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)

A cohort of 282 patients who underwent mitral valve replacement with a xenograft bioprosthesis was strictly segregated according to etiology of mitral dysfunction and analyzed regarding the impact of arteriographic coronary artery disease (CAD) and concomitant coronary artery bypass grafting (CABG) on operative risk, functional result, and survival. CAD was present in 21% of the 122 patients with predominant mitral stenosis (MS) and 59% of the 155 patients with mitral regurgitation (MR); moreover, discordance between the presence of angina and anatomic CAD was found in 27% (33 of 122) of the MS subgroup and 36% (56 of 155) of the MR subgroup. Etiology of the valvular dysfunction was rheumatic in 148 patients, myxomatous degeneration in 83, and ischemic in 32. Within these subgroups, 41 patients (27%), 40 patients (48%), and 32 patients (100%), respectively, had CAD. Of those patients with CAD, 85% of the rheumatic subgroup, 90% of the degenerative subgroup, and 81% of the ischemic subgroup underwent concomitant CABG at the time of valve replacement. Within each subgroup no statistically significant (P greater than 0.05) differences in operative mortality rate, perioperative myocardial infarction rate, incidence of late angina or late infarction, or late actuarial survival were evident when compared on the basis of CAD, and/or CABG, with one exception. The exception was the 10% incidence of perioperative myocardial infarction in the rheumatic subgrohp with coronary disease versus 2% in the rheumatic subgroup without coronary disease (P = 0.05). Within the time constraints of this study (mean follow-up = 2.3 years; maximum follow-up = 5.9 years), these results support simultaneous MVR and CABG when hemodynamically appreciable CAD is found. Moreover, the overall 43% incidence of arteriographic CAD warrants routine coronary angiography in most adults undergoing preoperative catheterization for mitral valvular disease.
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PMID:Impact of simultaneous myocardial revascularization on operative risk, functional result, and survival following mitral valve replacement. 56 31

Patients with mitral valve prolapse (MVP) frequently experience chest pain which may, expecially in older subjects and males, be difficult to differentiate from angina pectoris. Electrocardiographic (ECG) changes, ventricular arrhythmias, metabolic abnormalities and rare reports of myocardial infarction and sudden death further suggest the presence of an ischemic process in these patients. The recognition of accompanying coronary artery disease (CAD) and exclusion of other causes of ischemia, therefore, may be important in determining the prognosis and appropriate therapy for such patients.
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PMID:Myocardial perfusion scintigraphy in patients with mitral valve prolapse: Its advantage over stress electrocardiography in diagnosing associated coronary artery disease and its implications for the etiology of chest pain. 61 88

Between September 1966 and September 1976, a group of 48 patients with normal coronary arteries or nonsignificant coronary atherosclerosis documented in a first coronary arteriogram underwent a second angiogram because of persistent or recurrent chest pain. The interval between studies was 13 to 108 months (mean 42 months). The indication for the first angiogram was typical or atypical anginal pain. The patients were separated into two groups according to the results of the first angiogram. Group I included 22 patients, 9 men and 13 women, with normal coronary arteries (mean age 49 years, range 28 to 62). Group II included 26 patients, 18 men and 8 women, with coronary stenosis of less than 50% of intraluminal diameter (mean age 49 years, range 38 to 63). The second angiogram revealed normal coronary arteries in all 22 patients in Group I but showed progression of diseases in 7 (27%) of the 26 patients in group II. The coronary arterial narrowings were greater than 50% in four patients and greater than 70% in only two patients. The clinical course, coronary risk factors and interval between angiograms were not useful predictors of progression of disease. The data suggest that coronary artery disease is unlikely to developed in adults with normal coronary arteries and that roughly 75% of adults with nonsignificant atherosclerosis will not show progression of disease over a 3 to 4 year period.
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PMID:Angiographic evaluation of the natural history of normal coronary arteries and mild coronary atherosclerosis. 62 15

A follow-up study of 1,402 patients with a positive maximal treadmill stress test was made to evaluate the significance of angina during the test. Life tables were constructed and evaluated for significance of age, sex and work load at onset of angina. Coronary events (myocardial infarction, progression of angina and coronary death) were twice as frequent in subjects with angina and S-T segment depression as in those without angina. The increased incidence in 4 years held for all coronary events and was still doubled at 7 years for progression of angina and coronary death. The incidence of coronary events was more than twice as great when the angina was induced by a light work load (4 metabolic equivalents = METS) as when it was induced by a heavy work load (8 to 9 METS). Men aged 41 to 50 years having angina during exercise testing had a 3-fold greater incidence of coronary events and a 4-fold greater incidence of myocardial infarction compared with their counterparts who had S-T segment depression alone. In this study, angina during exercise testing identified 85% of true positive tests for coronary artery disease, whereas S-T depression alone identified only 64% of such tests. Thus, angina during exercise testing increases the sensitivity of the test and identifies cohorts of subjects at high risk for subsequent coronary events.
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PMID:Significance of chest pain during treadmill exercise: correlation with coronary events. 62 16

To determine whether regional myocardial ischemia plays a role in patients with the mitral valve prolapse syndrome, we examined myocardial perfusion with exercise stress testing and thallium-201 myocardial scintigraphy. Twelve patients were studied, 11 women and one man aged 18 to 56 years, mean age 30 years. In all patients, mitral valve prolapse was documented by echocardiography or phonocardiography. Patients over 35 years of age underwent cardiac catheterization. Electrocardograms disclosed abnormalities during maximal exercise in eight of the 12 patients. In two patients, angina developed during exercise. Thallium-201 (201Tl) scintigrams were normal in the 11 patients with presumed or documented normal coronary arteries. One patient, in whom an apical defect was demonstrated on scintigraphy, had significant disease of the left main and left anterior descending coronary artery. Repeat testing after successful aortocoronary bypass grafting revealed improved exercise capacity and a normal 201Tl myocardial scintigram. The data indicate that patients with mitral valve prolapse alone do not have regional myocardial ischemia and that the presence of a defect on 201Tl myocardial scintigraphy following maximal stress testing would suggest the existence of concomitant coronary artery disease.
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PMID:Thallium-201 myocardial perfusion studies in patients with the mitral valve prolapse syndrome. 62 33

Selective coronary angiography and left ventriculography was performed in 14 patients with conduction disturbances of the heart or chronic complete heart block. Occlusive coronary arterial diseas was present in 3 patients: 2 of these had had extensive previous myocardial infarction and 1 complained of angina pectoris. The other patients gave no history of coronary artery disease and conduction abnormalities were the consequence of idiopathic fibrosis of the conducting system. The coronary arteries were normal or dilated and were remarkably free of atheroma in this group of older patients. Left ventricular function, as measured by ejection fraction, was normal except in the 2 patients who had had previous myocardial infarction.
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PMID:Selective coronary angiography in patients with conduction disturbances of the heart. 62 17

After more than ten years of clinical application, direct myocardial revascularization with saphenous or mammary vein grafts is becomining one of the most common types of elective major surgery performed in the United States. The need for and the results of revascularization surgery are determined by cine coronary arteriography. The principles on which this type of surgery is based are simple. Critical occlusion of a coronary artery may produce an arteriographically identifiable area of myocardial perfusion deficit in the left ventricle. The functional demand for blood that results is usually manifested by anginal pain. When the occlusion is reduced by rest and administration of vasodilators, the immediate threat of infarction is alleviated. When pain persists in spite of treatment, direct revascularization surgery should be considered. This type of surgery need not involve ultrasophisticated adjuncts. Some of these adjuncts increase morbidity and contribute appreciably to the cost of operation and hospitalization. The record of myocardial revascularization suggests that the surgical treatment of coronary artery disease can and should be done in qualified community hospitals.
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PMID:Myocardial revascularization 1978. 62 32

In 12 patients with coronary artery disease and typical exercise-induced angina pectoris hemodynamic and ECG studies were performed at rest and during ergometer load in supine position. During the attacks of angina there was a significant ST-depression in all cases accompanied by elevated pulmonary capillary wedge pressures (PCP) and pulmonary artery mean pressures (PAM). Intravenous administration of 40 mg furosemide showed consistent hemodynamic changes. Cardiac output (CO) dropped significantly by 15.9 per cent at rest (p is less than 0.001) and by 6.9 per cent during exercise (p is less than 0.005). The PCP during exercise following furosemide decreased from 32.9 mmHg to 11.8 mm Hg (p is less than 0.001) and was paralleled by a significant decrease of PAM, indicating reduction of ischemia-related hemodynamic impairment. Furthermore, there was a striking improvement of Ecg findings during ergometer load in 9 of 12 patients as well as a relief of anginal pain in 11 of 12 patients. The present demonstration of antianginal properties of furosemide may be explained by the reduction of ventricular volumes and pressures, resulting in a decrease of myocardial wall stress. These effects are suggested to be related to the peripheral venodilator capacity of furosemide in conjunction with its diuretic properties. Thus, in patients with left ventricular dysfunction secondary to ischemia, intravenous furosemide may have salutary effects on myocardial oxygen requirements resembling the action of nitroglycerin, but without its oxygen-wasting effects on tachycardia.
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PMID:[Effects of furosemide on hemodynamic, electrocardiographic, and symptomatic responses to exercise in patients with angina pectoris (author's transl)]. 63 18

The syndrome of angina pectoris or acute myocardial infarction without obstructive coronary artery disease has been the subject of much interest. We studied nine autopsied patients with progressive systemic sclerosis and evidence of ischemic heart disease but morphologically normal coronary arteries. Three patients had angina pectoris and three others chest pains of unknown etiology, six had ventricular arrhythmias, four had clinically suspected acute myocardial infarction, and eight had sudden cardiac death. At autopsy extensive focal myocardial necrosis was present in seven patients and myocardial scarring in all nine, but all patients had widely patent intramural and extramural coronary arteries. The finding of contraction band myocardial necrosis in seven of the eight patients who experienced sudden death suggests that the myocardial damage was a consequence of reperfusion of focally nonperfused myocardium, and thus due to a myocardial Raynaud's phenomenon. Patients with PSS may provide a model of spasm of intramyocardial vessels causing angina pectoris or myocardial infarction with morphologically normal coronary arteries.
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PMID:Angina pectoris, myocardial infarction and sudden cardiac death with normal coronary arteries: a clinicopathologic study of 9 patients with progressive systemic sclerosis. 63 97

Intraaortic balloon pumping improves coronary blood flow characteristics while simultaneously reducing myocardial oxygen demands by reducing aortic systolic pressure. Clinical application of intraaortic balloon pumping has largely been in the "high risk" patient (cardiogenic shock, postinfarction angina, left main coronary artery disease and unstable angina) for support during diagnostic studies or cardiac surgery, or both. In addition, there is some evidence that balloon pumping immediately after coronary occlusion reduces the size of experimentally induced myocardial infarcts. In this study, myocardial infarcts were produced by ligation of the left anterior descending coronary artery in 12 dogs, 6 of which were treated with balloon counterpulsation beginning 3 hours after coronary occlusion. All dogs were killed 8 hours after coronary ligation. Intraaortic balloon pumping resulted in the expected hemodynamic changes (decreased aortic systolic pressure, left ventricular end-diastolic pressure and heart rate and increased aortic peak diastolic pressure). In addition, there was a significant reduction in infarct size in the group with balloon pumping as determined with epicardial S-T segment mapping, myocardial imaging with technetium-99m-glucoheptonate and histochemical staining with nitroblue tetrazolium. These results suggest that even when instituted as long as 3 hours after coronary occlusion, intraaortic balloon pumping results in significant reduction in infarct size and, it might be speculated, the mortality and morbidity associated with acute myocardial infarction may also be decreased.
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PMID:Role of delayed intraaortic balloon pumping in treatment of experimental myocardial infarction. 66 26


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