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At least 505 records · Page 28Linked to original sources
PubMed1983

Prevention of cardiovascular events in variant angina by long-term diltiazem therapy.

In 43 patients with variant angina, the cardiovascular event rate during diltiazem therapy was compared with that in an equal time period before initiation of therapy. Cardiovascular events, that is, myocardial infarction, sudden death and hospitalization for prolonged angina, were decreased significantly (p less than 0.01) during the initial 6 months and mean 19.6 months of therapy. Based on the binomial principle, there were 22 events during the mean 19.6 months before therapy and 2 events during the equal time period on therapy. No patient died during follow-up. The frequency of angina was decreased by 94%. Diltiazem was well tolerated by all patients and no patient had to discontinue therapy because of adverse effects. It is concluded that long-term diltiazem therapy reduces cardiovascular events in patients with variant angina.

Adult↗
PubMed1996

Relation between severity of magnesium deficiency and frequency of anginal attacks in men with variant angina.

OBJECTIVES: We evaluated whether the severity of magnesium deficiency was correlated with the frequency of attacks of variant angina. BACKGROUND: Magnesium deficiency may be associated with the development of variant angina. However, the relation between the activity of variant angina and magnesium deficiency remains to be elucidated. METHODS: We assessed the body magnesium status of 18 men with variant angina: Group 1 (> or = 4 attacks/week, n = 7) and Group 2 (< 4 attacks/week, n = 11). Concentrations of magnesium were determined in serum, urine, mononuclear cells and erythrocytes, and the 24-h magnesium retention rate was determined. RESULTS: Group 1 showed a higher 24-h magnesium retention rate (mean +/- SEM 63.5 +/- 7.6% vs. 24.9 +/- 2.7%, p < 0.01) and a lower intracellular concentration of magnesium in mononuclear cells and erythrocytes than did Group 2 (respectively, 156.3 +/- 13.5 vs. 212.1 +/- 6.9 fg/cell, p < 0.01; and 3.5 +/- 0.5 vs. 5.2 +/- 0.4 fg/cell, p < 0.05), demonstrating the presence of magnesium deficiency in Group 1. The 24-h magnesium retention rate and intracellular concentrations of magnesium in mononuclear cells and erythrocytes correlated well with the frequency of anginal attacks (r = 0.78, p < 0.01; r = -0.78, p < 0.01; r = -0.62, p < 0.01, respectively) for all patients. CONCLUSIONS: Data suggest that the magnesium status of men with variant angina is closely related to disease activity.

Aged↗
PubMed2006

Thyrotoxicosis-induced prinzmetal variant angina.

We describe a postmenopausal women with new onset of variant angina caused by thyrotoxicosis due to Graves' disease. During exercise bicycle ergometry at 50 Watts, the patient developed typical angina with ST segment elevation in the precordial leads. A coronary angiogram revealed normal coronary arteries. Graves' disease with overt hyperthyroidism was diagnosed. After achieving an euthyroid state with administration of propylthiouracil, the symptoms resolved completely and the patient had a normal exercise capacity without electrocardiographic changes. Thus, we conclude that in patients with thyrotoxicosis, variant angina and normal coronary arteries, restoration of normal thyroid function may be curative.

Angina Pectoris, Variant↗
PubMed1995

Is cardiac migraine a clinical entity?

Chest pain because of a disorder of the coronary circulation is assumed to be ischemic in nature. Irrespective of the underlying pathophysiological mechanism, it is accepted that all routes lead to myocardial ischemia in the pathway to anginal pain. The authors describe a patient with a history of vasoactive disorders including migraine, asthma, documented variant angina with prolonged episodes of chest pain, and scintigraphic evidence of inferior and posterior wall ischemia during exercise and ergonovine testing in the absence of significant underlying stenoses. Remarkably, severe retrosternal chest pain, ST segment depression in multiple leads, and relative increased uptake in the inferior and posterior walls on Tc-99m sestamibi tomographic images developed during pharmacologic coronary vasodilatation with dipyridamole, leading the authors to speculate as to the possible existence of a nonischemic chest pain syndrome caused by coronary vasodilatation either in association with variant angina or as a separate entity.

Angina Pectoris, Variant↗
PubMed1981

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.

Adult↗
PubMed1978

Coronary arterial spasm and Prinzmetal's variant form of angina induced by hyperventilation and Tris-buffer infusion.

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.

Angina Pectoris↗
PubMed1986

Autopsy findings of the coronary arteries of variant angina with Raynaud's phenomenon of the tongue.

A 42 year old man with variant angina occasionally associated with syncopal attacks died of acute myocardial infarction 17 months after the onset of angina. Prior to the onset of variant angina, he had Raynaud's phenomenon of the tongue for 2 years. Both Valsalva maneuver and hyperventilation could repeatedly provoke chest pain and ST segment elevation in leads II, III and aVF. The infusion of prostaglandin E1 at a rate of 0.05 microgram/kg/min, was able to prevent the attack of variant angina induced by these maneuvers. Although coronary angiography performed 15 months prior to death revealed no organic lesions except for complete spastic occlusion at segment 1 following intravenous ergonovine, autopsy revealed marked intimal proliferation and accumulation of abundant glycosaminoglycans in three coronary vessels, as well as in small and muscular arteries of other organs. This suggests that a rapid systemic progression of narrowing due to proliferation of the intima might occur in some cases of variant angina.

Adult↗
PubMed1979

Similarities of ergonovine-induced and spontaneous attacks of variant angina.

Ergonovine has been shown to provoke attacks of variant angina, but a question remains whether spontaneous and ergonovine-induced attacks of variant angina are similar. Seven patients with variant angina undergoing cardiac catheterization were studied during transient episodes of spontaneous and ergonovine-induced rest angina with ST-segment elevation. Clinical, electrocardiographic, left ventricular hemodynamic and coronary angiographic observations were made before and repeated after ergonovine (0.05-0.2 mg I.V.). The character and duration of chest pain were similar during both spontaneous and ergonovine-induced episodes. ST-segment elevation (greater than 1 mm) was present inferiorly in three patients, anteriorly in three patients, and both inferiorly and anteriorly in one patient during both episodes. Mean heart rate and systolic arterial pressure changed little, while left ventricular end-diastolic pressure increased significantly during spontaneous or ergonovine-induced attacks. We observed subtotal or total dynamic obstruction in the left anterior descending (three patients), right coronary arteries (three patients) and both arteries in one patient during both attacks. Thus, in selected patients ergonovine-induced attacks of variant angina were remarkably similar to spontaneous episodes.

Adult↗
PubMed1984

Magnesium sulfate in the treatment of variant angina.

41 episodes of anginal attacks were promptly terminated by a bolus of Mg sulfate administered intravenously in 15 patients with variant angina. Pretreatment with parenterally administered Mg sulfate in four of these patients prevented further attacks.

Aged↗