Abstract
The effects of diltiazem were tested in chronically instrumented dogs in a model of exercise-induced myocardial dysfunction. Since various bradycardiac agents have beneficial effects on myocardial function during ischemia, it was of interest to find out how a decrease in afterload, possibly combined with a decrease in myocardial oxygen demand, influences dysfunction. Therefore, diltiazem (1 mg/kg i.v.) was tested during critical stenosis of the circumflex branch of the left coronary artery, which led to exercise-induced myocardial dysfunction. At rest, diltiazem causes a reflex increase in heart rate. During exercise, a decrease in heart rate and hence in myocardial oxygen demand was neutralized by a decrease in arterial blood pressure and hence a lowered myocardial perfusion pressure. Therefore, systolic shortening in the ischemic area improved neither at rest nor during exercise after diltiazem.
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