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)

Spasm of coronary arteries can cause chest pain indistinguishable from classic angina pectoris in patients without atherosclerosis of these vessels or recognizable heart disease. Associated electrocardiographic changes usually correspond to the coronary artery affected and disappear when the attack of pain ends. Sublingual nitrates are excellent agents for the control of the episodic anginal symptoms. There have been scattered reports of myocardial infarction occurring in patients with normal coronary arteries; a role of arterial spasm in these cases in speculative.
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PMID:Myocardial ischemia from coronary arterial spasm. 0 82

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.
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PMID:Coronary arterial spasm and Prinzmetal's variant form of angina induced by hyperventilation and Tris-buffer infusion. 2 20

A randomized, double-blind study was carried out in 24 patients with stable angina pectoris to compare the efficacy of nadolol, a new beta-adrenoceptor antagonist, and propranolol. After a period on placebo, 14 patients received nadolol once daily and 10 patients propranolol 4-times daily over a 10-week dose-ranging period followed by a maintenance period of 4 weeks. Optimal daily dosage for nadolol was 100 mg, and 112 mg for propranolol. Parameters used for evaluation of therapeutic effects included the number of anginal attacks, number of nitroglycerine tablets needed, time before onset of chest pain during exercise test, exercise time, and overall clinical impression of response. The results indicated that nadolol given once daily was equally as effective as propranolol 4-times daily in treating angina pectoris.
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PMID:Comparison of the new beta-adrenoceptor antagonist, nadolol, and propranolol in the treatment of angina pectoris. 2 20

Medical versus surgical treatment of unstable angina was compared in a prospective nonrandomized study of 118 patients. Acute transient ST-T wave changes were present during chest pain in all patients. Acute infarction was excluded by serial electrocardiograms and enzyme studies. All patients admitted to the coronary care unit from 1970 to 1975 who fulfilled the entry criteria were included in the study. The starting point for data evaluation was 5 days after hospital admission. Characteristics at entry were similar in 66 medically treated patients and 52 patients who had coronary bypass vein graft surgery. During a mean follow-up period of 23 months in 66 medically treated patients with unstable angina the incidence rate of nonfatal myocardial infarction was 17% and the total mortality rate 21 percent compared with respective rates of 19% and 5.8% in 52 surgically treated patients. In the surgical group 8 patients (15%) had a perioperative infarction and only 2 (4%) had a late infarction; one patient (2%) died at operation. Symptomatic improvement was observed more frequently in the surgically treated group. Sixty percent of surgically treated patients were free of angina compared with 21% of medically treated patients. Eight medically treated patients (12%) required late surgical treatment for persistent severe angina despite optimal medical management.
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PMID:Unstable angina: comparison of medical and surgical management. 6 99

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.
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PMID:Similarities of ergonovine-induced and spontaneous attacks of variant angina. 10 58

31 patients presenting with Prinzmetal variant angina were divided into three groups according to their angiographic appearances. Group I comprised 9 patients with normal or coronary arteries with lesions less than 50% narrowing. Group II comprised 12 patients with single vessel disease. Group III comprised the other 10 patients with significant lesions on two or all three principal arteries. No clinical or electrocardiographical differences were found between the groups as to age, sex or the clinicapresentation of the chest pain. Most patients with normal or nearly normal coronary arteries had normal electrol cardiogrammes between attacjs (8 out of 9) and electrical changes mainly over the inferior wall (8 out of 9). Exercise electrocardiography reproduced ST elevation in 4 of the 9 patients but, in contrast to the patients in the other two groups, never ST depression. However, these features are not specific for patients in Group I as they were observed in 4 patients in the other two groups. Spontaneous or induced coronary spasm were observed in 27 patients, confirming its role as the mechanism of Prinzmetal angina, whatever the anatomical appearance of the coronary tree.
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PMID:[Clinical and angiographic study and pathogenic mechanism of Prinzmetal's angina. Apropos of 31 cases]. 10 80

This coronary spasm provocation test with methyl-ergometrine maleate was carried out during coronary arteriography in 47 patients presenting with spontaneous chest pain. Coronary spasm was triggered in 16 cases, reproducing the chest pain in 11 patients, and accompanied by electrical changes in 15 cases, 12 subepicardial ischaemias and 3 subendocardial ischaemias. This test is not without danger to the patient as arrhythmias and conduction defects were recorded in 6 cases although the spasm was readily reversible on injection of intravenous glyceryl trinitrate. Of 7 patients with Prinzmetal variant angina, the test was positive 6 times, in three of which on pre existing severe organic lesions, so confirming the mechanism of this syndrome and the reliability of the test. Of 40 patients presenting with spontaneous chest pain, 10 had a positive test. In 2 of these cases the chest pain was subsequently observed with subepicardial ischaemic electrical changes, so confirming the screening value of this test. In the 7 cases where coronary spasm gave rise to electrical changes with or without pain, the logical diagnosis would appear to be spastic angina. In the 30 cases where the test was negative the subsequent outcome did not provide any proof in favour of a coronary origin of the chest pain.
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PMID:[Methyl-ergometrin maleate test during coronary arteriography in spontaneous chest pain]. 10 81

One thousand forty-five spontaneous episodes of S-T segment elevation were observed in three patients over a total of 72 days of continuous electrocardiographic monitoring. Eighty-nine percent of episodes were asymptomatic; chest pain tended to occur with episodes longer than 3 minutes, and ventricular ectopy occurred almost exclusively with symptomatic episodes. Nitroglycerin regularly relieved angina or S-T elevation, or both. Plasma and urinary catecholamines and their metabolites were normal. Episodes of variant angina were not associated with a generalized increase in sympathetic outflow because serum catecholamine levels at the onset and termination of the S-T abnormalities were not elevated. Controlled trials of propranolol showed no significant beneficial effect. Propranolol significantly increased the length of episodes of S-T elevation in one patient, increasing ventricular irritability. The overall course of variant angina was quite variable, with spontaneous and long-lasting remissions, necessitating cautions interpretation of clinical trials.
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PMID:Variant angina pectoris: investigation of indexes of sympathetic nervous system function. 10 89

Five male patients, aged between 31 and 58 years, presented with anginal chest pain with nausea and sweating after the interruption of exercise. Prinzmetal variant angina was observed during the recovery phase of exercise tolerance testing. Coronary arteriography and selective left ventricular angiography were normal in all cases. Ergonovine, used in one case, induced coronary artery spasm. The angina was eased by Nifedipine in three patients and passed off with time in the other two patients. In one case attack occurred with amiodarone therapy and in another with glyceril trinitrate, after normal exercise tolerance tests. Vagotonia, all the more pronounced when sympathetic tonus is increased, and hyperventilation seem to be the causative factors of what probably results from coronary artery spasm. Nifedipine, a calcium-blocking agent would appear to be the treatment of choice.
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PMID:[Prinzmetal's angina initiated by interruption of exercise. 5 cases with normal coronary radiograms]. 11 38

75 cases of mitral valve prolapse (MVP) for which no cause was found underwent electromyography (EMG). In 64 cases (85.3%) EMG showed changes suggestive of spasmophilia. The symptoms observed were those already described in this condition. The specific clinical signs of spasmophilia were often elicited with a positive Chvostek sign in 20 out of 30 cases (73.3%). Radiological, echocardiographical and haemodynamic studies underlined the hyperkinetic state of the left ventricle. Biochemical investigations showed a high incidence of low erythrocytic magnesium levels. Chest pain suggestive of angina pectoris, mitral valve prolapse and spasmophilia are frequently associated. The role of the low erythrocyte magnesium on left ventricular hyperkinesis and the production of MVP is discussed.
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PMID:[Mitral valve prolapse and spasmophilia in the adult]. 11 69


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