Primary Prevention of Sudden Cardiac Death in Idiopathic

Dilated Cardiomyopathy
The Cardiomyopathy Trial (CAT)
Dietmar Bänsch, MD; Matthias Antz, MD; Sigrid Boczor; Marius Volkmer, MD;
Jürgen Tebbenjohanns, MD; Karlheinz Seidl, MD; Michael Block, MD; Frank Gietzen, MD;
Jürgen Berger, MD; Karl Heinz Kuck, MD; for the CAT Investigators

Background—Patients with idiopathic dilated cardiomyopathy (DCM) and impaired left ventricular ejection fraction have
an increased risk of dying suddenly.
Methods and Results—Patients with recent onset of DCM (ⱕ9 months) and an ejection fraction ⱕ30% were randomly
assigned to the implantation of an implantable cardioverter-defibrillator (ICD) or control. The primary end point of the
trial was all-cause mortality at 1 year of follow-up. The trial was terminated after the inclusion of 104 patients because
the all-cause mortality rate at 1 year did not reach the expected 30% in the control group. In August 2000, the vital status
of all patients was updated by contacting patients, relatives, or local registration offices. One hundred four patients were
enrolled in the trial: Fifty were assigned to ICD therapy and 54 to the control group. Mean follow-up was 22.8⫾4.3
months, on the basis of investigators’ follow-up. After 1 year, 6 patients were dead (4 in the ICD group and 2 in the
control group). No sudden death occurred during the first and second years of follow-up. In August 2000, after a mean
follow-up of 5.5⫾2.2 years, 30 deaths had occurred (13 in the ICD group and 17 in the control group). Cumulative
survival was not significantly different between the two groups (93% and 80% in the control group versus 92% and 86%
in the ICD group after 2 and 4 years, respectively).
Conclusions—This trial did not provide evidence in favor of prophylactic ICD implantation in patients with DCM of recent
onset and impaired left ventricular ejection fraction. (Circulation. 2002;105:1453-1458.)
Key Words: cardiomyopathy 䡲 defibrillation 䡲 tachycardia 䡲 fibrillation 䡲 death, sudden

I mplantable cardioverter-defibrillators (ICD) terminate

ventricular tachycardias (VT) and ventricular fibrillation
(VF) with high efficacy.1–3 In secondary prevention trials of
patients with DCM represent a minor subgroup of the overall
study population. Mortality rates after 1 year have been
reported to range between 14% and 44% in New York Heart
sudden cardiac death (SCD), ICD treatment was superior to Association functional class III to IV; 21% to 51% of deaths
antiarrhythmic drug therapy.4 – 6 In primary prevention of are supposedly due to ventricular tachyarrhythmias.10 –19
SCD, data on ICD treatment compared with conventional In 1991, we started a primary prevention trial in patients
therapy are inconclusive. ICD treatment did not provide with DCM of recent onset (ⱕ9 months) and impaired LV
survival benefits over bypass graft surgery alone in the ejection fraction (EF ⱕ30%) without documented symptom-
Coronary Artery Bypass Graft Patch Trial (CABG-Patch).7 In atic ventricular tachyarrhythmias who were randomly as-
contrast, the Multicenter Automatic Defibrillator Implanta- signed to ICD therapy or to a control group.20 –23 The results
tion Trial (MADIT) revealed a striking survival benefit of of the pilot phase are reported in this article.
ICD treatment compared with drug therapy in patients with
spontaneous nonsustained VTs, impaired left ventricular Methods
(LV) function, and inducible VTs that could not be sup- Patients
pressed by procainamide.8 These results are supported by the Patients were eligible if they were between 18 and 70 years of age,
had symptomatic DCM for ⱕ9 months and impaired LV function
Multicenter Unsustained Tachycardia Trial (MUSST).9
(LVEF ⱕ30% obtained during LV angiography), and were in NYHA
Only limited information is available in patients with class II or III. Coronary artery disease (coronary stenosis ⬎70%) had
dilated cardiomyopathy (DCM). In most heart failure studies, to be excluded by angiography. Patients with a history of prior

Received October 18, 2001; revision received January 18, 2002; accepted January 18, 2002.
From the Department of Cardiology, St Georg Hospital, Hamburg, Germany (D.B., M.A., B.B., M.V., K.H.K.); the Department of Cardiology,
University Hospital, Hannover, Germany (J.T.); the Department of Cardiology, Klinikum Ludwigshafen (K.S.); the Department of Cardiology and
Angiology, University Hospital, Münster (M.B.); the Department of Mathematics and Data Processing in Medicine, University Hospital Eppendorf,
Hamburg, Germany (J.B.); and the Department of Cardiology, Central Hospital, Bielefeld, Germany (F.G.).
Correspondence to Dr Karl Heinz Kuck, St Georg Hospital, Lohmühlenstr 5, D-20099 Hamburg, Germany. E-mail [email protected]
© 2002 American Heart Association, Inc.
Circulation is available at http://www.circulationaha.org DOI: 10.1161/01.CIR.0000012350.99718.AD

1453
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1454 Circulation March 26, 2002

myocardial infarction, myocarditis, or excessive alcohol consump- TABLE 1. Primary and Secondary End Points
tion were not included in the trial. Furthermore, patients were
excluded if they had a history of symptomatic bradycardia, VT, and Incidence at
VF or if they were listed for heart transplantation at the time of End Point 1y
presentation. Patients with significant valvular disease and hypertro- All-cause mortality
phic or restricted cardiomyopathy were also excluded from the trial,
ICD 4 (8.0)
as were patients in NYHA class I or IV and patients who were
mentally unable to understand the protocol. Control 2 (3.7)
Sudden death
Randomization ICD 0
The trial was conducted at 15 German centers. The protocol was
approved by the institutional review board in Freiburg, Germany, Control 0
and by the review boards at each clinical center. Enrollment began in Cardiac death
May 1991 and ended in March 1997. ICD 4 (8.0)
Patients were enrolled after written informed consent had been
obtained. Random assignment was performed centrally. Closed Control 1 (1.9)
envelopes with the assigned study group were sent to each center. Heart transplantation
The envelopes were opened when a patient was enrolled. ICD 2 (4.0)

Baseline Examinations Control 1 (1.9)

Detailed information on the study protocol has been published Values are numbers of patients (%). Total number of patients in the ICD
previously.21–23 In short, all patients underwent the following exam- group was 50; total number of patients in the control group was 54.
inations: physical examination, baseline ECG, exercise test, and
echocardiography. A Holter ECG was performed to document
bradycardia and tachycardia. Bradycardia was defined as a docu- Medicine. For quality control and completeness of data forms, data
mented heart rate ⬍40 bpm caused by sinus arrest and atrioventric- monitoring was performed.
ular block. Wide-complex tachycardias, QRS complex ⬎120 ms,
were defined as VT if there was no evidence for supraventricular Study Design and Statistical Considerations
tachycardia with aberrant conduction. VTs with ⬎3 beats and a On the basis of the literature in the late 1980s, all-cause mortality
duration of ⬍30 seconds were defined as nonsustained; with a rate was assumed to be 30% in the first year, with 40% of deaths
duration of ⬎30 seconds, they were defined as sustained. Left heart being sudden.10 –16 On this assumption, 1348 patients had to be
catheterization was performed to exclude coronary artery disease. included to show a 1-year survival benefit of 6% for ICD treatment,
Ventricular function and EF were calculated on the basis of LV with a power of 80% and a probability value of 0.05.
angiography. Electrophysiological study and right ventricular stim- Because all-cause mortality rate varied considerably between
ulation were performed with a maximum of 3 extrastimuli at 2 different heart failure studies and included mostly patients with heart
different cycle lengths at the right ventricular apex and outflow tract failure caused by coronary artery disease, it was decided to perform
until VT or VF was induced. a blinded interim analysis after the inclusion of 100 patients at 1 year
of follow-up (pilot phase).
Implantation Procedure In June 1997, a survival analysis of all patients with at least 1 year
Patients assigned to ICD therapy underwent implantation of a of follow-up was performed. The interim analysis showed that the
transvenous defibrillator system, under general anesthesia. ICD overall 1-year mortality rate for all patients was only 5.6% and
testing was performed according to current guidelines for ICD markedly below the assumed value of 30%. The difference between
implantation.24 A defibrillation threshold of ⬍20 J was mandatory. the survival rates of the two groups was only 2.6%. According to the
Guidant/CPI provided transvenous electrode systems (Endotak, Car- protocol, the randomization was stopped, and all randomly assigned
diac Pacemakers, Inc [CPI]) and pulse generators capable of deliv- patients completed the scheduled follow-up period of 2 years.
ering biphasic shocks (Ventak P2, P3, PrX II, CPI). All devices were In August 2000, at the time of final analysis, the vital status of all
capable of storing episode data and electrograms. A VT zone with a patients was assessed to determine long-term mortality rate. The
detection rate of 200 bpm was programmed in all patients. All shocks survival rates for the groups were presented as Kaplan-Meier curves
were programmed to a maximum output of 30 J. The pacemaker rate and compared by log-rank statistics.25 Despite having an interim
was programmed to 40 bpm. analysis, there was no need to perform an ␣-adjustment on signifi-
cance for the primary end point because no differences were detected
between the groups.
End Points To estimate the prognostic relevance of patient characteristics,
The primary end point of the trial was all-cause mortality at 1 year. Cox proportional regression models were calculated. Data were
Secondary end points were heart transplantation, cardiac mortality described by the arithmetic mean⫾SD if normally distributed or
(sudden and nonsudden cardiac death), sustained VT (adequate ICD otherwise by median with 25% to 75% percentiles. Quantitative
therapy), and symptomatic ventricular tachyarrhythmias requiring comparisons between groups were performed by 2-sided analysis,
antiarrhythmic treatment (Table 1). Adequate ICD therapy was with the use of the Mann-Whitney exact test; qualitative character-
assumed if documented tachycardia electrograms had a morphology istics were compared by means of the exact Fisher ␹2 test. Statistical
different from sinus rhythm and if tachycardias started suddenly with analysis was performed with SPSS for Windows, release 9.0.1.
no cycle length variation, indicative of atrial fibrillation. Further-
more, complications caused by ICD therapy, such as revision
procedures, infection, and so forth, were documented. Results
Study Sample and Comparison of Groups
Follow-Up A total of 104 patients were enrolled between July 1991 and
Patients were scheduled for follow-up visits every 3 months and March 1997. Fifty patients were randomly assigned to ICD
were encouraged to schedule additional visits if the first shock,
cluster of shocks, or syncope had occurred. treatment and 54 to the control group. Baseline characteristics
The central data registry was at the University Hospital of did not differ between groups except for bradycardias caused by
Eppendorf, Department of Mathematics and Data Processing in sinus arrest and atrioventricular block I and II (Wenckebach),
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 Bänsch et al Cardiomyopathy Trial 1455

TABLE 2. Baseline Characteristics of Patients

Patients All ICD Treatment Control Group P
Randomized 104 50 54
Sex, male/female 83/21 43/7 40/14 NS
Follow-up, mo (per protocol) 22.8⫾4.3 22.7⫾4.5 22.9⫾4.2 NS
Follow-up, y (per August 2000) 5.5⫾2.2 5.7⫾2.2 5.2⫾2.1 NS
Age, y 52⫾11 52⫾12 52⫾10 NS
Duration of symptoms, mo (median) 3.0 3.0 2.5 NS
Baseline violators 19 8 11 NS
Class of heart failure
NYHA II 65.3% 66.7% 64.1% NS
NYHA III 34.6% 33.3% 35.8%
Orthopnoe 3.0% 4.1% 2.0% NS
Edema 8.9% 8.3% 9.4% NS
Ejection fraction, % 24⫾7 24⫾6 25⫾8 NS
LVED pressure, mm Hg 17⫾10 16⫾9 18⫾10 NS
Echocardiography
LV diastolic, mm 69⫾8 69⫾7 69⫾8 NS
LV systolic, mm 58⫾9 58⫾9 59⫾10 NS
Baseline ECG
Rhythm
Sinus rhythm 83.3% 79.6% 86.8% NS
Atrial fibrillation/flutter† 15.7% 20.4% 11.3%
Paced 1% 0% 1.9%
QRS morphology
Normal 63.9% 72.9% 55.1% NS (0.091)
Not normal 36.1% 27.1% 44.9%
LBBB 82.9% 84.6% 81.8% NS
RBBB 2.9% 7.7% 0%
Other or undefined BB 14.3% 7.7% 18.2%
QRS width,‡ ms 108⫾29 102⫾29 114⫾29 NS
QT duration,‡ ms 358⫾58 347⫾69 369⫾43 NS
Holter ECG
Patients with nsVTs 52.9% 53.1% 58.0% NS
Median duration of nsVT, s (25%/75%) 4.0 (3.0/6.0) 5 (3.0/6.5) 3.5 (2.3/6.0) NS
Rate of nsVTs, bpm 165⫾32 175⫾39 157⫾23 NS
Bradycardias, % of patients 10.4% 2.1% 18.8% 0.015
SA block 2.1% 0% 4.2%
AV block 8.3% 2.1% 14.6% NS
Baseline EPS
AH, ms 91⫾27 86⫾22 97⫾31 NS
HV, ms 53⫾14 51⫾15 55⫾14 NS
Inducible VT 2.9% 6.1% 0% NS
Inducible VF 9.6% 16.0% 3.7% NS
Medication
␤-Blocker 3.8% 4.0% 3.7% NS
Ca antagonist 11.5% 16.0% 7.4% NS
Digitalis 80.8% 86.0% 75.9% NS
Diuretics 86.5% 88.0% 85.2% NS
Nitrates 28.8% 32.0% 25.9% NS
ACE inhibitor 96.2% 94.0% 98.1% NS
Warfarin 29.8% 24.0% 35.2% NS
AA indicates antiarrhythmic agent; ACE, angiotensin-converting enzyme; LBBB, left bundle-brunch block;
LVEDD, left ventricular end-diastolic diameter; mVT, monomorphic ventricular tachycardia; PVS, programmed
ventricular stimulation; pVT, polymorphic ventricular tachycardia; RBBB, right bundle brunch block; VTC,
ventricular tachycardia cluster; EPS, electrophysiological study; AH, AH interval; and HV, HV interval.
*Echocardiographic M-mode data available for 70 patients only.
†Chronic or intermittent.
‡Patients with pacemakers not included.

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1456 Circulation March 26, 2002

Complications Caused by ICD Therapy

No deaths occurred as a result of the implantation procedure,
that is, within 30 days of ICD implantation. Two revisions
caused by device dislocation and bleeding had to be per-
formed; two electrodes dislocated and had to be revised
during surgery. During the following 24 months, 10 compli-
cations occurred in 7 patients: 7 incidences of electrode
dislocation and sensing/isolation defects, 2 incidences of
infection with total device replacement, and 1 perforation.

Predictors of Death
The only predictor of total mortality was impaired LVEF.
Compared with patients with EF ⱖ28%, the odds ratio was
4.1 (95% CI, 1.5 to 11.3, P⫽0.006) for patients with EF
ⱕ21% and 2.1 (95% CI, 0.7 to 6.2, P⫽0.19) for patients with
EF 22% to 27%.
Survival in patients with nonsustained (ns)VTs during
baseline Holter monitoring was 87%, 72%, and 63%, as
opposed to 98%, 93%, and 77% in patients without nsVTs
after 2, 4, and 6 years, respectively (NS). Survival of patients
with nsVTs during baseline Holter monitoring was not
improved by ICD therapy, whereas 85%, 77%, and 72% of
patients with nsVTs survived in the ICD group and 90%,
67%, and 55% survived in the control group after 2, 4, and 6
Figure 1. Survival in the ICD group vs the control group. years, respectively (NS).
All baseline variables presented in Table 2, such as age,
sex, and so forth, were tested accordingly but did not show
which were noted more frequently during Holter monitoring in
any statistically significant impact on survival.
the control group (18.8% versus 2.1%, P⫽0.015). Furthermore,
mean QRS duration was longer in the control group than in the Shocks and Syncope in Patients With ICD
ICD group (114 versus 102 ms) as the result of a higher Eleven patients received adequate therapies for VTs ⬎200
incidence of left bundle-branch block (36.7% versus 22.9%). bpm, and 6 patients had syncope during VTs in the ICD
This difference did not reach statistical significance. Further- treatment group. Survival free of VTs and adequate therapies
more, 3 patients (6.1%) had monomorphic VTs induced during in the ICD group was 90%, 87%, and 82% after 2, 4, and 6
electrophysiological study. All were randomly assigned to ICD years, respectively. All-cause mortality rates were different in
therapy. In 10 patients, VF was inducible. Eight patients were patients with and without adequate therapies in the ICD
randomly assigned to ICD treatment and 2 patients were ran- group. Whereas 92%, 90%, and 83% of patients survived, if
domly assigned to the control group. This difference was not no VT was stored in the ICD (n⫽39), only 91%, 73%, and
statistically significant. 44% survived 2, 4, and 6 years if VTs were stored and
ACE inhibitors were used in 96% of patients without any adequately terminated by the ICD (n⫽11, P⫽0.024).
difference between the groups. Four percent of patients
received ␤-blocker therapy in both study arms at baseline Discussion
(Table 2). No changes in the medication of ACE inhibitors, This study revealed that short- and long-term overall mortal-
digitalis, and diuretics between baseline and 24-month ity rates in patients with DCM and significantly impaired LV
follow-up were documented. function were surprisingly low. Therefore, ICD therapy did
not provide any survival benefit in these patients.
Mortality Only 4 patients in the ICD group and 2 in the control group
All-cause mortality rates were neither different between ICD died during the first year of follow-up. Long-term survival
treatment and control group after 1 year (primary end point) nor was 92%, 86%, and 73% in the ICD group versus 93%, 80%,
during long-term follow-up: Four patients the ICD group and 2 and 68% in the control group after 2, 4, and 6 years,
patients in the control group died during the first year of respectively (Figure 1). This is in strong contrast to most
follow-up. No sudden death occurred in either group during this series of patients with DCM or heart failure published before
time. All four deaths were cardiac in the ICD group, whereas this trial was started: One-year mortality rate had been
both patients died of noncardiac causes in the control group. reported to be between 14% and 44% in NYHA functional
After a mean follow-up of 5.5⫾2.2 years, 13 patients in the class III-IV, with 30% to 50% of deaths being be sud-
ICD group and 17 in the control group died. Cumulative den.10 –14,18,19,26 Patients in NYHA class II show a lower
survival was 92%, 86%, and 73% in the ICD treatment group 1-year-mortality rate of 6% to 14%.10,13 However, most of
versus 93%, 80%, and 68% in the control group after 2, 4, and these data had been collected before the ACE inhibitor era.
6 years, respectively (log rank P⫽0.554, Figure 1). ACE inhibitors have significantly improved survival in pa-
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 Bänsch et al Cardiomyopathy Trial 1457

the study had been continued to include 1348 patients, the

power to show the expected difference of 6% would have
been ⬍50%. Thus, the trial was stopped for futility after 1
year.
Even in patients with an increased mortality rate, such as
patients with a lower EF or nsVTs during Holter monitoring
(Figure 2), ICD therapy did not reveal any significant survival
benefit in the Cardiomyopathy Trial (CAT). This is in
contrast to other studies, which revealed a strong association
between nsVTs and the risk of sudden death.10 –16,26 –30 How-
ever, it is in concordance with the results of the Amiodarone
Versus Implantable Defibrillators trial in patients with nonis-
chemic cardiomyopathy and nonsustained ventricular
tachycardias (AMIOVIRT), which did not reveal any survival
benefit of ICD treatment over the treatment with amiodarone.
The survival rates were 88% and 85% in the amiodarone-
treated group versus 89% and 79% in the ICD treatment
group after 2 and 4 years, respectively.30
In contrast to CAT and AMIOVIRT, which did not show
any survival benefit of ICD therapy, a subgroup analysis of
patients with DCM in the secondary prevention trial AVID
demonstrated a survival benefit despite similar low mortality
rates in the ICD arm (11% after 2 years compared with 8% in
Figure 2. Survival of patients with and those without nsVTs dur-
ing baseline Holter ECG. CAT). However, because the control arm in AVID had a
higher mortality rate (18% after 2 years) compared with CAT
tients with impaired LV function11–13,16 –19; 65.4% of patients (7% after 2 years), mortality rate was significantly reduced by
were in NYHA class II in our trial and 96.2% of patients ICD treatment.
received ACE inhibitors. This may explain the rather low Interestingly, survival in patients with an ICD with VTs
mortality rate, even though only a minority of patients was stored in the ICD was significantly impaired compared with
treated with ␤-blockers. patients without VTs (Figure 3). Only 44% of patients with
The lack of any survival benefit of ICD therapy is most VTs survived 6 years compared with 83% if no VT had
likely due to the overall low event rate in our cohort. Even if occurred (P⫽0.024). One explanation may be that the occur-

Figure 3. Survival of patients with and those with-

out VTs in the ICD group.

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1458 Circulation March 26, 2002

rence of VTs may be closely associated with a progression of surgery: Coronary Artery Bypass Graft (CABG) Patch Trial Investigators.
N Engl J Med. 1997;337:1569–1575.
heart failure, such that VTs are a sign of cardiac deterioration
8. Moss AJ, Hall WJ, Cannom DS, et al, for the Madit Investigators. Improved
rather than an independent risk factor of SCD. One study in survival with an implantable defibrillator in patients with coronary artery
patients with DCM and clusters of VTs supports this hypoth- disease at high risk of ventricular arrhythmia. N Engl J Med. 1996;335:
esis. In this study, only 16% of patients survived and were not 1933–1940.
9. Buxton AE, Lee KL, Fisher JD, et al. A randomized study of prevention of
given transplantation 4 years after the first cluster of VTs, as sudden death in patients with coronary artery disease: Multicenter Unsus-
opposed to 80% of patients without VTs.31 tained Tachycardia Trial Investigators. N Engl J Med. 1999;341:1882–1890.
10. Massie BM, Kramer B, Haughom F. Acute and long-term effects of vaso-
dilator therapy on resting and exercise hemodynamics and exercise tolerance.
SCD and Defibrillator Use Circulation. 1981;64:1216–1226.
VTs have been made responsible for 30% to 51% of sudden 11. Creager MA, Faxon DP, Halperin JL, et al. Determinants of clinical response
deaths in DCM.13,15,16,26 In CAT, 11 patients received ade- and survival in patients with congestive heart failure treated with captopril.
quate therapies for VTs ⬎200 bpm and 6 patients had Am Heart J. 1982;104:1147–1154.
12. King J, Steingo L, Barlow JB, et al. Further experience with long-term
syncope during VTs. However, this did not lead to a survival captopril therapy in severe refractory congestive heart failure. S Afr Med J.
benefit. It has been suggested that the occurrence of fast VTs 1983;64:510–515.
(⬎240 bpm) or VTs associated with syncope be used as a 13. Chatterjee K, Parmley WW, Cohn JN, et al. A cooperative multicenter study
of captopril in congestive heart failure: hemodynamic effects and long-term
surrogate end point for SCD.32 This concept is called into response. Am Heart J. 1985;110:439– 447.
question by the findings of the present study. 14. Kao W, Gheorghiade M, Hall M, et al. Relation between plasma norepineph-
rine and response to medical therapy in men with congestive heart failure
secondary to coronary artery disease or idiopathic dilated cardiomyopathy.
Limitations Am J Cardiol. 1989;64:609–613.
Because the overall mortality rate was too low, the study was 15. Huang SK, Messer JV, Denes P. Significance of ventricular tachycardia in
stopped for futility after the pilot phase. Even if 1348 patients idiopathic dilated cardiomyopathy: observations in 35 patients. Am J Cardiol.
had been included, as initially planned, the trial would have 1983;51:507–512.
16. Schwarz F, Mall G, Zebe H. Determinants of survival in patients with
been underpowered. congestive cardiomyopathy: quantitative morphologic findings and left ven-
tricular hemodynamics. Circulation. 1984;70:923–928.
Conclusions 17. Dec GW, Fuster V. Medical progress: idiopathic dilated cardiomyopathy.
ICD therapy did not reveal any survival benefit in the setting of N Engl J Med. 1994;331:1564–1575.
18. Diaz RA, Obasohan A, Oakley CM. Prediction of outcome in dilated car-
DCM of recent onset and impaired LV function (EF ⱕ30%). diomyopathy. Br Heart J. 1987;58:393–399.
This was most likely due to the low overall mortality rate in the 19. Sugrue DD, Rodeheffer RJ, Codd MB, et al. The clinical course of idiopathic
control group. However, even in patients with a significantly dilated cardiomyopathy: a population based study. Ann Intern Med. 1992;
117:117–123.
increased mortality rate caused by a lower EF and nonsustained 20. Kuck KH. Value of prophylactic implantable cardioverter defibrillator
VTs, ICD therapy did not reveal any survival benefit. Therefore, therapy. Pacing Clin Electrophysiol. 1994;17:514–516.
the results of CAT do not favor prophylactic ICD implantation 21. Cardiomyopathy Trial Investigators. Cardiomyopathy trial. Pacing Clin Elec-
trophysiol. 1993;16:576–581.
in patients with DCM of recent onset and impaired LVEF 22. German Dilated Cardiomyopathy Study Investigators. Prospective studies
without any further risk stratification. assessing prophylactic therapy in high risk patients: the German Dilated
CardioMyopathy Study (GDCMS): study design. Pacing Clin Electro-
physiol. 1992;15:697–700.
Acknowledgments 23. Kuck KH. Ein-Jahres-Mortalität bei Patienten mit dilatativer Kardiomyop-
This study was supported by a grant from Guidant, Giessen, athie und implantiertem Kardioverter/Defibrillator: CAT, eine randomisierte,
Germany. kontrollierte klinische Studie. Z Kardiol. 1998;87:207–207. Abstract.
24. Breithardt G, Camm AJ, Campbell RWF, et al. Guidelines for the use of
References implantable cardioverter defibrillators. Eur Heart J. 1992;13:1304–1310.
1. Mirowski M, Reid PR, Mower MM, et al. Termination of malignant 25. Kaplan EL, Meier P. Nonparametric estimation from incomplete obser-
ventricular arrhythmias with an implanted automatic defibrillator in vations. J Am Stat Assoc. 1958;457–481.
human beings. N Engl J Med. 1980;303:322–324. 26. Franciosa JA, Wilen M, Zische S, et al. Survival in men with severe chronic
left ventricular failure due to either coronary artery disease or idiopathic
2. Block M, Breithardt G. Long-term follow-up and clinical results of
dilated cardiomyopathy. Am J Cardiol. 1983;51:831–836.
implantable cardioverter defibrillators. In: Zipes DP, Jalife J, eds. Cardiac
27. Fuster V, Gersh BL, Giuliani ER. The natural history of idiopathic dilated
Electrophysiology: From Cell to Bedside. Philadelphia, Pa: WB Saunders;
cardiomyopathy. Am J Cardiol. 1981;47:525–531.
1995:1412–1425.
28. Stevenson LW, Fowler MB, Schroeder JS. Poor survival of patients with
3. Fazio G, Veltri EP, Tomaselli G, et al. Long-term follow-up of patients with
idiopathic cardiomyopathy considered to well for transplantation. Am J Med.
nonischemic dilated cardiomyopathy and ventricular tachyarrhythmias
1987;83:871–876.
treated with implantable cardioverter defibrillators. Pacing Clin Electro- 29. Steinberg JS, Ehlert FA, Cannon DS. Dilated cardiomyopathy vs coronary
physiol. 1991;14:1905–1910. artery disease in patients with VT/VF: differences in presentation and
4. AVID Investigators. A comparison of antiarrhythmic-drug therapy with outcome in the antiarrhythmic versus implantable defibrillator (AVID)
implantable defibrillators in patients resuscitated from near-fatal ventricular registry. Circulation. 1997;96:715–715.
arrhythmias. N Engl J Med. 1997;337:1576 –1583. 30. Bänsch D, Böcker D, Brunn J, et al. Clusters of ventricular tachycardias
5. Kuck K, Cappato R, Siebels J, et al. Randomized comparison of antiar- signify impaired survival in patients with idiopathic dilated cardiomyopathy
rhythmic drug therapy with implantable defibrillators in patients resuscitated and implantable cardioverter defibrillators. J Am Coll Cardiol. 2000;36:
from cardiac arrest: the Cardiac Arrest Study Hamburg (CASH). Circulation. 557–565.
2000;102:748 –754. 31. Strickberger AS. Amiodarone vs implantable defibrillator in patients with
6. Connolly SJ, Gent M, Roberts RS, et al. Canadian implantable defibrillator nonischemic cardiomyopathy and asymptomatic nonsustained ventricular
study (CIDS): a randomized trial of the implantable cardioverter defibrillator tachycardia. Circulation. 2000;102:2794. Abstract.
against amiodarone. Circulation. 2000;101:1297–1302. 32. Bocker D, Bänsch D, Heinecke A, et al. Potential benefit from implantable
7. Bigger JT. Prophylactic use of implanted cardiac defibrillators in patients at cardioverter-defibrillator therapy in patients with and without heart failure.
high risk for ventricular arrhythmias after coronary-artery bypass graft Circulation. 1998;98:1636–1643.

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 Correction

The following Appendix was intended to appear in the article “Primary Prevention of Sudden
Cardiac Death in Idiopathic Dilated Cardiomyopathy: The Cardiomyopathy Trial (CAT)” by
Bänsch et al in the March 26, 2002, issue of the journal (Circulation. 2002;105:1453–1458).

Appendix D. Bänsch, MD, M. Castrucci, MD; Bielefeld-Mitte Municipal

The investigators of the Cardiomyopathy Trial are as follows: St Hospital: H. Kuhn, MD, F. Gietzen, MD; Würzburg University
Georg General Hospital, Hamburg: T. Meinertz, MD, M.Volkmer, Hospital: M. Meesmann, MD, W. Peters, MD; Ludwigshafen Gen-
eral Hospital: J. Senges, MD, K.-H. Seidl, MD, B. Hauer, MD; Bonn
MD; as of 1994: K.-H. Kuck, MD, M.Volkmer, MD, M. Antz, MD;
University Hospital: M. Manz, MD, B. Lüderitz, MD, W. Jung, MD,
Hannover School of Medicine: H. Klein, MD, H.-J. Trappe, MD, H.
C. Wolpert; München University Hospital: A. Schömig, MD, C.
Drexler, MD, W. Schöhl, MD, K. Gille, MD, J. Tebbenjohanns, MD, Schmitt, MD, P. Barthel, MD, H. Kreuzberg, MD, A. Plewan, MD,
M. Niehaus, MD, R. Cierpka, MD, B. Kielblock; University Hospital M. Leibig, MD; Marburg University Hospital: B. Maisch, MD, W.
Eppendorf, Hamburg: K.-H. Kuck, MD, M. Antz, MD; as of 1994: Grimm, MD, J. Hoffmann, MD; Fulda Municipal Clinic: T. Bonzel,
T. Meinertz, MD, C. Weiß, MD; Göttingen University Hospital: MD, G. Strupp, MD, H. von Korn, MD, T. Vogtmann, MD; Bad
B.-D. Gonska, MD, A. Schaumann, MD, C. Fleischmann, MD, A. Bevensen Heart–Circulation Clinic: W. Kupper, MD, R. Mletzko,
Hareuther, MD; Mainz University Hospital: J. Meyer, MD, A. MD, J. Zimmer, MD; Biometrical support: J. Berger, MD; Biometri-
Liebrich, MD, D. Nebeling; Münster University Hospital: G. cal assistance, central study coordination and data management: S.
Breithardt, MD, M. Block, MD, D. Böcker, MD, F.-M. Isbruch, MD, Boczor.

(Circulation. 2002;106:888.)
© 2002 American Heart Association, Inc.
Circulation is available at http://www.circulationaha.org DOI: 10.1161/01.CIR.0000030856.26596.8B

888
Primary Prevention of Sudden Cardiac Death in Idiopathic Dilated Cardiomyopathy: The
Cardiomyopathy Trial (CAT)
Dietmar Bänsch, Matthias Antz, Sigrid Boczor, Marius Volkmer, Jürgen Tebbenjohanns,
Karlheinz Seidl, Michael Block, Frank Gietzen, Jürgen Berger and Karl Heinz Kuck
for the CAT Investigators

Circulation. 2002;105:1453-1458; originally published online March 18, 2002;

doi: 10.1161/01.CIR.0000012350.99718.AD
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2002 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539

The online version of this article, along with updated information and services, is located on the
World Wide Web at:
http://circ.ahajournals.org/content/105/12/1453

An erratum has been published regarding this article. Please see the attached page for:
http://circ.ahajournals.org/content/106/7/888.full.pdf

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