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可卡因滥用者动脉粥样硬化和外膜肥大细胞增加:可卡因相关冠状动脉痉挛和血栓形成的另一种机制。

Increase in atherosclerosis and adventitial mast cells in cocaine abusers: an alternative mechanism of cocaine-associated coronary vasospasm and thrombosis.

作者信息

Kolodgie F D, Virmani R, Cornhill J F, Herderick E E, Smialek J

机构信息

Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, D.C. 20306-6000.

出版信息

J Am Coll Cardiol. 1991 Jun;17(7):1553-60. doi: 10.1016/0735-1097(91)90646-q.

Abstract

Coronary vasospasm has been implicated as a cause of myocardial ischemia and sudden cardiac death in cocaine abusers. However, the mechanism or mechanisms remain unknown. Autopsy records (n = 5,871) from the medical examiner's files at Baltimore, Maryland and northern Virginia were examined and 495 persons (8.4%) were identified with positive toxicologic findings for cocaine. Of these, six subjects (1.2%) had total thrombotic occlusion, involving primarily the left anterior descending coronary artery. The mean number of adventitial mast cells per coronary segment and the degree of atherosclerosis were determined. These observations were compared with findings in age- and gender-matched subjects who died from cocaine overdose and in patients who had sudden cardiac death (acute thrombosis) without a history of illicit drug abuse. There were significantly more mast cells in subjects with cocaine-associated thrombosis than in the other groups. The number of mast cells showed a significant correlation with the degree of cross-sectional luminal narrowing (r = 0.68) in subjects with cocaine-associated thrombosis but not in subjects with sudden death due to thrombosis (r = 0.34, p less than 0.03). Subjects with cocaine-associated thrombosis also had significant coronary atherosclerosis without plaque hemorrhage (five had one or more vessels with greater than 75% cross-sectional area luminal narrowing) despite a mean age of 29 +/- 2 years. These findings suggest that adventitial mast cells may potentiate atherosclerosis and vasospasm, thrombosis and premature sudden death in long-term cocaine abusers.

摘要

冠状动脉痉挛被认为是可卡因滥用者心肌缺血和心源性猝死的一个原因。然而,其机制仍不明。研究人员检查了马里兰州巴尔的摩市和弗吉尼亚州北部法医档案中的尸检记录(n = 5871),确定有495人(8.4%)可卡因毒理学检查呈阳性。其中,6名受试者(1.2%)出现完全血栓性闭塞,主要累及左前降支冠状动脉。测定了每个冠状动脉节段外膜肥大细胞的平均数量以及动脉粥样硬化程度。将这些观察结果与死于可卡因过量的年龄和性别匹配的受试者以及无非法药物滥用史的心源性猝死(急性血栓形成)患者的结果进行比较。可卡因相关血栓形成的受试者中的肥大细胞明显多于其他组。在可卡因相关血栓形成的受试者中,肥大细胞数量与横断面管腔狭窄程度呈显著正相关(r = 0.68),而在因血栓形成导致猝死的受试者中则无此相关性(r = 0.34,p < 0.03)。尽管平均年龄为29±2岁,但可卡因相关血栓形成的受试者也有显著的冠状动脉粥样硬化且无斑块出血(5人有一根或多根血管的横断面管腔狭窄超过75%)。这些发现表明,外膜肥大细胞可能会增强长期可卡因滥用者的动脉粥样硬化、血管痉挛、血栓形成和过早猝死。

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