User Manual Part 2

C-6
CLINICAL STUDY - MADIT II
MORTALITY
There were a total of 202 deaths that occurred during the trial and recorded as
of the stop date, November 20, 2001. These deaths occurred during the study
periods as shown in Table C-2 on page C-6 along with the cause of death as
adjudicated by an independent events committee.
Table C-2. Cause of deat h durin g the treatment period
Cause of Death
(as a percent of total pts)
ICD Therapy
(N=742) Patients (%)
Conventional The ra py
(N=490) Patients (% )
Total
(N=202)
Noncardiac
25 (3.4%) 21 (4.3%) 46 (3.7%)
Cardiac: Arrhythmic 28 (3.8%) 48 (9.8%) 76 (6.2%)
Cardiac: Non arrhythmic 45 (6.1%) 22 (4.5%) 67 (5.4%)
Cardiac: Undetermined cause 1 (0.1% ) 2 (0.4%) 3 (0.2%)
Unknown
6 ( 0.8% ) 4 (0.8%) 10 (0.8%)
Total Deaths
105 (14.2%) 97 (19.8%) 202 (16.3%)
SUMMARY OF CLINICAL STUDY
Guidant supported the MADIT II Clinical Study as conducted by the University
of Rochester to evaluate the potential survival benefit o f a prophylactically
implanted ICD in patients with a prior myocardial infarction and a left ventricular
ejection of ≤ 30 percent. Unlike MADIT I
1
, patients enrolled in MADIT II were
not required to undergo electrophysiologic testing to induce arrhythmias prior to
implant. Patients were randomized to either ICD or conventional therapy. All
cause mortality was the primary endpoint of the study.
The MADIT II trial was monitored using a sequential design and on November
20, 2001, after review of the data by the Data and Safety Monitoring Board, the
study was stopped. Results of the trial data indicated a 31percent decrease in
the mortality rate in patients implanted with an ICD device compared to patients
randomized to the conventional therapy group, thus meeting its effectiveness
endpoint.
The trial began July 11, 1997 and was conducted over a period of four years at
76 investigational centers both within and outside the United States.
1. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival w ith an implanted defibrillator in
patients with coronary disease at high risk for ventricular arrhythmia. NEJM 1996;33 5:1993-40
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