Lauschke Jörg, Maisch Bernhard
Department of Internal Medicine and Cardiology, Philipps-Universität Marburg, Marburg, Germany.
Clin Res Cardiol. 2009 Feb;98(2):80-8. doi: 10.1007/s00392-008-0721-2. Epub 2008 Oct 13.
Intensive endurance training is able to cause a distinct pattern of functional and structural changes of the cardiovascular system. In an unknown proportion of athletes a so called "athlete's heart" develops. There is an overlap between this type of physiologic cardiac hypertrophy and mild forms of hypertrophic cardiomyopathy (HCM), the most common genetic disorder of the cardiovascular system with a prevalence of 0.2%. HCM is caused by mutations in 14 genes coding for sarcomere proteins. In the literature up to 50% of cases of sudden cardiac death (SCD) in younger sportsmen were connected to hypertrophic cardiomyopathy. It is therefore the most common cause of SCD in highly trained young athletes. Because of this data a great interest in distinguishing these two diagnoses exists. Apart from clinical examination and some non-specific ECG-changes, Echocardiography is the method of choice. The athlete's heart shows an eccentric biventricular hypertrophy with wall thicknesses under 15 mm and a moderately dilated left ventricle (LVEDD up to 58 mm). HCM is commonly characterized by asymmetric left ventricular hypertrophy with a reduced LV-diameter. In up to 70% of cases left ventricular outflow tract obstruction is evident during stress echocardiography. Systolic function is normal in highly trained athletes and the majority of HCM patients as well. There are important differences regarding diastolic filling patterns. Physiological hypertrophy is consistent with a normal diastolic function with even increased early diastolic filling. In case of HCM diastolic dysfunction (mostly relaxation disturbances) occurs in the majority of patients and is therefore inconsistent with an athlete's heart. If the diagnosis could not be stated using echocardiography, methods like cardiac-MRI, metabolic exercise testing, histological studies of endomyocardial biopsies and genetic testing can provide further information. A correct diagnosis may on the one hand prevent some athletes from sudden cardiac death. On the other hand sportsmen with an athlete's heart are reassured and able to continue as competitors. New insights into electrophysiological changes during physiological hypertrophy could probably change this view.
高强度耐力训练能够引起心血管系统功能和结构的明显变化。在一定比例未知的运动员中会出现所谓的“运动员心脏”。这种生理性心脏肥大与轻度肥厚型心肌病（HCM）存在重叠，HCM是最常见的心血管系统遗传性疾病，患病率为0.2%。HCM由14种编码肌节蛋白的基因突变引起。文献报道，年轻运动员中心脏性猝死（SCD）病例高达50%与肥厚型心肌病有关。因此，它是训练有素的年轻运动员SCD的最常见原因。基于这些数据，人们对区分这两种诊断非常感兴趣。除了临床检查和一些非特异性心电图变化外，超声心动图是首选方法。运动员心脏表现为双心室离心性肥大，壁厚小于15mm，左心室中度扩张（左心室舒张末期内径可达58mm）。HCM通常表现为不对称性左心室肥大，左心室直径减小。在高达70%的病例中，负荷超声心动图检查时可见左心室流出道梗阻。训练有素的运动员和大多数HCM患者的收缩功能均正常。在舒张期充盈模式方面存在重要差异。生理性肥大与正常舒张功能一致，甚至早期舒张期充盈增加。而HCM患者多数存在舒张功能障碍（主要是舒张功能减退），因此与运动员心脏不同。如果超声心动图无法明确诊断，心脏磁共振成像、代谢运动试验、心内膜心肌活检组织学研究和基因检测等方法可提供更多信息。正确的诊断一方面可以预防一些运动员发生心脏性猝死。另一方面，患有运动员心脏的运动员可以安心并继续参加比赛。对生理性肥大期间电生理变化的新认识可能会改变这种观点。
