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Correlation of intracoronary ultrasound plaque characteristics in atherosclerotic coronary artery disease patients with clinical variables.

作者信息

Rasheed Q, Nair R, Sheehan H, Hodgson J M

机构信息

University Hospitals of Cleveland, Ohio 44106.

出版信息

Am J Cardiol. 1994 Apr 15;73(11):753-8. doi: 10.1016/0002-9149(94)90876-1.

Abstract

It was examined whether intracoronary ultrasound-defined plaque morphology of symptom-producing, severely stenosed, atherosclerotic coronary artery lesions is related to patient-related clinical variables. Data regarding anginal pattern (stable vs unstable), age, sex, history of smoking, diabetes, hypertension, hypercholesterolemia and lesion location were recorded in 146 hemodynamically stable patients referred for clinically indicated balloon angioplasty or directional atherectomy. Intracoronary ultrasound images of the lesions were obtained before and after the intervention. Lesions were classified as soft (homogeneous echoes less dense than adventitia) or hard (bright echoes with or without acoustic shadowing). Eighty-three lesions (57%) were classified as soft and 63 (43%) as hard. Univariate analysis showed anginal pattern, age, vessel location and history of smoking to be significantly related to plaque morphology. Multivariate analysis revealed only anginal pattern, age and vessel location to be independent predictors of plaque morphology. The frequency of echogenic hard plaque was significantly higher in patients aged > 60 years (56 vs 30%; p = 0.001), those with stable angina (69 vs 35%; p = 0.002), and lesions located in the distal arterial segments (68 vs 31%; p < 0.001) than in younger ones, those with unstable angina, and lesions in proximal segments, respectively. Based on previous studies, echogenic hard plaques are likely to be predominantly fibrous or calcific, or both, whereas low-echogenicity soft plaques are likely to be fibrocellular, lipid rich or thrombotic, or a combination. This difference in plaque morphology is probably due to differences in the predominant mechanism of plaque formation (i.e., slow growth vs rupture/thrombosis).(ABSTRACT TRUNCATED AT 250 WORDS)

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