Cardiovascular effects of a newer antiarrhythmic agent, disopyramide phosphate

Abstract

The effect on myocardial contractility of a new antiarrhythmic drug, disopyramide phosphate, was investigated and compared with that of quinidine using a Walton-Brodie strain gauge arch. Quinidine and disopyramide phosphate were compared at the same dosage, ranging from 1 to 10 mg. per kilogram of body weight. At 1 mg. per kilogram of body weight, the contractile force was unaffected by quinidine but was depressed 42 per cent by disopyramide phosphate. At higher dose (5 to 10 mg. per kilogram of body weight) the contractile force was depressed 50 to 100 per cent more by disopyramide phosphate than by quinidine. End-diastolic muscle segment length increased 5 per cent with disopyramide phosphate at 1 mg. per kilogram of body weight, whereas no change was observed with quinidine at this dosage. Both drugs widened QRS and P duration and prolonged PR interval to the same degree. Disopyramide appears to have no beta-adrenergic blocking activity, since it did not alter the contractile force or arterial blood pressure responses to isoproterenol, norepinephrine, or tyramine. Coronary blood flow was decreased by both drugs. The cardiac depressant effect of disopyramide phosphate would appear to limit its usefulness, but for the same degree of cardiac depression, disopyramide phosphate exhibited fewer ECG abnormalities and hence could be used as a replacement therapy for quinidine.