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)

The frequency and severity of "morphological" variables (fibrosis, proteoglycan accumulation, atheroma, intimal vascularization, calcification, acute intimal hemorrhage, and both adventitial and intimal lymphoplasmacellular infiltrates) in atherosclerotic plaques were related to plaque type, percentage of lumen reduction, plaque length, and intimal and medial thickness in 3,640 coronary artery sections sampled at the site of maximal lumen reduction in 8 selected segments from 100 cases of acute myocardial infarct, 50 of chronic angina, 208 of unexpected sudden coronary death with or without prodromata, and from 97 normal subjects dying accidentally. Morphological variables were occasionally observed in 1,519 sections with no lumen reduction. They were found only in sections from ischemic patients. With increasing luminal stenosis and intimal thickness, progression of the coronary plaque seemed to start as a fibrous change followed by proteoglycan accumulation in the deeper portion of the fibrous intima. Proteoglycan deposits appeared as a recurrent phenomenon. In them, atheroma or calcification develop. Intimal hemorrhage was a less frequent variable. It was found mainly in a vessel supplying an infarcted area. Lymphoplasmacellular inflammation correlated mainly with proteoglycan accumulation and atheroma, both showing a parallel increase with increasing intimal thickness and lumen reduction. No correlation was found between plaque variables and sex, age, heart weight, and infarct size. Significant variations in the distribution of plaque variables were observed among hearts of patients in the ischemic groups and between them and controls. In particular, inflammatory reaction was significantly more frequent and severe in ischemic groups than in controls, independent of the degree of coronary stenosis. Coagulative myocytolysis (contraction band necrosis), found in the majority of ischemic patients, correlated with the inflammatory reaction in supplying vessels. A peculiar tropism of mononuclear cell infiltrates for adventitial nerve structures was found. As a result, we question whether this inflammation may trigger coronary spasm and/or coagulative myocytolysis ("active" plaque vs "inactive" plaque).
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PMID:Correlation of morphological variables in the coronary atherosclerotic plaque with clinical patterns of ischemic heart disease. 320 98

Atherosclerotic cardiovascular disease is a major cause of morbidity and mortality in the Western world. Despite tremendous strides in understandings its pathogenesis, it still remains a challenge because of gaps in our understanding of its initiation, progression and complications leading to the clinical syndromes of angina, acute coronary syndrome, cerebrovascular disease and peripheral vascular disease. Recent studies have provided impetus on the shift from models of atherosclerosis based on cellular interactions to models where the important role of extracellular matrix is recognized. Proteoglycans, especially those belonging to the small leucine-rich proteoglycan family of which decorin is a representative example, have come under close scrutiny for their role in atherogenesis. There is evidence from in vitro and in vivo animal models as well as humans to suggest an important role of decorin in attenuating progression of atherosclerosis. Decorin distribution in different blood vessels has been shown to inversely correlate with the tendency to develop atherosclerosis. Decorin seems to interact closely with different cellular components of the plaque milieu, thereby suggesting its role in influencing atherogenesis at different steps. Here we review the current understanding of the role of decorin in the pathogenesis of atherosclerosis.
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PMID:Decorin in atherosclerosis. 2208 75