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PubMed1979

Coronary spasm.

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Angina Pectoris, Variant↗
PubMed1980

Exercise-induced coronary arterial spasm: angiographic demonstration, documentation of ischemia by myocardial scintigraphy and results of pharmacologic intervention.

Exercise-induced coronary arterial spasm is an infrequently recognized phemonemon whose mechanism and management are not well established. In two patients with reproducible exercise-induced S-T segment elevation and angina pectoris thallium-201 scintigraphy showed areas of reversible anteroapical hypoperfusion, and gated radionuclide ventriculography revealed anteroapical hypokinesia with a decrease in left ventricular ejection fraction at peak exercise. During coronary arteriography supine exercise provoked occlusive spasm of the left anterior descending coronary artery, which at rest had only minimal plaques. Consequently, treadmill testing was performed with five different pharmacologically provoked interventions: direct vasodilatation (nitrates), alpha adrenergic blockade (phenmoxybenzamine), beta adrenergic blockade (propranolol), calcium flux blockade (verapamil), and prostaglandin inhibition (indomethacin). Exercise-induced coronary arterial spasm, manifested as S-T segment elevation and angina, was prevented by nitrates, but was not eliminated by short-term oral administration of an alpha or beta blocking agent, a calcium antagonist or a prostaglandin inhibitor. Further, beta adrenergic blockade appeared to be detrimental. Thus, this study demonstrates (1) that coronary arterial spasm may be the underlying mechanism of at least some cases of exertional angina associated with transient perfusion deficits and left ventricular dysfunction, and (2) that it may be prevented by oral nitrates.

Angina Pectoris, Variant↗
PubMed1980

Comparative pharmacology of calcium antagonists: nifedipine, verapamil and diltiazem.

Calcium antagonists (slow channel blocking agents) are a very heterogeneous group of agents with dissimilar structural, electrophysiologic and pharmacologic properties. Nifedipine is a potent, long-acting vasodilator that has proved highly efficacious in relieving anginal symptoms caused by coronary vasospasm. In vivo, it exerts no myocardial depressant effects and has no antiarrhythmic properties. Treatment with nifedipine can safely be combined with administration of a beta receptor blocking agent. VErapamil prolongs atrioventricular (A-V) conduction (A-H interval) in a dose-dependent manner. It is the drug of choice for the treatment of reentrant supraventricular arrhythmias, irrespective of whether reentry occurs within the A-V node or through an accessory pathway (the Wolff-Parkinson-White syndrome). Verapamil is only moderately effective as an antianginal agent. Diltiazem is efficacious for the treatment of angiospastic angina, but its value as an antiarrhythmic agent remains to be delineated.

Angina Pectoris↗
PubMed1981

Unstable angina: natural history and determinants of prognosis.

One hundred one patients with unstable angina were treated conservatively without the routine use of beta receptor blocking agents, calcium antagonist drugs, anticoagulant agents or nitrates. Only two patients underwent arteriography and coronary arterial bypass surgery during hospitalization and one patient during the 1st year of follow-up study. The 28 day mortality rate was 4 percent and the total 1 year cardiac mortality rate 10 percent. Two patients died from carcinoma. The incidence rate of nonfatal myocardial infarction was 9 percent during the first 28 days and a further 3 percent for the 1st year. These results compare favorably with the immediate and 1 year prognosis reported from other studies using different treatment procedures, including modern intensive drug treatment and coronary arterial bypass surgery. Various factors studied during the acute stage of unstable angina were assessed in an effort to predict the immediate and long-term outcome. Only persistence of pain after admission to the hospital was found a significant indicator of an adverse prognosis. Modern medical treatment of unstable angina with beta receptor blocking agents, calcium antagonist drugs, anticoagulant agents, nitrates and antiarrhythmic agents is critically examined. The paucity of proper randomized controlled studies confirming the value of medication is underlined. There is little evidence to show that aggressive or intensive medical or surgical treatment is superior to a conservative approach to management in the coronary care unit. This approach includes bed rest until the pain has resolved, symptomatic drug treatment only, the minimal use of invasive investigations and careful risk factor intervention.

Adrenergic beta-Antagonists↗
PubMed1981

Comparison of ambulatory electrocardiography and exercise testing.

Ambulatory electrocardiography and exercise testing are two noninvasive diagnostic procedures widely employed to evaluate patients for cardiac arrhythmias and S-T segment changes. This review addresses the differences and similarities of the two techniques, and examines the relative diagnostic and prognostic merit of the arrhythmia and S-T segment changes detected with each method. Ambulatory electrocardiography is more sensitive than exercise testing in detecting cardiac arrhythmias. The recording of ventricular arrhythmia is of value in predicting sudden death in survivors of myocardial infarction, whereas exercise-induced ventricular arrhythmia has limited predictive value. Nevertheless, exercise-induced S-T depression is of great prognostic value in predicting mortality and sudden death in patients with acute and chronic coronary heart disease.

Ambulatory Care↗
PubMed1981

Nifedipine in the treatment of unstable angina, coronary spasm and myocardial ischemia.

The effects of nifedipine, a potent calcium antagonist, were studied in patients with unstable angina, coronary spasm and myocardial ischemia. Data from two separate groups of patients studied in the cardiac catheterization laboratory indicate that intracoronary injection of nifedipine promptly reversed coronary spasm--whether provoked or spontaneous--in five of six patients. In other patients, direct intracoronary injection of the drug was compared with intravenous administration. After intracoronary injection, local mechanical cardiac action virtually ceased, and the ventricular wall became thinner during systole. Thus, a specific inhibitory action on contractile energy expenditure could be demonstrated in the presence of increased coronary flow. This "oxygen-sparing" effect was tested in a group of 31 patients with symptomatic unstable angina whose pain at rest, with ST-T changes, had not responded to 8 hours of treatment with maximal beta adrenergic blockade, nitrates and bed rest. The addition of 6 X 10 mg of nifedipine rendered 27 of these patients asymptomatic within 1.5 hours. In the four patients who did not respond, coronary arteriography demonstrated severely stenotic lesions. Two of the four patients subsequently responded to intraaortic balloon pumping and bypass surgery; one patient had a myocardial infarction and one who had a 90 percent reduction in the diameter of the left main coronary artery, died. It is concluded that nifedipine should be added to beta adrenergic blockade therapy if the latter does not appear to be immediately effective. This combination has not been shown to cause any hemodynamic deterioration, and only a minority of the patients treated sustained a myocardial infarction during the first 3 months of follow-up. The use of nifedipine in unstable angina deserves further clinical evaluation.

Adult↗
PubMed1981

Comparison of coronary arteriographic findings during angina pectoris associated with S-T elevation or depression.

Coronary arteriographic findings during an attack of angina pectoris associated with S-T segment elevation and angina associated with S-T depression were compared in 54 patients. Thirty-eight attacks with S-T segment elevation included 2 that were spontaneous, 6 induced by methacholine, 4 by epinephrine with or without propranolol, 9 by arm exercise, 5 by hyperventilation with or without Tris-buffer infusion and 12 by ergonovine maleate. Twenty-nine of the 38 attacks were associated with total occlusion, 8 with subtotal occlusion and 1 with diffuse narrowing of a major coronary artery caused by spasm. Twenty-six attacks with S-T segment depression included 3 induced by methacholine, 13 by arm exercise, 3 by hyperventilation with or without Tris-buffer infusion and 7 by ergonovine maleate. Eight of the 26 attacks were associated with subtotal occlusion and 9 with diffuse narrowing of a major coronary artery caused by spasm; 3 attacks were associated with total occlusion of a major coronary artery well supplied with collateral vessels and 2 with total occlusion of a small coronary branch caused by spasm. Four attacks were associated not with spasm but with fixed subtotal occlusion of a major coronary artery (3 attacks) or total occlusion of a major coronary artery receiving collateral vessels (1 attack). Only 2 of the 31 patients with S-T segment elevation had collateral vessels compared with 8 of the 16 patients with S-T segment depression (p less than 0.001). It is concluded that angina pectoris associated with S-T segment elevation usually indicates more severe myocardial ischemia than angina associated with S-T segment depression.

Adult↗
PubMed1981

Nifedipine blockade of ergonovine-induced coronary arterial spasm: angiographic documentation.

To determine whether calcium-flux blockade with nifedipine blunts coronary vasospasm, four patients with angiographically demonstrable coronary arterial spasm in the absence of significant fixed coronary arterial stenosis were evaluated with coronary arteriography before and after treatment with nifedipine. After initial coronary arteriography, ergonovine was administered in successive doses of 0.05, 0.1 and (when necessary) 0.2 mg intravenously at 3 minute intervals. Three patients had symptomatic high grade focal coronary arterial spasm with electrocardiographic changes, and the fourth exhibited asymptomatic 60 percent constriction of the left anterior descending coronary artery. A maximal ergonovine challenge was repeated 30 minutes later after each patient had been pretreated with a 20 mg sublingual dose of nifedipine. Under these conditions, no patient had chest pain or electrocardiographic changes. Furthermore, neither focal nor diffuse coronary arterial spasm was demonstrable angiographically after the second challenge. Thus, in each case, a single dose of nifedipine precluded the angiographic expression of ergonovine-provoked coronary arterial spasm.

Angina Pectoris↗