 2003;4(suppl 2):S3-S13.Adapted from Leclercq C, et al. Circulation. 2001;106:1760-1763.

MRI-Tagged 3-D Cine-Imaging

Disparities in Regional WorkloadResulting From Dyssynchrony

Adapted from Kass DA. Rev Cardiovasc Med. 2003;4(suppl 2):S3-S13.

Fiber Strain

Early Activated Late Activated20

0-0.1 0.10.0

20

0-0.1 0.10.0

Area = Regional Work

Regional Blood Flow

Glucose Metabolism

Fib

er S

tres

s

Fib

er S

tres

s

Discoordinate Motion

Normal Sinus Rhythm

30 60 90

0

40

LV Volume (mL)

80

Acute Dyssynchrony (RV Pace)L

V P

ress

ure

(m

m H

g)


Adverse Effects on Global Function From RV-Pacing–Induced Dyssynchrony

Do We ResynchronizeWith Biventricular

or Left Ventricular Pacing?

CRT Enhances Cardiac Mechano-Energetic Efficiency

LV pacingDobutamine

P< 0.05

MV

O2/

HR

Adapted from Nelson GS, et al. Circulation. 2000;102:3053-3059.

*P< 0.01†P< 0.05Mean ±SEM

.24

40

20

0

-20

† †

*

*

dP/dtmax PP MeanCorF

AVO2 MVO2

.22

.20

.18

.16

.14500 600 700 800 900 1000

dP/dtmax (mm Hg)

(Rel

ativ

e U

nit

s)

Ch

ang

e (%

)

Single-Site LV PacingWorks Just as Well

LV Free Wall per CirculationBiventricular

LV Volume (mL) LV Volume (mL)

0 300200100 0 300200100

120

80

40

0

120

80

40

0


LV

Pre

ssu

re (

mm

Hg

)

LV

Pre

ssu

re (

mm

Hg

)

Regional Wall Motion With CRT

Septum

Lateral

Pacing OffPacing On

Reg

ion

al F

ract

ion

al A

rea

Ch

ang

e

Seconds 0.40

Seconds 0.40


Adapted from Kawaguchi M, et al. J Am Coll Cardiol. 2002;39:2052-2058.

Global Chamber Effects of CRT:Acute Human Studies

0.0 2.8 5.6 8.4 11.2

1151.0

870.0

113.0

0.4

114.0

54.7

1193.0

-841.0

Pacing ON Pacing OFF

0.0 2.5 5.0 7.5 10.0Seconds

1151.0

865.0

113.0

1.0

114.0

50.8

1120.0

-727.0

Seconds

2-Min Steady State

LV

Pre

ssu

re (

mm

Hg

)

LV

PA

OP

dP

/dt

LV Volume (mL)

120

80

40

0

0 300200100Adapted from Kass DA. Rev Cardiovasc Med. 2003;4(suppl 2):S3-S13.

LV

PA

OP

dP

/dt

Ventricular Reverse RemodelingWith Resynchronization

Adapted from Abraham WT, et al. N Engl J Med. 2002;346:1845-1853.

En

d-D

iast

olic

Dim

ensi

on

(m

m)

Eje

ctio

n F

ract

ion

(%

)6.0

6.5

7.5

10

20

P<0.001

Placebon=81

CRTn=63

CRTn=61

P<0.001

Placebon=63

30

CRT 6-monthControl 6-month CRT

How Important Are Pacing Site, Atrioventricular Delay,

and Ventricular to Ventricular Delay?

AV Interval Optimization

Adapted from Auricchio A, et al. Circulation. 1999;99:2993-3001.

AV delay(0 to PR – 30 msec)

AV delay(0 to PR – 30 msec)

LVBV

Ch

ang

e in

Ao

rtic

PP

(%

)

Ch

ang

e in

dP

/dt m

ax (

%)

24

18

12

6

0

-12

-6

16

12

8

4

0

-8

-41 1

LVBV

Synchronous vs Non-Synchronous BV Pacing: Is RV-LV Delay Important?

* P<0.01 vs. Simultaneous (s)Sogaard P, et al. Circulation. 2002;106:2078-2084.

RV Preactivation S LV PreactivationSys

toli

c F

un

ctio

n (

Ech

o I

nd

ex) * *

6

5

4

3

2

1

0

Can We Predict Responders?

Wide QRS complex– Widely used, but only broadly correlates with acute response

– Weak predictor of chronic response

Mechanical dyssynchrony– More direct target of CRT

– Measures of wall dyssynchrony (MRI, ECHO, TDI) best correlate with acute and chronic responsiveness

Basal dysfunction– Low contractile state and marked P-R delay are likely additional

features of responders


Ch

ang

e in

dP

/dt m

ax

(%)

QRS (msec)

QRS duration is only weakly correlated with acute

improvement1,2

However, change in QRS duration does not correlate with acute

improvement2

1. Adapted from Auricchio A, et al. Circulation. 1999;99:2993-3001.2. Nelson GS, et al. Circulation. 2000;101:2703-2709.

0

20

40

60

100 150 250200

Surface QRS (msec)

r =0.51

QRS as a Predictor of Response

100

75

50

25

0

-25-50 -30 50-10 0 10 30

%

Ch

ang

e in

dP

/dt m

ax

(%)

More Direct Methodsto Assess Dyssynchrony

Interventricular delay– RV/LV pressure plot (area in loop)

– Interventricular delay

– QRS onset-pulmonary flow onset – QRS onset-aortic flow onset >25 msec

Intraventricular delay– Strain rate TDI

– M-mode ECHO

– Echo contrast analysis

– QRS onset-end lateral wall contraction >290 msec

– QRS onset-end lateral wall contraction >QRS onset-mitral E-wave onset


M-mode Echo Assessmentfor Predicting Responders

Adapted from Pitzalis MV, et al. J Am Coll Cardiol. 2002;40:1615-1622.

D 20 60 380140 220 300

SPWMD (msec)

r =-.70P=.001

+20

0

-20

-40

-60

-80

-100

LV

ES

VI

(mL

/m2)

TDI Assessmentfor Predicting Responders

Adapted from Sogaard P, et al. J Am Coll Cardiol. 2002;40:723-730.

Percentage of LV Base With DLC-40

0

-20

20

40

60

80

20 40 60 80Ch

ang

e i

n L

VE

F (

%)

Potential Causesfor Lack of Response

Poor lead placement– Site matters; lateral placement is usually better

Improper setting of AV delay– Loss of preexcitation; suboptimal atrial filling,

exacerbation of mitral regurgitation

Infarcted underlying substrate– Cannot be stimulated and thus cannot be

resynchronized


Summary

Cardiac dyssynchrony reduces net systolic function and energetic efficiency, inducing marked regional heterogeneity of wall stress and molecular signaling

CRT is most effective if targeted to hearts with discoordinate contraction, rather than QRS widening

In appropriate patients, improvement in systolic functionand energetics from CRT can be marked

Defining intraventricular mechanical dyssynchronyseems at present to be the most reliable variable for predicting responders—but more work is needed to define the most reliable dyssynchrony measurement and test its prospective utility

Pathophysiologyof Congestive Heart Failure

Heart Failure

Heart failure is a clinical syndrome (ie, there are signs and symptoms) characterized in most patients by dyspnea and fatigue at rest and/or with exertion caused by underlying structural and/or functional heart disease

Francis GS, Tang WH. Rev Cardiovasc Med. 2003;4(suppl 2):S14-20.

Congestive Heart FailureScope of the Problem

Nearly 900,000 annual hospital admissions (increased 90% in past 10 years)1

Most common discharge diagnosis for patients olderthan 65 years2

6.5 million hospital days per year1

Single largest expense for Medicare1

Annual hospital/nursing home costs: $15.4 billion3

1. Hunt SA, et al. ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult. 2001. 2. Graves EJ, Gillum BS. 1994 Summary: National Hospital Discharge Survey. National Center for Health Statistics; 1996.3. AHA. 2002 Heart and Stroke Statistical Update; 2001.

Heart Failure Hospitalizations

The Number of Heart Failure Hospitalizations Is Increasing in Both Men and Women

CDC/NCHS: hospital discharges include patients both living and dead.

AHA. 2002 Heart and Stroke Statistical Update. 2001.

An

nu

al D

isch

arg

es

0

100,000

200,000

300,000

400,000

500,000

600,000

'79 '81 '83 '85 '87 '89 '91 '93 '95 '97

WomenMen

Year

'99

Diagnosis of CHF:Clinical Challenge

Signs and symptoms of heart failure, such as shortness of breath and edema, have a broad differential diagnosis1

Chest x-ray findings have limited accuracyfor CHF1

20% to 40% of patients with CHF have normal

systolic function2

1. Dao Q, et al. J Am Coll Cardiol. 2001;37:379-385.2. Hunt SA, et al. ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult; 2001.

New York Heart Association Functional Classification

None Ordinary physical activity does not cause

undue fatigue, palpitation, dyspnea, or anginal pain

Often were previously symptomatic but are now in a well-compensated state

Slight Patient comfortable at rest Ordinary physical activity results in

fatigue, shortness of breath, palpitations,or angina

Functional Class Patient Limitations

The Criteria Committee of the NYHA. Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis. 6th ed. 1964.

Class I

Class II

New York Heart Association Functional Classification

Marked Patient is comfortable at rest Less than ordinary activity leads

to symptoms

Severe Inability to carry on physical

activity without symptoms Patient is symptomatic at rest Any physical activity increases

symptoms

Functional Class Patient Limitations

The Criteria Committee of the NYHA. Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis. 6th ed. 1964.

Class III

Class IV

ACC/AHA Stages of Heart Failure: Stages A and B

Stage APatients at high risk of developing heart failure as a result of the presence of conditions that are strongly associated with the development of heart failure. These patients do not have any identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown signs or symptoms of heart failure

Stage BPatients who have developed structural heart disease that is strongly associated with the development of heart failure but who have never shown signs or symptoms of heart failure

Hunt SA, et al. J Am Coll Cardiol. 2001;38:2101-2113.

Stage CPatients who have current or prior symptoms of heart failure associated with underlying structural heart disease

Stage DPatients who have advanced structural heart disease and marked symptoms of heart failure at rest despite maximal medical therapy and who require specialized interventions

ACC/AHA Stages of Heart Failure: Stages C and D

Hunt SA, et al. J Am Coll Cardiol. 2001;38:2101-2113.

Heart FailurePathophysiology

Etiology of heart failure includes1-5:– Structural changes such as loss of myofilaments

– Disorganization of the cytoskeleton

– Apoptosis and necrosis

– Changes in heart size and shape (remodeling)

– Disturbances in Ca2+ homeostasis

– Alterations in receptor density and coupling to G-proteins

– Alterations in G-proteins

1. Francis GS, Tang WH. Rev Cardiovasc Med. 2003;4(suppl 2):S14-20. 2. Francis GS. Am J Med. 2001;110(suppl 7A):37S-46S.3. Shah M, et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2-S6. 4. Ceconi C, et al. Rev Port Cardiol. 1998;17(suppl 2):1179-1191. 5. Mann DL. Circulation. 1999;100:999-1008.

Heart FailurePathophysiology

Etiology of heart failure includes1-7:– Alterations in signal transduction pathways– Switch to fetal gene programs—increase -myosin heavy chain,

decrease -myosin heavy chain, increase ANP, increase BNP– Increase collagen synthesis, increase matrix

metalloproteinases– Na+ and water retention– Reflex control disturbances– Myocyte hypertrophy– Altered myocardial energetics

1. Katz AM. Med Clin North Am. 2003;87:303-316. 2. Francis GS. Am J Med. 2001;110(suppl 7A):37S-46S. 3. Iwanaga Y, et al. J Am Coll Cardiol. 2000;36:635-642. 4. Francis GS, Tang WH. Rev Cardiovasc Med. 2003;4(suppl 2):S14-S20. 5. Shah M, et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2-S6. 6. Wilson EM, et al. J Card Fail. 2002;8:390-398. 7. Jugdutt BI. Curr Drug Targets Cardiovasc Haematol Disord. 2003;3:1-30.

Heart Failure Pathophysiology

Myocardial Injury Fall in LV Performance

Activation of RAAS, SNS, ET,and Others

Myocardial ToxicityPeripheral VasoconstrictionHemodynamic Alterations

Remodeling andProgressive

Worsening ofLV Function Heart Failure SymptomsMorbidity and Mortality

ANPBNP

Shah M, et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2-S6.

Heart FailureLeft Ventricular Dysfunction

Mechanisms by which elevated LV filling pressure could contribute to mortality in HF include1-3:– Stretch-induced angiotensin II release

– Mechanically induced myocardial structural remodeling

– Progressive atrioventricular valvular regurgitation

– Myocardial stretch-induced increase in intracellular cAMPand calcium

– Decrease in vagal activity secondary to stretching of cardiac mechanoreceptors

1. Leri A, et al. J Clin Invest. 1998;101:1326-1342.2. Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7-S12.3. Cerati D, Schwartz PJ. Circ Res. 1991;69:1389-1401.


Changes associated with LVAD bridge to transplant experience 1990s1-4:– Decrease in chamber size

– Enhanced -adrenergic response

– Reversal of defects in sarcoplasmic reticulum (SR) Ca2+ cycling

– Normalization of gene expression

– Normalization of neurohormones and cytokines

1. Mann DL, Willerson JT. Circulation. 1998;98:2367-2369.2. Heerdt PM, et al. Circulation. 2000;102:2713-2719. 3. Ogletree-Hughes ML, et al. Circulation. 2001;104:881-886.4. McCarthy PM, Hoercher K. Prog Cardiovasc Dis. 2000;43:37-46.

Transition from LV dysfunction to HF1-3:

– Cell dropout (apoptosis)

– Myocyte elongation, hypertrophy

– Myocyte slippage

1. Mann DL. Circulation. 1999;100:999-1008. 2. Francis GS. Am J Med. 2001;110(suppl 7A):37S-46S. 3. D'Armiento J. Trends Cardiovasc Med. 2002;12:97-101.


Effects of Resynchronizationon LV Performance

225

200

175

150

125

100

Left Ventricular Volume (mL)

Baseline 1wk 1mo 3mo off-immed

off-1wk

off-4wk

45

40

35

30

25

20

Ejection Fraction (%)


off-1wk

off-4wk

1000

900

800

700

600

500

400Baseline 1wk 1mo 3mo off-

immedoff-1wk

off-4wk

dP/dtmax (mm/Hg/sec)

Yu CM, et al. Circulation. 2002;105:438-445.

500

450

400

350

300

250

Left Ventricular Filling Time (msec)


off-1wk

off-4wk

off-4wk

10

15

20

25

30

35

40


off-1wk

Mitral Regurgitation (%)

160150140130120110100

9080706050

Isovolumetric Contraction Time (ms)


off-1wk

off-4wk

Yu CM, et al. Circulation. 2002;105:438-445.

Effects of Resynchronizationon LV Performance

Summary

Heart failure is a major medical and economic burden that is growing in incidence with the aging of America

The pathogenesis of heart failure begins with an index event and is characterized by progressive remodeling of the heart

Neurohormones are an important part of the pathogenesis of heart failure; only those drugs that inhibit the RAAS and SNS have been shown to slow or reverse remodeling and improve survival

Devices also can reverse the remodeling process and improve survival

Device placement will likely complement pharmacologic therapies in the HF patient with dyssynchrony

Device Selection:CRT Alone Versus

CRT Plus Implantable Cardioverter Defibrillator

(ICD)

Arrhythmia PVCs; VT-NSVT-S; VF

Heart Disease Absent PresentPresent Present

LV Dysfunction Absent AbsentAbsent PresentPresent Present

Potential Risks for SCD

Minimal IntermediateIntermediate High

PVCsPVCs

VT-NSVT-NS

Risk-Stratification for Sudden Cardiac Death

PVC=premature ventricular complexes; VT-NS=nonsignificant ventricular tachycardia;VT-S=significant ventricular tachycardia; VF=ventricular fibrillation.

Prystowsky EN. Am J Cardiol. 1988;61:102A-107A.

CAST: Survival

CAST Investigators. N Engl J Med. 1989;321:406-412.

P=0.0003

Sur

viva

l (%

)

100

95

90

85

0 400 450 50050 100 150 200 250 300 350

Days After Randomization

Placebo (N=725)

Encainide or flecainide (N=730)

Julian DG, et al. Lancet. 1997;349:667-674.

EMIAT: All-Cause Mortality LVEF and by Group

Months Since Randomization Months Since Randomization

Pro

bab

ility

of

Su

rviv

al

Pro

bab

ility

of

Su

rviv

al

Amiodarone

PlaceboEjection fraction < 30%

Ejection fraction 31%-40%

CAMIAT: All-Cause Mortalityand Nonarrhythmic Death

Cairns JA, et al. Lancet. 1997;349:675-682.

Months Since Randomization

Cu

mu

lati

ve

Ris

k (

%)

Months Since Randomization

Cu

mu

lati

ve

Ris

k (

%)

P=0.072

P=0.130

Amiodarone

Placebo

Primary Prevention Post-MI Trials

1. Buxton AE, et al. N Engl J Med. 1999;341:1882-1890.2. Moss AJ, et al. N Engl J Med. 1996;335:1933-1940.3. Moss AJ, et al. N Engl J Med. 2002;346:877-882.

0

10

20

30

40

50

60

70

80

MUSTT1

27 MonthsMADIT2

27 MonthsMADIT-II3

20 Months

Mo

rtal

ity

Red

uct

ion

w/IC

D R

x (%

)

55 54

31

Mean time (MI to enrollment)

% Prior CABG or PTCA

LVEF (mean)

VT-NS (mean beats)

% Beta-blocker at discharge

Class II-III (% patients)

MADIT(N=196)

27 mos

71%

26%

9

18%

65%

MUSTT (N=704)

39 mos

66%

30%

5

40%

64%

MUSTT and MADIT: Overview

Adapted from Prystowsky EN. Am J Cardiol. 2000;86(Suppl 1):K34-K39.

MUSTT Study

Hypothesis: Antiarrhythmic therapy guidedby EP testing can reduce the risk of arrhythmic death and cardiac arrest in patients with:

– Coronary artery disease– LVEF <40%– Nonsustained VT

(3 beats – 30 sec; rate >100 bpm)

Buxton AE, et al. N Engl J Med. 1999;341:1882-1890.

MUSTT Randomized Patients:Arrhythmic Death or Cardiac Arrest

Eve

nt-

Fre

e R

ate

P=0.04

EP-Guided

Control

Months After Enrollment

0.0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1.0

0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60


MUSTT Randomized Patients:Arrhythmic Death or Cardiac Arrest

Eve

nt-

Fre

e R

ate

P<0.001

EP ICD

Control


EP no ICD


0.0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1.0

0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60

MUSTT Randomized Patients:Total Mortality

Eve

nt-

Fre

e R

ate

P<0.001

EP ICD

Control


EP no ICD


0.0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1.0

0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60

MADIT and MADIT-II:Inclusion Criteria

1. Moss AJ, et al. N Engl J Med. 1996;335:1933-1940.2. Moss AJ, et al. N Engl J Med. 2002;346:877-882.

MADIT1

Prior MI

Asymptomatic,

Inducible, nonsuppressible VT at EP

MADIT-II2

Prior MI

LVEF 30%

MADIT1

Prior MI

Asymptomatic,non-sustained VT

Inducible, nonsuppressible VT at EP

MADIT-II2

Prior MI

LVEF 35%

NYHA Class I, II, or III

<

<

MADIT: Survival by Treatment Groups

Moss AJ, et al. N Engl J Med. 1996;335:1933-1940.


Pro

bab

ility

of

Su

rviv

al

ICD

Conventional Therapy

P=0.009

0.0

0.2

0.4

0.6

0.8

1.0

0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60

MADIT-II: Survival byTreatment Group

Moss AJ, et al. N Engl J Med. 2002;346:877-882.

0.78

0.69

P=0.007

0 1 2 3 4

Defibrillator Group

Conventional Group

Pro

bab

ilit

y o

f S

urv

ival

Years

0.5

0.6

0.7

0.8

0.9

1.0

Secondary Prevention Trials:AVID, CASH, CIDS

1. AVID Investigators. N Engl J Med. 1997;337:1576-1583.2. Kuck KH, et al. Circulation. 2000;102:748-754.3. Connolly SJ, et al. Circulation. 2000;101:1297-1302.

0

10

20

30

40

50

60

70

80

AVID1

3 YearsCASH2

3 YearsCIDS3

3 Years

Mo

rtal

ity

Red

uct

ion

w/IC

D R

x (%

)

31

2820

AVID Trial

Eligibility criteria– Resuscitation from ventricular fibrillation– Sustained VT with syncope– Sustained VT with LVEF ≤40% and

severe hemodynamic compromise (near-syncope; CHF; angina)

Therapy– ICD (N=507)– Antiarrhythmics (N=509)

• Amiodarone (N=493)

• Sotalol (N=13)

• Other (N=3)

AVID Investigators. N Engl J Med. 1997;337:1576-1583.

AVID: Overall Survival

0 1 2 3Years After Randomization

Defibrillator Group

Antiarrhythmic Drug Group

Pro

po

rtio

n S

urv

ivin

g

P<0.02


0.0

0.2

0.4

0.6

0.8

1.0

AVID: Hazard Ratios forAll-Cause Mortality

Age

<60 yr

60-69 yr

70 yr

LVEF

<0.35%

0.35%Cause ofarrhythmia CAD Other

RhythmVentricularFibrilation

Ventricualr Tachycardia

Other

0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6Hazard Ratio


CASH: Long-Term Overall Survival in ICD and Drug Arms

Kuck K-H et al. Circulation. 2000;102:748-754

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.1

0.00 1 2 3 4 5 6 7 8 9

Years

Pro

po

rtio

n S

urv

ivin

g

ICD

Amiodarone/metoprolol

P=0.081

Update of CIDS Trial:11-Year Follow-Up From One Center

Original study randomized amiodarone vs ICD in VT/VF survivors (N=659) Long-term follow-up from 1 center–amiodarone (N=60) All-cause mortality higher in amiodarone (N=28) vs ICD (N=16) Annual mortality rate–amiodarone, 8.4%–ICD, 4.8% Amiodarone patients

– 82% had side effect

– 50% had significant side effect

Bokhari FA, et al. Circulation. 2002;106(19 suppl II):II-497.

CIDS Update: 11-Year Follow-Up

ICDAmiodarone

100

80

60

40

20

020 40 60 80 100 120 140

P=0.021

Months

Act

uar

ial S

urv

ival

(%

)

Bokhari FA, et al. Circulation. 2002;106(19 suppl II):II-497.

Selection of CRT vs CRT-ICD

CRT– Consider for patients who require chronic ventricular

pacing, especially those with LV dysfunction or mitral regurgitation

CRT-ICD– Consider for patients who meet criteria for MADIT II,

and MUSTT/MADIT with VT induced

– Consider for any patient with an ACC/AHA/NASPE Class I indication for an ICD

Prystowsky EN. Rev Cardiovasc Med. 2003;4(supp/2):S47-S53.

Summary

Trials of antiarrhythmic drugs failed to preventor significantly reduce SCD in patients post-MI

– CAST, CAST-II, EMIAT, CAMIAT

The ICD conferred a reduction of approximately 50%in overall mortality in the randomized trials MUSTTand MADIT

The ICD has been shown in multiple randomizedstudies to be the most significant therapy availablefor the primary prevention of SCD in patientswith a previous MI

Summary

The ICD was associated with reductions in all-cause mortalityin three randomized secondary prevention trials of SCD

– AVID, CASH, CIDS In 2002, the FDA approved the combination CRT-ICD for treatment of heart failure in patients at risk for SCD

The CRT-ICD may be more appropriate than CRT without defibrillation in patients who meet eligibility criteria for primary prevention post-MI trials

Preliminary results of the COMPANION trial strongly suggest that many CRT candidates will benefit even more from CRT-ICD

Further studies of the CRT-ICD are warranted to determinethe most appropriate candidates

cardiac resynchronization and defibrillation therapies: complementary approaches to the management...

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