This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Sandrock, M. Articles by Dickhuth, H.-H. Search for Related Content PubMed PubMed Citation Articles by Sandrock, M. Articles by Dickhuth, H.-H.

Influence of Physiologic Cardiac Hypertrophy on the Prevalence of Heart Valve Regurgitation

Department of Rehabilitative and Preventive Sports Medicine, Center for Internal Medicine, Freiburg University Hospital, Freiburg, Germany (H.-H.D.); Department of Sports Medicine, Technical University Munich, Munich, Germany (A.S.-T.); Department of Sports Medicine, Center for Internal Medicine, Tübingen University Hospital, Tübingen, Germany (M.S., A.N.); and Center for Anesthetics, Mannheim University Hospital, Mannheim, Germany (D.S.).

Address correspondence to Markus Sandrock, MD, Department of Sports Medicine, Center for Internal Medicine, Tübingen University Hospital, Silcherstrasse 5, 72076 Tübingen, Germany. E-mail: markus.sandrock{at}gmx.de

Objective. Chronic dynamic exercise leads to regulative and structural adaptations of the heart (athlete’s heart). To what extent the enlargement and physiologic hypertrophy of the heart lead to changes in the function of the valves, particularly regurgitation, is not yet clear. The aim of this study was to examine the regurgitation levels of different states of "athlete’s heart." Methods. Our study population consisted of 5124 healthy subjects (4046 male and 1078 female, 18–60 years), regularly exercising 1 to 20 h/wk. Subjects were divided into 3 groups depending on their relative heart volumes (RHVs): (1) very enlarged heart group (VEHG; male, n = 1251; female, n = 201), with RHVs of greater than 14 (male) and 13 (female) mL/kg; (2) mildly enlarged heart group (MEHG; male, n = 702; female, n = 224), with RHVs of 12 to 14 (male) and 11 to 13 (female) mL/kg; and (3) control subjects (CS; male, n = 2093; female, n = 653), with RHVs of less than 12 (male) and 11 (female) mL/kg. Results. According to US Food and Drug Administration criteria for valve regurgitation, it could be shown by Doppler sonography that as physiologic enlargement and hypertrophy increased significantly, the frequency and severity of aortic valve regurgitation (mean ± SD: VEHG, 0.04 ± 0.09; MEHG, 0.09 ± 0.10; CS, 0.10 ± 0.11; P < .05) and high mitral regurgitation (VEHG, 0.10 ± 0.17; MEHG, 0.20 ± 0.29; CS, 0.26 ± 0.32; P < .01) decreased. On the contrary, pulmonary regurgitation (VEHG, 0.79 ± 0.45; MEHG, 0.47 ± 0.33; CS, 0.35 ± 0.38; P < .01) and tricuspid valve regurgitation (VEHG, 0.42 ± 0.29; MEHG, 0.47 ± 0.33; CS, 0.35 ± 0.38; P < .01) increased highly significantly with heart size. Conclusions. These findings strongly support the view of athlete’s heart as a physiologic adaptation of the heart, at least on the left side, not causing increased valvular regurgitation.

Key Words: athlete’s heart • prevalence • relative heart volume • regurgitation level

Abbreviations: AHV, absolute heart volume • AR, aortic regurgitation • CS, control subjects • IVSTd, septum thickness • LVIDd, left ventricular end-diastolic diameter • Man-U, Mann-Whitney U test • MEHG, mildly enlarged heart group • MR, mitral regurgitation • PR, pulmonary regurgitation • PWTd, posterior wall thickness • RHV, relative heart volume • TDV, total diastolic volume • TEDD, total end-diastolic diameter • TLD, total longitudinal diameter • TR, tricuspid regurgitation • VEHG, very enlarged heart group • VO₂max, maximum oxygen consumption