Abstract des Autors

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 lethal misjudgements due to sports's forensic medical mistakes. Verf.-Referat