Clark James, Bakhit Yasir, Motwani Manish
Department of Cardiology, Betsi Cadwaladr University Health Board, Wrexham Maelor Hospital, Wrexham LL13 7TD, UK.
Division of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
Eur Heart J Case Rep. 2023 Jan 10;7(1):ytad002. doi: 10.1093/ehjcr/ytad002. eCollection 2023 Jan.
The wide-ranging benefits of frequent and moderate exercise are well recorded in the literature. Chronic deleterious remodelling in response to exercise is less well described. We describe an amateur endurance cyclist who, in addition to developing a heart failure syndrome and electrocardiographic evidence of arrhythmia, also developed severe functional tricuspid regurgitation.
After developing palpitations during long distance cycle rides as part of his fitness regimen, a 69-year-old male presented to emergency services but was discharged. While continuing to enjoy long-distance cycling, he began to develop peripheral swelling and presented for a second time to hospital. Subsequent investigation found he had a dilated right heart, exercise-induced arrhythmia, and mid-wall myocardial fibrosis. A diagnosis of exercise-induced cardiomyopathy was made. He was managed with diuretics and immediate cessation of exercise. His symptoms improved and he remains symptom free.
The volume of blood passing through the right heart increases during exercise. In vulnerable individuals undertaking frequent endurance exercise, this can promote structural remodelling and fibrotic change. It is unclear if cessation of exercise can reverse the remodelled heart. There are some early advances in predictive biomarkers and imaging techniques in categorizing those in the population who would be at risk of developing this cardiomyopathy, and those who can undergo intense exercise regimens without concern. If those at risk of developing an exercise-induced cardiomyopathy can be accurately identified, the next dilemma is how can their risk of heart failure or sudden death be acceptably minimized.
文献中充分记载了频繁适度运动的广泛益处。而关于运动导致的慢性有害重塑的描述则较少。我们描述了一名业余耐力自行车运动员，他除了出现心力衰竭综合征和心律失常的心电图证据外，还出现了严重的功能性三尖瓣反流。
一名69岁男性在作为健身计划一部分的长途骑行中出现心悸后，前往急诊，但被出院。在继续享受长途骑行的过程中，他开始出现外周水肿，并再次入院。随后的检查发现他右心扩大、运动诱发的心律失常以及中层心肌纤维化。诊断为运动诱发的心肌病。他接受了利尿剂治疗并立即停止运动。他的症状有所改善，目前无症状。
运动期间流经右心的血量会增加。对于经常进行耐力运动的易感个体，这可能会促进结构重塑和纤维化改变。目前尚不清楚停止运动是否能逆转重塑的心脏。在预测生物标志物和成像技术方面，在对人群中哪些人有患这种心肌病的风险以及哪些人可以毫无顾虑地进行高强度运动方案进行分类方面有一些早期进展。如果能够准确识别有患运动诱发心肌病风险的人，下一个难题是如何将他们发生心力衰竭或猝死的风险合理地降至最低。
