Beneficial effects of timolol on infarct size and late ventricular tachycardia in patients with acute myocardial infarction.

This investigation was undertaken to study the effects of beta-adrenergic blockade with timolol on infarct size and on the incidence of late ventricular tachycardia in patients with acute myocardial infarction of less than 6 hr of evolution. Patients were assigned randomly either to a placebo-treated group (98 patients) or to a timolol-treated group (102 patients). The patients were treated with 5.5 mg iv timolol (or matched placebo) as a bolus divided into four doses during the first 2 hr followed by 10 mg orally twice daily for 1 month. Cumulative total creatine kinase (CK) release, which reflects the amount of myocardial necrosis was 1677 +/- 132 IU/liter in the placebo group (n = 83) and 1274 +/- 73 IU/liter in the timolol group (n = 81, p less than .01), a 24% reduction. Cumulative release of CK-MB was 138 +/- 8 IU/liter in the placebo group and 106 +/- 8 IU/liter in the timolol group (p less than .01), a 23% reduction. Twenty-four hour Holter electrocardiograms were obtained on days 7, 14, 21, and 28 after the onset of the acute myocardial infarction in 80 patients in the placebo group and 82 patients in the timolol group. The incidence of ventricular tachycardia was lower in the timolol than in the placebo group (7 vs 16 patients, p = .05). We conclude that early administration of intravenous timolol followed by oral treatment in patients with acute myocardial infarction reduces infarct size as assessed by CK and CK-MB serum activity, and decreases the occurrence of late ventricular tachycardia.

Efficacy of chronic amiodarone therapy in patients with variant angina pectoris and inhibition of ergonovine coronary constriction.

In three patients with vasospastic angina pectoris, chronic amiodarone administered orally at doses of 800 and 1,000 mg/day totally suppressed spontaneous episodes of ischemic chest pain for 8 to 14 months. Before treatment, ergonovine maleate 0.2 to 0.4 mg intravenously provoked chest pain and similar ischemic ECG changes as those occurring spontaneously. During amiodarone treatment ergonovine vasoconstriction was totally or partially inhibited. In addition to calcium-blocking agents, amiodarone is another spasmolytic drug which effects smooth muscle relaxation by different mechanisms and appears to be useful for the chronic treatment and prevention of variant angina. The vasodilator property of amiodarone is achieved by both direct action and noncompetitive alpha receptor antagonism of coronary vasculature.

Spontaneous remission in variant angina.

Four cases of variant angina are reported, in which total remission of anginal pain was documented during a follow-up of seven months, four years, five years, and 15 years, respectively. During this relatively long follow-up, the clinical course of the disease was apparently benign. The possibility of spontaneously and complete recovery may be postulated. The natural history of relatively benign forms a variant angina is poorly known and understood.

Electrophysiologic and pharmacologic studies in a patient with acute myocardial infarction complicated by intraventricular and atrioventricular block.

A patient with an acute anterior wall myocardial infarction complicated by bilateral bundle branch block and paroxysmal AV block is presented. The following new, uncommon or unreported phenomena were documented: the simultaneous occurrence of phase-3 block in the right bundle branch and phase-4 block in the left bundle branch; the simultaneous occurrence of phase-4 block in both main bundle branches; phase-4 left posterior hemiblock associated with escape beats arising from the injured posterior division of the left bundle branch; supernormal conduction in the right bundle branck and 2:1 right bundle branch block related to supernormality. Most of these changes were, of course, not simultaneous, and their successive appearance was related to day-to-day and sometimes hour-to-hour variations in the degree and quality of the multifascicular injury caused by the infarct. In addition, the actions of several drugs upon automaticity and conduction were tested. The effects of amiodarone, lidocaine and isoproterenol were similar to those previously reported under comparable circumstances. At a moment when the patient had repeated episodes of paroxysmal AV block with severe Adams-Stokes seizures, the administration of a single i.v. dose of 0.25 mg of strophanthin suppressed totally the Adams-Stokes attacks through a significant enhancement of ventricular automaticity. If rapid implantation of an artifical pacemaker is not at hand, strophanthin may be life-saving in patients with acute paroxysmal AV block.