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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary artery bypass graft surgery has been available and widely successful for the symptomatic treatment of ischemic heart disease. Despite its widespread use, there is little information available on the pathological consequences of this procedure on the human heart. In this article, morphological consequences of coronary artery bypass graft surgery is reviewed. Intimal changes occurring within the vein graft itself consist predominately of fibrous initimal proliferation, which in some patients may progress to from an occlusive plaque. Most occlusions, however, occur at the coronary artery bypass graft anastomosis site and the mechanisms of occlusion include compression of the vascular lumen, thrombosis, and dissection of the coronary artery. Most graft failure occurs in the setting of too small a native coronary artery lumen. The myocardium is also at risk for alterations as a result of the bypass operation. Contraction band or reperfusion necrosis is the type of injury most commonly seen, and it appears to occur most often in the distribution of patent grafts. Accelerated atherosclerosis in vein grafts and the myocardial injury associated with revascularization require further detailed morphological studies, but these are important areas for pathological exploration since they bear on important and yet unanswered questions about coronary bypass surgery: can it in the long run perserve myocardium and prolong life?
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PMID:Pathology of coronary artery bypass graft surgery. 30 6

The heart of an elderly person functions well in ordinary circumstances but has lost much of its physiologic reserve. The effects of aging myocardium are difficult to spearate from those of coronary atherosclerosis. In addition to ischemic heart disease, a high index of suspicion must be maintained for the sick sinus syndrome, valvular heart disease, cardiomyopathies, congenital lesions, corpulmonale and thyroid disease. Management requires the judicious use of drugs and the prescription of appropriate physical activity.
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PMID:The aging heart. 30 6

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

The injury-vasospasm hypothesis of IHD was discussed in relation to coronary artery autoregulation and the anoxic-feedback mechanism. Observations in the recent literature, not usually attributed to spasm, were examined in light of this phenomenon. This includes reperfusion models of experimental AMI, the association of AMI with myocarditis, and findings in AMI and SCD as necrotic microlesions, prodromata, and epicardial arterial plaque rupture and hemorrhage. The disparity between the severity of coronary disease and the occurrence of the various types of IHD suggest that atherosclerosis itself does not precipitate attacks of chest pain. It was emphasized that plaque rupture due to spasm might help induce CAT. With exercise, the possible importance of the autoregulatory system was explored in the prevention and induction of AMI and SCD, and the improvement of AP. The role of spasm in IHD should be defined.
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PMID:The injury-vasospasm hypothesis of ischemic heart disease, revisited. 33 91

Heart disease continues to be a major cause of disablement and death in Canada. Elevated serum cholesterol concentrations, hypertension and cigarette smoking are among the standard risk factors associated with ischemic heart disease. Research attention has also been directed at the role of behavioural factors in the development of atherosclerosis and myocardial infarction. Experimental findings support a conceptual approach to the interplay of psychologic stress, the type A "coronary"-prone behaviour pattern and pathophysiologic mechanisms that have been implicated in the development of coronary artery disease. It is concluded that type A behaviour and stress contribute substantially to the pathogenesis of cardiovascular disease. However, assessment of the manner in which these two variables influence the pathophysiology of ischemic heart disease requires further research, with systematic examination of physiologic and biochemical processes. Potential strategies for modifying type A behaviour are reviewed. However, unequivocal support for the preventive efficacy of behavioural approaches must await future research.
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PMID:Behavioural prevention of ischemic heart disease. 36 Nov 91

There were under observation 440 patients with ischemic heart disease due to atherosclerosis of the coronary arteries in the phase of exacerbation of the disease and 52 patients suffering from hypertensive disease with a clinical picture of ischemic heart disease; 192 practically healthy individuals were examined as controls. Significant increase in the levels of cholesterol, triglycerides, and glucose in blood of the patients with ischemic heart disease and of those with hypertensive disease was revealed. In patients with ischemic heart disease marked by pain and disorders of the rhythm as well as in individuals with hypertensive disease hormonal-metabolic shifts, monotypical in character, were noted. It is suggested that hormonal-regulatory disorders are of primary character in atherogenesis.
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PMID:[Hormonal and metabolic disorders in ischemic heart disease]. 36 20

Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic cardiomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.
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PMID:Myocardial bridges in man: clinical correlations and angiographic accentuation with nitroglycerin. 40 19

A significant increase of the relative phosphatidyl serine level, a decrease in the percentage of lipoleic and arachidonic acids, and an increase in the oleic acid level were revealed in blood platelet phospholipids of patients with ischemic heart disease and severe coronary atherosclerosis. In the entire group of patients with ischemic heart disease (with coronary atherosclerosis of various degree), these changes are less marked and only the decrease in the linoleic acid level as compared to that in healthy individuals is significant. It was established that besides these changes in the phospholipid structures, blood platelet aggregation increases when the severity of the atherosclerotic process in the coronary arteries becomes more pronounced.
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PMID:[Thrombocyte phospholipids in ischemic heart disease with a varying degree of coronary arteriosclerosis severity]. 43 12

It was established that in blood of patients with ischemic heart disease due to atherosclerosis of the coronary arteries (the diagnosis was verified in selective coronaroangiography) the content of acylhydroperoxides grows while the activity of glutathione-peroxidase II decreases. In blood of patients with no damage to the coronary vessels (according to the results of angiography), glutathione-peroxidase II activity does not differ significantly from the values in the control group. The decrease of glutathione-peroxidase II activity was most marked in patients with ischemic heart disease and hypercholesterolemia. It is suggested that the increase in the peroxide content in blood of patients with ischemic heart disease may be due to the sharp decrease in the activity of glutathione-peroxidase II.
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PMID:[Lipid peroxides and atherosclerosis. The enzymatic detoxication of lipid peroxides in the blood in ischemic heart disease due to coronary artery arteriosclerosis]. 45 35

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


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