6631948

Cardiac
Resynchronization
and Defibrillation
Therapies:
Complementary Approaches
to the Management
of Heart Failure

Ventricular
Resynchronization
Pathophysiology and
Identification of Responders

Mechanisms of Dysfunction Due
to 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 increased
energetic 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 Workload
Resulting From Dyssynchrony
Fiber Strain
Early Activated Late Activated
20
0
-0.1 0.10.0
20
0
-0.1 0.10.0
Area = Regional Work
Regional Blood Flow
Glucose Metabolism
FiberStress
FiberStress

Discoordinate Motion
Normal Sinus Rhythm
30 60 90
0
40
LV Volume (mL)
80
Acute Dyssynchrony (RV Pace)
LVPressure(mmHg)
Adverse Effects on Global Function From RV-Pacing–Induced Dyssynchrony

Do We Resynchronize
With Biventricular
or Left Ventricular Pacing?

CRT Enhances Cardiac
Mechano-Energetic Efficiency
LV pacing
Dobutamine
P< 0.05
MVO2/HR
Adapted from Nelson GS, et al. Circulation. 2000;102:3053-3059.
*P< 0.01
†P< 0.05
Mean ±SEM
.24
40
20
0
-20
† †
*
*
dP/dtmax PP Mean
CorF
AVO2 MVO2
.22
.20
.18
.16
.14
500 600 700 800 900 1000
dP/dtmax (mm Hg)
(RelativeUnits)
Change(%)

Single-Site LV Pacing
Works 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
LVPressure(mmHg)
LVPressure(mmHg)

Regional Wall Motion With CRT
Septum
Lateral
Pacing Off
Pacing On
RegionalFractionalAreaChange
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 10.0
Seconds
1151.0
865.0
113.0
1.0
114.0
50.8
1120.0
-727.0
Seconds
2-Min Steady State
LVPressure(mmHg)
LVPAOPdP/dt
LV Volume (mL)
120
80
40
0
0 300200100
Adapted from Kass DA. Rev Cardiovasc Med.
2003;4(suppl 2):S3-S13.
LVPAOPdP/dt

Ventricular Reverse Remodeling
With Resynchronization
Adapted from Abraham WT, et al. N Engl J Med. 2002;346:1845-1853.
End-DiastolicDimension(mm)
EjectionFraction(%)
6.0
6.5
7.5
10
20
P<0.001
Placebo
n=81
CRT
n=63
CRT
n=61
P<0.001
Placebo
n=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)
LV
BV
ChangeinAorticPP(%)
ChangeindP/dtmax(%)
24
18
12
6
0
-12
-6
16
12
8
4
0
-8
-4
1 1
LV
BV

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 Preactivation
SystolicFunction(EchoIndex)
* *
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

ChangeindP/dtmax
(%)
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
% D
ChangeindP/dtmax
(%)

More Direct Methods
to 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 Assessment
for 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 =-.70
P=.001
+20
0
-20
-40
-60
-80
-100DLVESVI(mL/m2)

TDI Assessment
for 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 80
ChangeinLVEF(%)

Potential Causes
for 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 function
and energetics from CRT can be marked
 Defining intraventricular mechanical dyssynchrony
seems 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

Pathophysiology
of 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 Failure
Scope of the Problem
 Nearly 900,000 annual hospital admissions
(increased 90% in past 10 years)1
 Most common discharge diagnosis for patients older
than 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.
AnnualDischarges
0
100,000
200,000
300,000
400,000
500,000
600,000
'79 '81 '83 '85 '87 '89 '91 '93 '95 '97
Women
Men
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 accuracy
for 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 A
Patients 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 B
Patients 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 C
Patients who have current or prior symptoms of heart failure
associated with underlying structural heart disease
Stage D
Patients 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 Failure
Pathophysiology
 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 Failure
Pathophysiology
 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.
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 Toxicity
Peripheral Vasoconstriction
Hemodynamic Alterations
Remodeling and
Progressive
Worsening of
LV Function Heart Failure SymptomsMorbidity and Mortality
ANP
BNP
Shah M, et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2-S6.

Heart Failure
Left 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 cAMP
and 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.

Heart Failure
 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.
3. D'Armiento J. Trends Cardiovasc Med. 2002;12:97-101.
Heart Failure

Effects of Resynchronization
on 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 (%)
immed
off-
1wk
off-
4wk
1000
900
800
700
600
500
400
immed
off-
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)
immed
off-
1wk
off-
4wk
off-
4wk
10
15
20
25
30
35
40
immed
off-
1wk
Mitral Regurgitation (%)
160
150
140
130
120
110
100
90
80
70
60
50
Isovolumetric Contraction Time (ms)
immed
off-
1wk
off-
4wk
Yu CM, et al. Circulation. 2002;105:438-445.
Effects of Resynchronization
on 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-NS
VT-S; VF
Heart Disease Absent Present Present
LV Dysfunction Absent Absent Present Present
Potential Risks for
SCD
Minimal Intermediate High
PVCs
VT-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
Survival(%)
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
ProbabilityofSurvival
Amiodarone
Placebo
Ejection fraction < 30%
Ejection fraction 31%-40%

CAMIAT: All-Cause Mortality
and Nonarrhythmic Death
Cairns JA, et al. Lancet. 1997;349:675-682.
Months Since Randomization
CumulativeRisk(%)
Months Since Randomization
CumulativeRisk(%)
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.
0
10
20
30
40
50
60
70
80
MUSTT1
27 Months
MADIT2
27 Months
MADIT-II3
20 Months
MortalityReductionw/ICDRx(%)
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 guided
by 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
Event-FreeRate
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

Arrhythmic Death or Cardiac ArrestEvent-FreeRate
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

Total MortalityEvent-FreeRate
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
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.
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 by
Treatment 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
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 Years
CASH2
3 Years
CIDS3
3 Years
MortalityReductionw/ICDRx(%)
31
28
20

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 3
Years After Randomization
Defibrillator Group
Antiarrhythmic Drug Group
ProportionSurviving
P<0.02
0.0
0.2
0.4
0.6
0.8
1.0

AVID: Hazard Ratios for
All-Cause Mortality
Age
<60 yr
60-69 yr
70 yr
LVEF
<0.35%
0.35%
Cause of
arrhythmia
CAD
Other
Rhythm
Ventricular
Fibrilation
Ventricualr
Tachycardia
Other
0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6
Hazard 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
0.0
0 1 2 3 4 5 6 7 8 9
Years
ProportionSurviving
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
ICD
Amiodarone
100
80
60
40
20
0
20 40 60 80 100 120 140
P=0.021
Months
ActuarialSurvival(%)
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 prevent
or 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 MUSTT
and MADIT
 The ICD has been shown in multiple randomized
studies to be the most significant therapy available
for the primary prevention of SCD in patients
with a previous MI

Summary
 The ICD was associated with reductions in all-cause mortality
in 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 determine
the most appropriate candidates

6631948

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