Haemodynamic effects of dextro-propranolol in acute myocardial infarction.

Racemic propranolol has been shown to be an effective antidysrhythmic agent in many circumstances (Frieden, 1967; Gettes and Surawicz, 1967; Gibson and Sowton, 1969), including the management of ventricular fibrillation following infarction (Sloman, Robinson, and McLean, 1965). Its depressant effects on myocardial function (Bay, Lund-Larsen, Lorentsen, and Sivertssen, 1967) limit its use in seriously ill patients, although Stannard, Sloman, and Sangster (1968) reported that the reduction in cardiac output could be largely prevented by the addition of atropine. The dextro-isomer of propranolol (I.C.I. 47,319) is almost devoid of blocking activity during an isoprenaline challenge in animal investigations (Howe and Shanks, 1966) and in normal volunteers (Shanks, 1968, personal communication). D-Propranolol possesses considerable antidysr&hythmic activity and will rapidly revert ouabain-induced tachycardia in dogs and cats to sinus rhythm (Howe and Shanks, 1966). Howitt was able to control various dysrhythmias in 59 patients (Howitt, Husaini, Rowlands, Logan, Shanks, and Evans, 1968) and reported that 5-20 mg. of dextropropranolol given intravenously was as effective as the racemic drug in treating ventricular and supraventricular ectopic beats. In six of his patients the dextro-isomer terminated digitalisinduced dysrhythmias. It seems possible that dextro-propranolol might be indicated in preference to the racemic drug in patients following cardiac infarction. This report concerns the haemodynamic effects of D-propranolol in 13 patients with recent cardiac infarction.