Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The opinion is emerging that beta-blocking drugs have an important role in management of patients following acute myocardial infarction. Already beta-blocking drugs are accepted as the treatment of choice in hypertension and in angina pectoris--in the major risk factor and consequence respectively of coronary atherosclerosis, and both commonly recognized in patients who survive acute myocardial infarction. But beta-blocking drugs also may be of benefit in reducing the incidence and risk of subsequent infarction, and so may be of value for long term treatment of patients who have no symptoms whatever following acute infarction.
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PMID:The role of long term beta-blockade after myocardial infarction: Paper 1. 3 Apr 41

Serum milk, egg, and gluten antibody titres were measured in ninety men with acute myocardial infarction and compared with those of thirty-six age-matched male controls. None of the antibody titres was higher in the patients with myocardial infarction, nor was there a significant correlation between antibody titres and the Norris prognostic index or death before hospital discharge. The results do not support the suggestion that immunological mechanisms are involved in the pathogenesis of coronary heart-disease and atherosclerosis.
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PMID:Dietary antibodies and myocardial infarction. 5 87

A postmortem coronary angiography technique employing aortic injection of contrast medium and double contrast visualization of the aortic bulb and large epicardial coronary trunks was applied to the study of coronary ostia in a series of 124 deaths from acute myocardial infarction and a series of 89 sudden deaths without recent infarction and 42 violent deaths. A stenosis of 50 per cent or more of the lumen was found in the right ostium in 45 per cent and in the left ostium in 8 per cent of infarct cases. The corresponding figures in sudden deaths were 37 per cent on the right and 4.5 per cent on the left side, and in violent deaths 7 per cent in the right ostium and none in the left. Most ostial stenoses were caused by coronary atherosclerosis. In 9 patients, two with a recent infarct and 7 sudden deaths, an ostial stenosis was the only stenosed site in the coronary arterial tree. Of theses 9 patients, 7 were known to have suffered from symptomatic heart disease during life, chest pain on effort and arrhythmias being the most common complaint.
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PMID:Occurrence of coronary ostial stenosis in a necropsy series of myocardial infarction, sudden death, and violent death. 12 64

Certain clinical and morphologic observations are described in 27 patients with severe isolated angina pectoris of either the stable (five patients) or the unstable form (22 patients). Twenty-four patients died during or shortly after cardiac operations designed to relieve angina pectoris and three died during cardiac catheterization. During life none had had clinical evidence of acute myocardial infarction or congestive cardiac failure. At necropsy, each had diffuse, extensive coronary atherosclerosis with severe luminal narrowing: the lumens of at least two, an average of three, of the four major epicardial coronary arteries were narrowed greater than 75% in cross-sectional area by old atherosclerotic plaques. Despite the severe coronary narrowing, there was little myocardial damage. Left ventricular scarring (excluding papillary muscle) was observed grossly in only 14 (52%) of the 27 patients and in each it involved only a small portion of myocardial wall. The left ventricular cavity was of normal size in all except two patients. The hearts were of normal weight in 15 (56%) patients, and the average increase above the upper range of normal for the other 12 hearts was 19%. Thus, clinically isolated, severe angina pectoris is associated with severe, diffuse luminal narrowing but relatively little myocardial damage.
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PMID:The coronary arteries and left ventricle in clinically isolated angina pectoris: a necropsy analysis. 13

Platelets may contribute to the pathogenesis of atherosclerosis and to the complications of coronary atherosclerosis, acute myocardial infarction, unstable angina, and sudden cardiac death. In addition, platelets may contribute to saphenous vein aortocoronary graft occlusion. Of 104 men with coronary artery disease, platelet survival (SURV) (chromium51 labeling) was shortened in 68% (3.1+/-0.03 days [average+/-SEM]; normal, 3.7+/-0.03 days; P greater than .001). Three platelet-suppressant drugs, sulfinpyrazone, clofibrate, and dipyridamole increased SURV. Saphenous vein graft occlusion was associated with shortened SURV. Of 36 men with occlusion of at least one graft, SURV was shortened in 35 (2.5+/-0.08 days), whereas in 19 with all grafts open, SURV was shortened in six (3.5+/-0.10 days; P less than .01). These drugs increased SURV (2.3 +/- 0.08 to 2.7 +/- 0.11 days; P less than 0.1) and were associated with improved graft patency (four of 32 grafts after initial bypass vs 30 of 34 grafts open after second operation).
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PMID:Platelet-suppressant therapy in patients with coronary artery disease. 30 69

The condition of the distal bed of the cardiac coronary arteries was studied in 150 patients with ischemic heart disease. It proved to be affected with stenotic atherosclerosis in 20,6% of cases. The distal bed in patients with the chronic stage of ischemic heart disease hardly differed from that in patients with acute myocardial infarction. Total revascularization may be accomplished in 33% of cases with affection of three vessels of the cardiac coronary bed with stenotic atherosclerosis and in 96,5% of cases with affection of one vessel.
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PMID:[State of the distal bed of the cardiac coronary arteries in ischemic heart disease]. 31 Apr 86

A population-based study was conducted in metropolitan Baltimore, in which the prognosis of 504 patients hospitalized with acute myocardial infarction (MI) from July 1966 through June 1967 was compared with that of 803 patients hospitalized from January through December 1971. For patients admitted to coronary care units (CCUs), the in-hospital case-fatality rate (CFR) in 1971 (20%) was found to be significantly lower than that in 1966/67 (27.5%) (p less than .025), after simultaneous adjustment for 16 variables which may affect prognosis. No such significant difference was detected for patients not admitted to CCUs when the two time periods were compared. As a result of these time trends, CFRs were not significantly different between CCU and non-CCU patients in 1966/67, but in 1971 a significant advantage was shown for CCU patients (p less than .005). These results suggest that effectiveness of CCUs in prevention of in-hospital deaths increased between 1966/67 and 1971. For hospital survivors, regardless of admission to a CCU, no significant differences in long-term prognosis were found between patients discharged in 1971 and those discharged in 1966/67. This finding may reflect the lack of major therapeutic advances between the two study periods, aimed at reducing the progression of coronary atherosclerosis and/or the extent of the infarcted area.
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PMID:Time trends in prognosis of patients with myocardial infarction: a population-based study. 43 Sep 47

Arteriosclerotic and nonarteriosclerotic rats were treated with carbon tetrachloride (CCL4) to induce cirrhosis of the liver. Massive myocardial infarction was then induced in intact and CCL4-treated animals. During acute necrosis (Days 1 thru 3), animals were killed at 4, 8, 12 and 24 h on Days 1 and 2, and during myocardial repair on Days 4, 5 and 8. During the induction of cirrhosis, animals developed polydypsia, polyuria, and hyperglycemia; during myocardial infarction, the arteriosclerotic + cirrhotic animals developed severe and persistent congestive heart failure, i.e., hydrothorax. Adrenal and thymus gland weights and corticosterone levels indicated that cirrhosis per se increased pituitary--adrenal activity, particularly in arteriosclerotic animals. Enzyme levels of SGOT and SGPT demonstrated severe hepatic damage due to cirrhosis and acute myocardial infarction. Blood triglycerides and cholesterol responded abnormally in cirrhotic animals during acute myocardial ischemia due to their entrapment within hepatic cells. The cirrhotic animals manifested poor myocardial repair with persistent foci of necrosis, calcification, and a high incidence of large, occlusive, atrial thrombi. It is suggested that cirrhosis interferes with lipid metabolism and adrenal steroid conjugation leading to abnormal levels of mineralocorticoids which favor congestive heart failure, poor myocardial repair, and atrial thrombosis.
Atherosclerosis 1979 Mar
PMID:Effect of CCL4-induced cirrhosis on the pathophysiologic course of acute myocardial infarction in nonarteriosclerotic vs arteriosclerotic male rats. 46 16

Clinical and morphologic features of transmural myocardial infarction (associated with insignificant or absent atherosclerosis of the extramural coronary arteries) are described in seven patients with hypertrophic cardiomyopathy. Marked chronic congestive heart failure associated with supraventricular arrhythmias occurred in six of the seven patients, each of whom had no or mild left ventricular outflow tract obstruction under basal conditions. No patient had typical angina pectoris, and only one patient had clinically evident acute myocardial infarction. Infarction may have caused cardiac arrest in one other patient, but was "silent" in the remaining five patients. At necropsy, six of the seven patients had extensive myocardial scarring involving the ventricular septum, left ventricular free wall and one or both left ventricular papillary muscles; in four patients portions of the right ventricular wall were also scarred. Six patients had dilated ventricular cavities, including two who were known to have nondilated ventricular cavities earlier in their clinical course. It is concluded that transmural myocardial infarction in the absence of significant coronary atherosclerosis is a not uncommon finding (prevalence rate 15 percent) in a population of patients who had died from hypertrophic cardiomyopathy. Although transmural infarction is possibly a secondary event, it more likely contributes causally to the clinical deterioration of some patients with hypertrophic cardiomyopathy, leading to ventricular dilatation and progressive fatal cardiac failure.
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PMID:Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries. 57 70

Male and female, arteriosclerotic and non-arteriosclerotic rats were treated with the anti-lipemic agent, clofibrate, for 8 days and then subjected to an acute myocardial infarction by injecting them with two large doses of isoproterenol spaced 24 hours apart. The animals were killed at sequential time intervals during the acute necrosis and early repair phases of myocardial infarction. Pre-treatment with clofibrate caused a definite improvement in survival, less shock and prostration, and ECG evidence of little or no ischemia. Increased SGOT levels, hepatic lipid and necrosis were indicative of advanced liver damage. Although clofibrate-treated animals showed little change in serum lipids during the acute cardiac necrosis phase, they were hyperglycemic and showed the greatest increase in BUN levels. Clofibrate-treated animals had higher serum corticosterone levels than those given isoproterenol alone. Despite superior survival rates, both the arteriosclerotic and non-arteriosclerotic, clofibrate-treated animals exhibited equally severe histopathologic evidence of myocardial damage. It is suggested that the protective effect of prophylactic treatment with clofibrate against isoproterenol-induced myocardial infarction in rats may be due to its ability to change corticosterone levels in the circulation.
Atherosclerosis 1978 Mar
PMID:Protective effects of clofibrate on isoproterenol-induced myocardial infarction in arteriosclerotic and non-arteriosclerotic rats. 66 86


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