RT-179
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Amiodarone in post-infarction
patients at high risk: lessons from EMIAT
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Michiel J. Janse, A. John Camm*,
Gerald Frangin**, Desmond G. Julian***, Marek Malik°, Peter J. Schwartz°°.
Dept. of Clinical and Experimental Cardiology, Academic Medical Center,
University of Amsterdam, Amsterdam, The Netherlands, *Dept. of Cardiological Sciences, St.
George's Hospital Medical School, London, **Sanofi Recherche, Montpellier, France,
***London, °Dept. of Cardiological Sciences, St. George's Hospital Medical School,
London, UK, °°Dept. of Cardiology, Policlinico S. Matteo, Pavia, Italy
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Introduction
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The European Myocardial Infarct Amiodarone Trial
(EMIAT) was a prospective, randomized, double-blind placebo-controlled clinical trial
designed to assess the effect of amiodarone on all-cause mortality, cardiac mortality, and
arrhythmic death and resuscitated cardiac arrest in patients surviving an acute myocardial
infarction and with impaired left ventricular function1.
Entry criteria were a left ventricular ejection fraction < 40%, determined by
multiple-gated nuclear angiography assessed between 5 and 21 days after the onset of
myocardial infarction in patients between 18 and 75 years of age. Before randomisation, a
12 lead electrocardiogram was made and a 24-hour Holter recording was obtained, but the
findings did not influence entry into the trial. A total of 1486 patients was enrolled,
who were followed for a mean of 21 months. Of the 205 patients who died, 31 died from an
unknown or non-cardiac cause. The other 174 deaths were assumed to be of cardiac origin.
Of those, 126 were witnessed, and 44 were sudden (41 were documented or considered to be
arrhythmic). Of the 82 witnessed non-sudden deaths, six were arrhythmic. Of the 48
unwitnessed deaths, 36 were considered to be arrhythmic deaths. In addition, there were 26
patients who were resuscitated from documented ventricular tachycardia/fibrillation.
There were no differences between the placebo and the amiodarone group with regard to
all-cause mortality and cardiac mortality, but there was a 35% reduction in presumed
arrhythmic death in patients treated with amiodarone. Thus, the reduction of arrhythmic
deaths was offset by an excess of non-arrhythmic deaths in the amiodarone group. It might
be that some patients who were rescued from arrhythmic deaths eventually died from another
mode of death, such as pump failure. It would therefore be important to identify on the
one hand post-infarction patients at high risk for arrhythmic death, not likely to die
from pump failure, and on the other hand to identify patients not likely to benefit from
amiodarone treatment. For these reasons, an attempt was made to identify such patients on
the basis of several factors present before randomisation, and easy to obtain, such as
heart rate at rest, presence of ventricular arrhythmias on Holter, and concomitant
treatment with beta-blockers2. Heart rate was derived
from the resting ECG taken before randomisation, and not from the pulse. Pulse heart rates
were available but tended to cluster at round numbers and the figures were considered to
be less reliable than those obtained from the ECG.
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