Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Echocardiographic findings of 11 patients with dilated cardiomyopathy (DCM) were compared with those of 11 patient with coronary triple vessel disease, who showed extensive left ventricular (LV) wall motion abnormalities (abnormal LV regional wall motion observed in more than six of seven segments as classified by AHA) and a dilated LV cavity (LVEDVI: 120 ml/m2 or greater), consistent with so-called ischemic cardiomyopathy (ICM). Short-axis two-dimensional echocardiograms of the left ventricle at the mitral valve, papillary muscle, and apical levels were divided equally into eight segments starting from the posterior aspect of the right side of the interventricular septum. Non-uniformity of LV regional wall motion abnormalities was demonstrated in seven patients (64%) with DCM and 11 patients (100%) with ICM, and that of LV regional wall motion abnormalities of more than two degrees was observed in one patient (9%) with DCM and nine patients (82%) with ICM. LV regional wall thinning was observed in two patients (18%) with DCM and 11 patients (100%) with ICM. Increased echo intensity of the LV regional wall was observed in only four patients with ICM. Two patients (18%) with DCM and 11 patients (100%) with ICM had episodes of chest pain and the former two had LV regional wall thinning, suggesting the possibility of post-myocarditis cardiomegaly. Abnormal Q waves in the electrocardiograms were observed in 10 patients (91%) with ICM and in two (18%) with DCM. Exercise ECG tests were positive in nine of 11 patients with ICM, but in none of the five DCM examined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of echocardiographic findings in patients with coronary triple vessel disease and dilated cardiomyopathy]. 383 56

Atherosclerotic mouse models develop little ischemic organ damage and no infarctions, despite the presence of large atherosclerotic lesions. Therefore, we hypothesize that luminal changes do not follow atherosclerotic lesion development. Because a phenomenon that may explain the discrepancy between luminal changes and lesion size is vascular remodeling, we measured parameters of vascular remodeling in the carotid arteries (CAs), thoracic aorta (TA), and abdominal aorta (AA) of apolipoprotein E (apoE)-deficient (apoE(-/-)) and apoE*3-Leiden mice, 2 well-known mouse models of atherosclerosis. Atherosclerotic lesions were classified (American Heart Association [AHA] types II through V), and plaque thickness, compensatory enlargement versus constrictive remodeling, lumen diameter, stenosis, and media thickness were measured relative to the nondiseased arterial wall. In CAs, plaque thickness increased during atherogenesis. CAs showed compensatory enlargement (apoE(-/-) 55%, apoE*3-Leiden 38%). Regression analysis revealed a positive correlation between plaque and lumen area (for apoE(-/-), R=0.95; for apoE*3-Leiden, R=0.90). Medial thinning and elastolysis were also observed. During atherogenesis, lumen diameter decreased (apoE(-/-) -69%, apoE*3-Leiden -40%), and stenosis >70% developed. TA and AA showed similar features, but neither developed a progressive decrease in lumen diameter or stenosis >70%. In CAs, TA, and AA of apoE(-/-) and apoE*3-Leiden mice, atherogenesis is associated with compensatory enlargement, medial thinning, and elastolysis. A progressive decrease in lumen diameter and stenoses >70% occur only in CAs. Vascular remodeling is more prominent in apoE(-/-) mice.
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PMID:Compensatory enlargement and stenosis develop in apoE(-/-) and apoE*3-Leiden transgenic mice. 1149 66