Sotalol-Induced Beta Blockade in Cardiac Patients
Sotalol (MJ 1999), a beta-adrenergic blocking agent found to have no significant intrinsic myocardial depressant effects, was administered intravenously to 20 patients with heart disease. Eight of the patients had clinical and hemodynamic evidence of chronic heart failure. Doses ranged from 0.2 to 0.6 mg/kg.
In all studies, heart rate decreased significantly, accompanied by comparable decreases in cardiac index and tension-time index. There were, however, no significant changes in stroke index, mean blood pressure, or left ventricular end-diastolic pressure—even in those patients with advanced heart failure, indicating that the changes noted were primarily rate-related and could not be ascribed to myocardial depression. To confirm this, further studies were performed in which heart rate was held constant by atrial pacing in normal and catecholamine-depleted dogs. Sotalol, at doses much higher than the minimal beta-blocking dose, did not change stroke index, blood pressure, left ventricular end-diastolic pressure, or estimated maximal velocity of isotonic shortening (Vmax), confirming that myocardial contractility was unaffected.
It is concluded that sotalol-induced beta blockade had no observable myocardial depressant action in dogs or adverse hemodynamic effects in cardiac patients, even when advanced chronic heart failure was present.
- Beta-adrenergic influences in heart failure
- Force-velocity relationship in intact circulation
- Myocardial contractility
- Myocardial depression
- Received March 2, 1970.
- Accepted March 20, 1970.
- © 1970 American Heart Association, Inc.