Biomedical subjects
Publications and source records attributed to S Omote.
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In four patients with exertional angina induced by arm exercise, coronary arteriograms taken before, during and after the attack demonstrated that spasm appeared in the large coronary artery supplying the area of myocardium shown to be ischemic in the electrocardiogram during the attack. The spasm disappeared with subsidence of the attack after administration of nitroglycerin. Anginal attacks induced by treadmill exercise were not suppressed by propranolol, 60 mg orally, in two of the four patients. However, such attacks were suppressed in all patients by oral administration of diltiazem (90 mg, four patients) or nifedipine (20 mg, three patients) or intramuscular injection of phentolamine (0.2 mg/kg body weight, three patients). It is concluded that coronary arterial spasm can be induced by exercise and can cause exertional angina in some patients. Diltiazem and nifedipine, calcium antagonistic drugs, prevent spasm.
Thirteen patients with Prinzmetal's variant angina performed treadmill exercise tests in the early morning and in the afternoon of the same day. The attacks with ST elevation were induced repeatedly in all 13 patients in the early morning, but in only two patients in the afternoon. Propranolol did not suppress the exercise-induced attacks in all 13 patients. Diltiazem suppressed the attacks in all 13 patients and phentolamine in eight of the nine patients. Coronary arteriograms demonstrated that spasm occluding completely or almost completely the large coronary artery supplying the area of myocardium showing ST elevation appeared during the attacks and disappeared along with the attacks after nitroglycerin administration in all four patients in whom the attacks were induced by arm exercise in the catheterization laboratory. We conclude that there is circadian variation of exercise capacity in patients with Prinzmetal's variant angina caused by coronary arterial spasm induced by exercise in the early morning but not in the afternoon.
Vigorous hyperventilation was induced for five minutes immediately after a five-minute infusion of 100 ml of Tris-buffer (pH 10) in nine patients with Prinzmetal's variant angina. In eight of the patients, chest pain with ischemic changes in the electrocardiogram occurred during this procedure or within five minutes after it ended. Coronary arterial spasm appeared after the procedure and disappeared after the administration of nitroglycerin in all four patients in whom coronary cinearteriography was performed. This was evident both before and after the procedure and after sublingual administration of nitroglycerin (0.6 mg). The oral administration of 90 mg of diltiazem, a calcium antagonistic drug, two hours before, completely suppressed the attack induced by the procedure in all of the five patients who received this drug. We conclude that hyperventilation plus Tris-buffer infusion induces coronary arterial spasm and anginal attack in patients with Prinzmetal's variant angina and that diltiazem suppresses these reactions.
To twenty six patients with angina at rest (including 13 patients with Prinzmetal's variant angina), propranolol 40--50 mg, dilitiazem 60--90 mg, dipyridamole 50 mg, atropine sulfate 0.6 mg and phenoxybenzamine 10--20 mg were given at 9:00 p.m. and 2:00 a.m. (except phenoxybenzamine which was given only at 9:00 p.m.) to examine the effect of these drugs on the attack. Propranolol was not only ineffective in suppressing the attack but rather tended to aggravate it in all the cases of Prinzmetal's variant angina. It was effective to some degree in 5 of 13 cases of angina at rest other than Prinzmetal's variant angina. Diltiazem suppressed the attack completely and dramatically in all the cases of angina at rest (including Prinzmetal's variant angina). Dipyridamole was ineffective in all the cases except one in suppressing the attack. Atropine sulfate and phenoxybenzamine suppressed the attack in 13 of 21 cases and in 6 of 12 cases respectively. Coronary arteriography was done before and after the intravenous administration of 10 mg of diltiazem in 8 patients and it was demonstrated that diltiazem dilates large coronary arteries in all these patients. It is concluded that diltiazem, a calcium antagonistic drug, is specifically effective in suppressing the attack of angina at rest by dilating large coronary arteries and that the autonomic nervous system plays a role in the genesis of the attack probably by constricting large coronary arteries by way of alpha adrenergic receptors.