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1 Cardiovascular Division, Department of Medicine, Peter Bent Brigham Hospital, Harvard Medical School, and the Department of Cardiology, Boston University Hospital, Boston, Massachusetts
The inotropic time course of acetylstrophanthidin (AS) in man was assessed noninvasively with systolic time interval (STI) measurements. Changes in myocardial contractility were determined from shortening of left ventricular ejection time index and electromechanical systolic index. AS was administered intravenously to 12 subjects, none of whom had congestive heart failure. Two had coronary atherosclerosis and the others were normal. Two AS infusion schedules were employed: 1) a 1.0-mg injection completed within 5 minutes in five cases; 2) successive 0.2-mg injections every 6 minutes with a total of 1.0 mg of AS given within 24 minutes in seven cases. With the slower drug schedule, maximal shortening of STI occurred within 1 minute after the last AS dose. Mean apparent half-time (T
) for subsidence of drug effect was 34.0 ± 4.4 minutes for left ventricular ejection time index and 34.0 ± 4.9 minutes for electromechanical systolic index. With the faster AS schedule, maximal shortening of STI was noted 15 to 22 minutes after completion of drug infusion. T
for disappearance of drug action was 59.2 ± 10.8 minutes for left ventricular ejection time index and 55.5 ± 8.2 minutes for electromechanical systolic index. Plasma level T
for AS nadioimmunoassay determined in three of these cases averaged 136 minutes. Mechanical action of AS upon the heart is brief, paralleling an abbreviated rate slowing period in atrial fibrillation. T
for dissipation of STI shortening is 22 to 33 times less than rapidly acting cardiac glycosides in clinical usage.