Author + information
- Received April 16, 1985
- Revision received August 7, 1985
- Accepted August 16, 1985
- Published online January 1, 1986.
- Vilma Torres, MD,
- David Tepper, BA,
- David Flowers, MD,
- Jonathan Wynn, MD,
- Stanley Lam, PhD,
- Deborah Keefe, MD, FACC,
- Dennis S. Miura, MD and
- John C. Somberg, MDa,1
- ↵aAddress for reprints: John C. Somberg, MD, Albert Einstein College of Medicine, 1300 Morris Park Avenue, F-208, Bronx, New York 10461.
Amiodarone is an antiarrhythmic agent known to cause prolongation of action potential duration which is reflected in the electrocardiogram as a prolongation of the QT interval. Prolongation of the QT interval in patients dying suddenly was compared with that in patients who remained alive to determine whether a difference existed between these two groups. The electrocardiogram and amiodarone levels were evaluated in 33 patients who presented with cardiac arrest and symptomatic ventricular tachycardia in whom no other antiarrhythmic agent was found effective in preventing induction of ventricular tachycardia during electrophysiologic studies. There were 30 men and 3 women (mean age 62 ± 10 years). Twenty-three are alive after a mean follow-up period of 12 ± 7 months. Ten died: six suddenly, three of non-cardiac causes and one of congestive heart failure.
Using a two-way analysis of variance, the percent change in QT, QTc, JT and JTc intervals before and after amiodarone therapy was analyzed. Marked prolongation in the QT interval was present in patients who remained alive with amiodarone therapy: A significant difference in percent QT prolongation was seen between the latter patients and those who died suddenly (p < 0.005). No difference was observed in the percent change in QRS interval between the two groups. The levels of amiodarone (2.5 versus 3.2 μg/ml) and its metabolite (desethylamiodarone) were not significantly different between the living patients and those who died suddenly. These findings suggest that a prolongation of the QT interval may be a marker for the therapeutic antiarrhythmic effect of amiodarone.
- Received April 16, 1985.
- Revision received August 7, 1985.
- Accepted August 16, 1985.
- American College of Cardiology Foundation