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与运动医学相关的高危心律失常的结构性和非结构性疾病。

Structural and non-structural disease underlying high-risk cardiac arrhythmias relevant to sports medicine.

作者信息

Rossi L

机构信息

Department of Pathology, University of Milan, Italy.

出版信息

J Sports Med Phys Fitness. 1995 Jun;35(2):79-86.

PMID:7500631
Abstract

Problems of arrhythmogenic sudden death (ASD) in athletes have been re-assessed on the clinicopathological plane, encompassing the emerging, unsolved, question of so-called idiopathic ventricular tachycardia, and its debated diagnostics versus arrhythmogenic right ventricular dysplasia-cardiopathy. Ischemic-infarction ASD from coronary artery pathology in young athletes has been seen to present with atherosclerotic "soft" subintimal plaques, rich in newly formed smooth myocytes, often attended by adventitial mast cell, as suspect microscopic markers of spasm, relevant to reperfusion; these features can be found also in precociously intramural arteries, responsible for ASD. Rare congenital abnormalities of the coronary ostia occasionally underlie ASD, together with the acquired aneurysmic coronaritis of chronic Kawasaki disease. Ischemic ASD can also be due to coronary arteriolopathy attending hypertrophic cardiomyopathy, a not uncommon disease in athletes, to be carefully discriminated from training heart hypertrophy. Young South-American sportsmen with Chagas' chronic cardiopathy seem to be at particular risk of ASD. Minor, but specific arrhythmogenic cardiac malformations such as accessory AV pathways have been detected in athletes succumbing to otherwise unexplained ASD, undergone careful post-mortem investigation. The need of more attentive and extended histopathologic control emerges from the hitherto ignored cardiac neuropathological substrates of reflexogenic ASD, which is cogent to problems of ASD in competing athletes. The thorough examination of the cardiac vascular centers in the brain stem, and of the peripheral cardiac innervation, at either abutments of the arc of dive- and/or Bezold-Jarisch cardioinhibitory-vasodepressor reflex, made it possible to suggest novel clinicopathological explanations in controversial cases of athletes' ASD, safeguarding from grave leval misjudgements due to sport's forensic medical mistakes.

摘要

运动员致心律失常性猝死(ASD)问题已在临床病理层面重新评估,涵盖了新出现的、尚未解决的所谓特发性室性心动过速问题,以及其与致心律失常性右心室发育不良-心肌病的诊断争议。年轻运动员因冠状动脉病变导致的缺血性梗死性ASD表现为富含新形成平滑肌细胞的动脉粥样硬化“软”内膜下斑块,常伴有外膜肥大细胞,这些被视为与再灌注相关的痉挛可疑微观标志物;这些特征也可在导致ASD的早熟壁内动脉中发现。罕见的冠状动脉开口先天性异常偶尔是ASD的基础,慢性川崎病的后天性动脉瘤性冠状动脉炎也是如此。缺血性ASD也可能归因于肥厚型心肌病伴发的冠状动脉小动脉病变,肥厚型心肌病在运动员中并不罕见,需仔细与训练性心脏肥大相鉴别。患有恰加斯慢性心脏病的年轻南美运动员似乎特别容易发生ASD。在因其他原因不明的ASD而死亡的运动员中,经过仔细的尸检后发现了一些轻微但特定的致心律失常性心脏畸形,如房室旁道。从迄今被忽视的反射性ASD的心脏神经病理基质中可以看出,需要更仔细和广泛的组织病理学检查,这与竞技运动员的ASD问题密切相关。对脑干中的心脏血管中枢以及外周心脏神经支配进行全面检查,在潜水弧和/或贝佐尔德-雅里什心脏抑制-血管减压反射的两端进行检查,有可能为运动员ASD的争议病例提出新的临床病理解释,避免因运动法医错误而导致严重的水平误判。

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