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PubMed1989

[Variant angina].

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Angina Pectoris, Variant↗
PubMed1981

Exercise-induced angina provoked by aspirin administration in patients with variant angina.

The effects of aspirin (4.0 g/day) given orally to eight patients with variant angina were observed. An exercise stress test performed in the morning was positive in two of seven patients during placebo administration, whereas a test performed in the afternoon at the same exercise work load resulted in negative findings. During aspirin administration, the afternoon exercise test repeatedly provoked anginal attacks associated with electrocardiographic changes (S-T segment elevation in five and S-T depression in two). Rate-pressure product at the end of the exercise test during aspirin administration was significantly lower than that during placebo administration (p less than 0.01). During aspirin administration, the frequency of angina increased markedly, and the attacks occurred not only during the night or early morning but also in the daytime in six of the eight patients. Our observations suggest that aspirin, in this large dose, reduces the capacity for exercise and provokes exercise-induced coronary arterial spasm in patients with variant angina.

Adult↗
PubMed1987

Prinzmetal's angina during 5-fluorouracil chemotherapy.

Variant angina developed during intravenous 5-fluorouracil therapy in a patient without prior history of angina pectoris. Ambulatory electrocardiography demonstrated S-T segment elevation and ventricular ectopy during pain, whereas no symptoms or S-T segment changes occurred during placebo therapy. Prophylaxis with both nifedipine and diltiazem was successful in preventing recurrence. It is believed that 5-fluorouracil induced coronary vasospasm and that this was prevented by prophylactic calcium antagonist therapy. Drug-induced coronary artery spasm may be the cause of 5-fluorouracil-associated chest pain.

Angina Pectoris, Variant↗
PubMed1982

Surgical therapy for Prinzmetal's variant angina.

Fifty-two patients underwent coronary artery bypass grafting between 1973 and 1979 for variant angina, defined as pain, usually at rest, associated with S-T segment elevation. Only patients with fixed occlusive coronary artery disease, defined as greater than 70% narrowing in diameter, were included. When fixed coronary artery stenosis is present, variant angina--whether presenting as stable, unstable, or postinfarction angina, and regardless of the number of vessels diseased--is effectively treated by myocardial revascularization. Preoperative intraaortic balloon pumping is a useful therapeutic adjunct in the unstable subset refractory to medical therapy. The results of revascularization in patients with Prinzmetal's variant angina and fixed coronary disease were no different from those in patients with classic angina pectoris of comparable clinical categories.

Adult↗
PubMed1991

Usefulness of intracoronary injection of acetylcholine as a provocative test for coronary artery spasm in patients with vasospastic angina.

In order to examine both the sensitivity and specificity of coronary artery spasm induced by intracoronary injection of acetylcholine in patients with vasospastic angina, incremental doses of acetylcholine (20, 30, and 50 micrograms) were injected directly into each coronary artery in 21 patients with variant angina (group A), in 28 patients with other types of vasospastic angina (group B), and in 20 patients without any significant coronary artery disease (group C). Coronary artery spasm was defined as severe vasoconstriction (greater than or equal to 90% of reduction in luminal diameter) with chest pain and/or ischemic changes in the electrocardiogram. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in 20 patients (95%) of group A, in 27 patients (96%) of group B, and in only 2 patients (10%) of group C. The low dose of acetylcholine (20 micrograms) induced coronary spasm more frequently in group A patients (81%) than in group B patients (43%) (P less than 0.05). ST-segment elevation associated with anginal attacks was significantly (P less than 0.05) more frequent in group A (71%) than in group B (39%). When acetylcholine was injected separately into the left and right coronary arteries, spasm of both coronary arteries was observed in 7 out of 14 of group A (50%), in 8 out of 22 of group B (36%), and in none of the 20 of group C. We concluded that intracoronary injection of acetylcholine is a sensitive and reliable method for the induction of coronary spasm in patients with vasospastic angina as well as in those with variant angina.

Acetylcholine↗
PubMed1984

Mechanisms of methacholine-induced coronary vasospasm in an experimental model of variant angina in the anesthetized rat.

Methacholine (Mch), when injected near the ostia of the coronary arteries, induces an intense coronary vasospasm which can be measured by the degree of S wave elevation monitored from an electrocardiogram (ECG). The observed ECG changes resemble those occurring in patients with variant angina. The effects of Mch were blocked by atropine, but not by d-tubocurarine, hexamethonium, adrenergic receptor blockade, or prior reserpinization, indicating that Mch is acting directly on muscarinic receptors to produce a vasoconstriction of the coronary arteries. This model of Mch-induced coronary vasospasm appears to be useful for testing spasmolytic agents which might be of benefit in variant angina.

Angina Pectoris, Variant↗