Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transmural myocardial infarction occurred in a 48-year-old woman with syndrome X -- atypical angina pectoris and angiographically normal coronary arteries. Before the infarction her electrocardiogram had been normal at rest but showed ischemia after exercise. Angiography 3 months after infarction revealed a normal coronary tree but hypokinesia of the posterior left ventricular wall.
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PMID:Syndrome X: case report. 84 23

In this study of human autopsy hearts, coronary arteries were divided by morphologic criteria into classes A (branching-type) and B (straight-type) arteries. Infarcted hearts and normal hearts were investigated mainly by means of coronary angiography, as well as by gross and histologic examinations. Transmural myocardial infarction originated in the inner half of the myocardial layer, which was predominantly supplied by class A arteries, followed by gradual extension to the outer layer. The early infarcted focus revealed an angiographically avascular state. This may have been the result of shrinkage of the peripheral branches of class A arteries due to increased extravascular resistance rather than to arteriolar obstruction by small thrombi and/or leukocyte plugs. By contrast, class B arteries remained patent and were almost entirely free from such phenomena. They usually penetrated the infarcted focus to drain into the papillary muscles and trabeculae carnae. As the process of myocardial infarction progressed, various patterns of vascular reactions corresponding to the healing phase were demonstrated by these branches within the infarcted foci. The passive response of class A arteries during acute ischemia characterized the early myocardial lesion. Subsequently, neovascularization from the surviving class B arteries in the infarcted focus occurred as a part of the formation of granulation tissue. Newly formed small arteries from class A arteries also participated in this reaction at the marginal area of the lesion. These well-coordinated vascular reactions revealed in greater detail the initiation and progression of the healing process and were reflective of the clinical prognosis.
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PMID:An angiographic study of intracardiac coronary arteries from human autopsy hearts: their clinicopathologic significance and characterization during transmural myocardial infarction. 231 48

One of the primary limitations of cell therapy for myocardial infarction is the low survival of transplanted cells, with a loss of up to 80% of cells within 3 days of delivery. The aims of this study were to investigate the distribution of nutrients and oxygen in infarcted myocardium and to quantify how macromolecular transport properties might affect cell survival. Transmural myocardial infarction was created by controlled cryoablation in pigs. At 30 days post-infarction, oxygen and metabolite levels were measured in the peripheral skeletal muscle, normal myocardium, the infarct border zone, and the infarct interior. The diffusion coefficients of fluorescein or FITC-labeled dextran (0.3-70 kD) were measured in these tissues using fluorescence recovery after photobleaching. The vascular density was measured via endogenous alkaline phosphatase staining. To examine the influence of these infarct conditions on cells therapeutically used in vivo, skeletal myoblast survival and differentiation were studied in vitro under the oxygen and glucose concentrations measured in the infarct tissue. Glucose and oxygen concentrations, along with vascular density were significantly reduced in infarct when compared to the uninjured myocardium and infarct border zone, although the degree of decrease differed. The diffusivity of molecules smaller than 40 kD was significantly higher in infarct center and border zone as compared to uninjured heart. Skeletal myoblast differentiation and survival were decreased stepwise from control to hypoxia, starvation, and ischemia conditions. Although oxygen, glucose, and vascular density were significantly reduced in infarcted myocardium, the rate of macromolecular diffusion was significantly increased, suggesting that diffusive transport may not be inhibited in infarct tissue, and thus the supply of nutrients to transplanted cells may be possible. in vitro studies mimicking infarct conditions suggest that increasing nutrients available to transplanted cells may significantly increase their ability to survive in infarct.
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PMID:Effects of myocardial infarction on the distribution and transport of nutrients and oxygen in porcine myocardium. 2308 96