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)

Features of infarction can be divided into two types--the spasmodic and the mechanical. The former (pre-infarct angina and emotional factors in infarction) seem readily explainable by spasm, and are similar to the findings in angina which prompted Heberden to consider angina as spasmodic. The mechanical features of infarction (association with thrombosis and arteriosclerosis, and severe and unremitting chest pain) seem to be the antithesis of spasm and probably account for the reluctance to consider spasm seriously in infarction. The injury-vasospasm hypothesis of acute myocardial infarction explains both spasmodic and mechanical features. Spasm represents a dominance of vasoconstricting over vasodilating forces. Coronary sclerosis can result in both ischaemia (vasodilating) and ischaemic injury-spasm (vasoconstricting). The fight-flight component of the autonomic nervous system is considered to be vasodilating, and the conservation-withdrawal portion to be vasoconstricting. Once spasm occurs, a new balance of forces obtains which can lead either to vasodilatation and relief of symptoms or to infarction.
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PMID:Coronary artery vasospasm: the likely immediated cause of acute myocardial infarction. 38 Jun 5

Coronary artery spasm is an important pathogenetic mechanism in some forms of myocardial ischemic disease. Factors that may be important in the genesis of spasm include the autonomic nervous system, prostaglandins, endoperoxides, thromboxanes, and the calcium availability to the contractile apparatus. Spasm results in myocardial ischemia with attendant chest pain and electrocardiographic and hemodynamic changes; it is the primary pathogenetic mechanism in Prinzmetal's variant angina and has been found in association with classic angina pectoris and acute myocardial infarction. Diagnosis of coronary artery spasm is firmly made only by coronary angiography. Treatment includes the use of both short- and long-acting nitrates and the slow-channel blocking agents such as verapamil, nifedipine, and perhexiline.
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PMID:Coronary artery spasm. 38 40

The effect of a single oral dose of a plasma FFA-lowering drug (5-(3-pyridyl) tetrazole), which does not act by conversion into nicotinic acid, on exercise tolerance and ECG reaction was studied on a double-blind basis in 15 men with stable angina pectoris. Exercise was performed on a bicycle ergometer in the sitting position with a load increase of 10 W/min. In addition to ECG, time to onset of chest pains and to termination of exercise because of strong chest pains was recorded. 5-(3-pyridyl) tetrazole decreased plasma FFA during exercise from 523 to 299 mumol/l. It reduced significantly the ST depression at corresponding work loads and permitted the patients to exercise 0.6 min longer, corresponding to a 7% higher work load, before the onset of chest pain. However, absolute exercise time was not significantly increased. The most probable explanation of the improved performance is a decreased lipid and increased carbohydrate oxidation by the ischemic heart, although a contribution may have come from hemodynamic effects of the drug, unrelated to effects on myocardial metabolism but perhaps involving heart rate and BP. The lack of a significant effect on performance time may have been due to general fatigue.
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PMID:Effect of plasma free fatty acid lowering on exercise tolerance and ST segment depression in patients with angina pectoris. 39 81

A patient experienced episodic pulmonary edema accompanying nocturnal angina pectoris. The symptoms were provoked at cardiac catheterization by atrial pacing. Simultaneous onset of chest pain, shortness of breath, and sudden appearance of a large V wave in the pulmonary artery wedge pressure contour confirmed acute mitral valve regurgitation. Rapid reversal of these changes after nitroglycerin administration supported "papillary muscle dysfunction" as the explanation for these hemodynamic changes.
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PMID:Severe papillary muscle dysfunction substantiated by atrial pacing during cardiac catheterization. 40 54

Fifty-eight patients with angina-like chest pain had esophageal manometric testing. Forty-three had no evidence of coronary artery disease at the time of referral or at subsequent contact; 15 patients were proven to have coronary artery disease. High-amplitude contraction waves were the most frequently found manometric abnormality (15 patients). Less frequent were increased duration of contractions, achalasia, and diffuse esophageal spasm; the latter was present in only 3 patients. An approach to the interpretation of information obtained during manometry is presented. Using this approach, the esophagus was strongly implicated as the cause of the pain in 20 patients and was suspect in 18 others. Seven patients had results that exonerated the esophagus, and in the 13 remaining individuals, the esophagus was probably not the offending organ.
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PMID:Esophageal manometrics in patients with angina-like chest pain. 40 71

This study related to 163 cases of chest pain with the typical clinical features of angina of effort (AE) selected from a continuous series of patients who had carotid arteriography (CA) for anginal pain. These 163 cases were divided into two groups: a study group (SG) consisting of 44 patients with a normal CA, and a control group (CG) which, when patients with ECG evidence of transmural necrosis had been excluded, consisted of 119 cases of coronary artery stenosis, almost all amounting to more than 75 percent. Among those with typical AE (without ECG evidence of transmural necrosis), the proportion of normal CA was 27 percent. It was reduced to 17 percent when those patients with ECG evidence of transmural necrosis were added to the CG. The clinical features of the pain were noted for the SG and the CG, as well as the incidence of "risk factors". By contrast, the SG contained significantly more young subjects and females than the CG (P less than 0.001). The proportion with normal ECGs at reat was the same in the two groups (32 percent). The proportion of non-ischaemic abnormalities of repolarisation was 32 percent in the SG and 18 percent in the CG. Ischaemic abnormalities of repolarisation were present in 23 percent of cases in the SG, and in 49 percent in the CG (p less than 0.01). The exercise test on a bicycle ergometer was carried out for 16 cases in the SG was positive in 7 (44 percent: one male, six females). Of the 33 tests in the CG, a positive response was obtained in 20 (60 percent: 18 males, 2 females) (NS). 37 percent of patients in the SG showed an abnormality of volume or of left ventricular kinetics on arteriography (5 cases) and/or elevation of the end-diastolic pressure before and after arteriography (9 cases). These findings are not significantly different from those in the CG. 9 patients in the SG were studied for myocardial metabolism under pacing: 2 were found to have abnormalities in lactate production.
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PMID:[Electrocardiogram in the "typical angina of effort with normal arteriography" syndrome]. 41 14

In a prospective study, 100 consecutive patients (mean age 51.3 years) with angina pectoris had propranolol abruptly discontinued 24 to 144 hours (mean 39.0 hours) prior to elective coronary arteriography. The mean duration of therapy was 8.2 months and the mean daily propranolol dose was 216.1 mg. New York Heart Association Class II, III and IV symptoms were present in 30, 41, and 29 patients and one, two, or three coronary arteries were more than 50 per cent narrowed in 37, 29, and 34 cases, respectively. Three patients experienced minor increases in chest pain and two suffered non-transmural myocardial infarctions prior to the time of scheduled cessation of therapy. The same number of minor and major complications occurred in the post-withdrawal period. All four patients who developed non-transmural myocardial infarction in this study had pre-existing Class IV symptoms. The course of the remaining 90 patients was uneventful. These findings do not support the concept of a rebound propranolol withdrawal reaction.
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PMID:Propranolol withdrawal in angina pectoris: a prospective study. 42 68

Mitral valve prolapse is a relatively common condition in the general population. The syndrome appears more common in females, and is often associated with a family history. Patients may be asymptomatic or may present with a variety of symptoms ranging from mild chest aches and anxiety to severe angina-like chest pain, palpitations and dizziness. The common auscultatory features include mid-systolic clicks and a late systolic murmur, either alone or in combination. The wide spectrum of symptoms and signs may be explained by ventriculovalvular disproportion, where either the ventricle is too small for the valve, or the valve is too large for the ventricle. The long-term prognosis is very good; severe mitral regurgitation can occasionally develop, but both sudden death and bacterial endocarditis are rare. No treatment is required for asymptomatic patients, beyond antibiotic cover for dental procedures and surgery.
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PMID:Mitral valve prolapse. 42 30

Four patients with variant angina pectoris exhibited reproducible exercise-induced chest pain and ST-segment elevation. Coronary arterial spasm was documented with arteriography during exercise-induced ST-segment elevation (three patients) or after intravenous administration of ergonovine maleate (one patient). Our observations show that in patients with variant angina exercise can trigger coronary arterial spasm, thus inducing anginal pain and ST-segment elevation.
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PMID:Coronary arterial spasm as a cause of exercise-induced ST-segment elevation in patients with variant angina. 42 7

Prinzmetal's variant of angina occurred in a 48-year-old man who sustained two attacks of subarachnoid hemorrhage within 10 days. The first anginal pain started at the same time that the second cerebrovascular accident developed, but subsequent anginal episodes were not accompanied by other symptoms or signs that indicated new development of subarachnoid hemorrhage. Twelve days later, when nuchal rigidity was fairly improved, the episodes of chest pain ended. A vasospasm of the large coronary arteries--probably due to the derangement of the autonomic nervous system caused by subarachnoid hemorrhage--was presumed to contribute to the occurrence of the variant angina. Based on this case and on review of the literature, we propose that coronary arterial spasm is one of several causes of the cardiac changes seen in subarachnoid hemorrhage.
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PMID:Prinzmetal's variant angina associated with subarachnoid hemorrhage: A case report. 43 81


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