Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently, in Prinzmetal's variant angina, many cases with normal coronary arteries have been reported. The anginal attacks frequently relapse after aortocoronary bypass grafting. It is frequently possible to induce an anginal attack by parasympathomimetic agents such as methacholine and pilocarpine. In this study, methacholine (0.13 mg per kilogram) was injected subcutaneously in three cases of this disease to induce an angina attack, and coronary arteriograms and left ventriculograms were recorded. In all cases a coronary arterial spasm corresponding to the site of the ST-segment elevation in the electrocardiogram was observed. Complete occlusion due to the spasm was observed even in the normal coronary artery. Asynergy was seen in the left ventricular wall corresponding to the site of the ST-segment elevation in the electrocardiogram.
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PMID:Prinzmetal's variant angina. Coronary arteriogram and left ventriculogram during angina attack induced by methacholine. 124 51

The attacks of vasospastic angina or coronary spasm can be induced by injection of epinephrine, cold pressor test, Valsalva maneuver, and exercise. The attacks induced by these procedures can be suppressed by injection of phentolamine, an alpha adrenergic blocking agent in 80 per cent of the patients. On the other hand, propranolol, a beta adrenergic blocking agent, is not only ineffective in suppressing the attacks but aggravates the attacks in 50 per cent of the patients. Thus, alpha adrenergic receptors seem to play an important role in the production of vasospastic angina. The attacks of vasospastic angina can also be induced by injection of methacholine, a parasympathomimetic agent, and this reaction is suppressed by atropine, a parasympathetic blocking agent. Thus, parasympathetic nervous system also seems to play a role in the production of vasospastic angina. The attacks of vasospastic angina can be easily induced by adrenergic or parasympathetic stimuli from midnight to early morning but is usually not provoked by these stimuli in the daytime. Thus, there is circadian variation in the reactivity of coronary arteries to adrenergic or parasympathetic stimuli. There are also weekly, monthly and yearly variations of the reactivity of coronary arteries to these stimuli. Thus, alpha adrenergic or parasympathetic activity is not the sole factor in the production of vasospastic angina. Angina pectoris caused by increased myocardial oxygen demand is induced by infusion of isoproterenol, a beta adrenergic stimulant, and is suppressed by propranolol but not by phentolamine. So, beta adrenergic receptors play an important role in the production of angina pectoris caused by increased myocardial oxygen demand or organic angina pectoris.
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PMID:Role of autonomic nervous system in the pathogenesis of angina pectoris. 630 98

Coronary arterial spasm plays an important role iun the production not only of variant angina but, also, of resting angina other than variant angina, of some exertional angina, and of some acute myocardial infarction. Coronary arterial spasm is most likely to occur at rest, particularly from midnight to early morning, and is usually not provoked by exercise in the daytime. This is related to the fact that the tone of coronary artery is increased from midnight to early morning, whereas it is decreased in the daytime after physical activities. Coronary arterial spasm can be induced by exercise, cold pressor test, hyperventilation, Valsalva maneuver, and the administration of pharmacological agents such as sympathomimetic agents (epinephrine, norepinephrine, etc.), beta-blocking agents (propranolol, etc.), parasympathomimetic agents (methacholine, pilocarpine, etc.), ergot alkaloids (ergonovine, ergotamine, etc.), alcohol, and others, particularly in the morning when spontaneous coronary arterial spasm is most likely to occur. Diltiazem and nifedipine, calcium-blocking agents, prevent coronary arterial spasm induced by these procedures in almost all patients. Phentolamine, an alpha-blocking agent, also suppresses coronary arterial spasm induced by these procedures in 81% of the patients. On the other hand, propranolol, a beta-blocking agent, is not only ineffective in suppressing coronary arterial spasm in 82% of the patients, but aggravates coronary arterial spasm in 41% of the patients. The acute attack of coronary arterial spasm can be promptly relieved by the administration of nitroglycerin.
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PMID:Coronary arterial spasm in ischemic heart disease and its pathogenesis. A review. 633 4

We report 13 patient with unequivocal Prinzmetal's variant angina pectoris as the entire experience with this syndrome during a 7-year period in a single institution. The clinical diagnosis of this relatively uncommon disorder is emphasized. Five patients were given 10 mg of methacholine subcutaneously. Three demonstrated subsequent delayed appearance of chest pain, ECG change, and coronary vasospasm following early appearance of muscarinic effects. Two Prinzmetal patients had no provocation of variant angina following methacholine, though they did experience significantly less blood pressure fall in response to muscarinic provocation. Another 23 subjects with incompletely explained chest pain given methacholine had neither ECG change nor spasm. Methacholine provocation of variant angina need not necessarily implicated a parasympathomimetic mechanism for otherwise spontaneous episodes. Rather, provocation would appear to occur via the customary reflex adrenergic response to drug-induced hypotension. Methacholine is probably safe though unreliable as an agent to be used for spasm provocation.
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PMID:Methacholine provocation of Prinzmetal's variant angina pectoris: a revised perspective. 674 64