Use of digitalis in
myocardial infarction is controversial. To determine the efficacy and toxic threshold, serial infusions of 3 mug/kg per min of acetyl-
strophanthidin were given to six intact conscious dogs 24 hr before and 1 hr, 2 days, and 7 days after
myocardial infarction induced by inflation of a balloon cuff implanted on the left anterior descending coronary artery. Within 1 hr after
myocardial infarction, heart rate increased by 28%. Left ventricular end-diastolic pressure increased from 7 to 20 mm Hg, and stroke volume decreased by 25%. At this time
acetylstrophanthidin caused no beneficial hemodynamic change, 1 wk later, the heart rate and left ventricular end-diastolic pressure had declined toward normal but remained elevated. At this time,
acetylstrophanthidin lowered left ventricular end-diastolic pressure by 25%, and increased the stroke volume and cardiac output by 25% and 21% respectively, without any change in heart rate or aortic pressure. Tolerance to
acetylstrophanthidin, defined as appearance of
ventricular tachycardia, declined the 1st hr after
myocardial infarction by 24% (P<0.05) from the control level of 43 +/-4 mug/kg (SEM), but subsequently returned to control.Thus, immediately after
myocardial infarction, tolerance to
acetylstrophanthidin was reduced, and left ventricular failure was not ameliorated. 1 wk later in the healing phase of
myocardial infarction, tolerance to
acetylstrophanthidin returned to normal and left ventricular performance was improved by this
drug. The study suggests a limited therapeutic role for digitalis in the treatment of left ventricular failure in the acute phase immediately after
myocardial infarction, but beneficial effects may occur in the healing phase 1 wk later.