Pitfalls in the differentiation between athlete’s heart and hypertrophic cardiomyopathy

Abstract

Dear Editors, With great interest we read the recently published article ‘‘Athlete’s heart or hypertrophic cardiomyopathy?’’ by Lauschke and Maisch [4]. We appreciate the work of the authors, but would like to mention some important aspects. First of all, it is important to mention that competitive sport does not necessarily result in an athlete’s heart. An athlete’s heart is typical for endurance athletes performing regular and intensive endurance training of at least 5 h/week, e.g. covering running distances of more than 70 km/week [1, 2]. In contrast to the endurance trained heart with an eccentric hypertrophy, there is less evidence for a strength trained heart with a concentric hypertrophy, hypothesized by Morganroth et al. in 1975 [6], as controversial data for left ventricular dimensions in strength athletes have been reported in the following years [7, 16]. In consequence, even the cited meta-analysis of Pluim et al. [9] can only be as good as the underlying data are. The concentric hypertrophy of strength trained athletes sometimes reported in the literature is probably due to the use of anabolic steroids [7, 15, 16] and not the result of the increase in blood pressure during strength training. Usually, the LV wall thickness is not increased in strength trained athletes. Therefore, an elevation of the LV wall thickness ([13 mm) without a concomitant increase in the LV end diastolic diameter, and especially if a relative wall thickness of 42–44% is exceeded [3, 16], has to be considered as pathological—regardless of the kind and amount of sports performed. In this context, it also seems necessary to warn of the upper reference values for LV mass given in the article by Lauschke and Maisch (122 g/m in men; 149 g/m in women) [4], because in healthy females the LV mass is not higher but lower than in healthy males [7, 10, 11, 14]. Second, a differentiation between athlete’s heart and hypertrophic cardiomyopathy (HCM) by the peak or maximal oxygen consumption (VO2max) bears a considerable risk. As the VO2max in healthy untrained subjects at ages between 20 and 40 years usually ranges between 40 and 50 ml/(min kg), the suggested cut-off value of 50 ml/ (min kg) can easily be exceeded by mildly trained athletes—even if a grey zone pathology is present. Furthermore, the suggested cut-off value is easily exceeded by well trained or professional athletes with initial or borderline HCM. In two professional athletes with a clear echocardiographic evidence of HCM and septal wall thicknesses of 15–18 and 14–17 mm, respectively, a maximal power output of 350 W during cycle ergometry and a VO2peak of 62 ml/(min kg) were measured, respectively, at our institute. Therefore, it is neither possible nor advisable to differentiate between athlete’s heart and HCM by spiroergometry in trained athletes—especially in those athletes with grey zone hypertrophy. In addition, an ergometric capacity clearly above average levels does not exclude a HCM or other forms of cardiomyopathies either [13]. Third, it is right that the ECG is a helpful screening tool in sports cardiology. But as stated correctly in the introduction, trained healthy athletes present a broad range of J. Scharhag (&) Hochschulambulanz der Universitat Potsdam, Zentrum fur Sportmedizin, Freizeit-, Gesundheitsund Leistungssport, Universitat Potsdam, Am Neuen Palais 10, Haus 12, 14469 Potsdam, Germany e-mail: Scharhag@uni-potsdam.de