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by the American Institute of Ultrasound in Medicine J Ultrasound Med 27:85-93 • 0278-4297 Influence of Physiologic Cardiac Hypertrophy on the Prevalence of Heart Valve RegurgitationDepartment 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
Chronic endurance training is associated with functional and morphologic heart adaptations, which include bradycardia and increases in wall thickness and the size of all 4 chambers. This is called "athlete’s heart."1–3 The function and structure of an athlete’s heart and the impact of different sports on cardiac structure have been investigated by several authors.4–7 However, the effect of physiologic cardiac hypertrophy on the function of the valves, particularly the frequency and extent of regurgitation, is unclear. In 1983, Dickhuth et al3 classified physiologic hypertrophy of endurance-trained athletes and untrained subjects using 2-dimensional echocardiographic measurements. The echocardiographic method developed combined 1-dimensional measurements of the diameter of the left ventricular mitral valve and papillary muscle levels with 2-dimensional determination of the long axis on an apical 4-chamber view. The end-diastolic left ventricular volume and total heart volume can be obtained from a modified Simpson rule and correlate highly to the radiographically and angiographically determined total heart volume.8,9 We used this classification in our study to differentiate between different stages of physiologic cardiac hypertrophy. Color Doppler echocardiography, a sensitive technique for detecting valvular regurgitation, provides a semiquantitative method for estimating the severity of regurgitation.10 Previous color Doppler echocardiographic studies reporting the prevalence of valvular regurgitation have been limited to small subsets of patients with heart insufficiency11–13 and acromegaly14 as well as athletes15 and children16 compared with untrained subjects with structurally normal hearts.12,17,18 There are no investigations on the sex-dependent prevalence rates of mitral regurgitation (MR), tricuspid regurgitation (TR), pulmonary regurgitation (PR), and aortic regurgitation (AR) in athletes. The purpose of this study was to describe the effect of increases in physiologic cardiac hypertrophy on the regurgitation level of the valves of the heart.
Study Population Our study population consisted of 5124 healthy subjects (4046 male and 1078 female, 18–60 years). They were examined between January 2001 and March 2006 in a major outpatient sports medicine clinic. The design of the study was a retrospective cross-sectional analysis of data. Each subject underwent a careful medical assessment, including a medical history, a drug intake history, a clinical examination, routine laboratory tests, and stress electrocardiography. All subjects with a history of cardiovascular events, pathologic findings, or a resting blood pressure of greater than 150/90 mm Hg and those who were taking cardiovascular drugs or noncardiovascular drugs such as anabolic steroids or anorectics, which might have interfered with the study results and are of potential interest to young and body-conscious people, were excluded from the study. None of the subjects had cardiac symptoms or abnormalities noted in the permanently registered electrocardiographic records during the ergometric test. The subjects were divided into 3 groups according to sex and their relative heart volumes (RHVs; in milliliters per kilogram)10 based on 2-dimensional echocardiograms. The RHV is not a commonly used parameter, nor is the total heart volume. Sonographic analysis of both parameters is more time-consuming than that of the actual left internal diameter used, but relative and absolute volumes give some additional information than does the internal diameter for evaluation of the physical heart size.12 The 3 groups were as follows: (1) very enlarged heart group (VEHG; male, n = 1251; mean age ± SD, 26.7 ± 7.8 years; female, n = 201; mean age, 24.7 ± 9.7 years), with RHVs of greater than 14 (male) and 13 (female) mL/kg; (2) mildly enlarged heart group (MEHG; male, n = 702; mean age, 28.4 ± 11.4 years; female, n = 224; mean age, 25.8 ± 11.2 years), with RHVs of 12 to 14 (male) and 11 to 13 (female) mL/kg; and (3) control subjects (CS; male, n = 2093; mean age, 28.4 ± 11.4 years; female, n = 653; mean age, 28.7 ± 13.4 years), with RHVs of less than 12 (male) and 11 (female) mL/kg. The research was carried out in accordance with the Declaration of Helsinki (1989) of the World Medical Association and was approved by the Freiburg University Research and Ethics Committee. Informed consent was obtained from all subjects.
Cardiorespiratory Fitness Bicycle tests were performed according to standardized testing protocols starting at 100 W and increasing by 20 W every 3 minutes. Treadmill tests commenced at 6 km/h with a constant augmentation of 1%. The velocity was increased 2 km/h every 3 minutes until subjective exhaustion with a 15-second break at the end of each step for lactate blood testing. Oxygen consumption was measured by the breath-by-breath method of respiratory gas exchange for maximum oxygen uptake (Jaeger Oxycon Delta, Würzburg, Germany) or was calculated from the maximum power of the exercise test.
Echocardiography M-mode echocardiography was used to determine the left ventricular end-diastolic diameter (LVIDd) and left ventricular posterior wall thickness (PWTd) as well as the septum thickness (IVSTd). The left ventricular total end-diastolic diameter (TEDD = LVEDD + LVIDd + PWTd) was determined on the mitral valve plane (TEDDm) and the papillary muscle plane (TEDDp). The left ventricular total longitudinal diameter (TLD) was determined in the 4-chamber-view. Parameters were measured 3 times, and mean values were used to calculate the left ventricular total diastolic volume (TDV; in milliliters) and absolute heart volume (AHV; in milliliters) by the following formulas16:
The RHV was calculated by dividing the AHV by the weight of the subject.13
Color Doppler Echocardiography Pulsed Doppler echocardiography was performed routinely in apical 4- and 5-chamber views. If Doppler echocardiographic regurgitation signals were present, the sample volume was selectively placed on the Doppler signal. Color Doppler variations were represented by different groups of brightness and color intensity. Flow directed toward the transducer was conventionally coded in red, and flow away from the transducer was coded in blue. Valvular regurgitation was diagnosed with color-coded Doppler imaging proximal to the valve plane during its closure and extended into the chamber proximal to the valve. For color Doppler studies, gain settings were adjusted to eliminate background speckling and to maximize the extent of intracavitary velocity coding. Mitral regurgitation was identified on the basis of views from the parasternal long-axis, apical 4- and 2-chamber, apical long-axis, and subcostal positions. For TR, the parasternal right ventricular inflow, parasternal short-axis, apical 4-chamber, and subcostal views were used. Parasternal long-axis, parasternal short-axis, apical 5-chamber, and apical long-axis views were used to identify AR, and the parasternal long-axis view was used for PR. Mitral regurgitation and TR were considered to be present if blue, green, or mosaic signals were seen originating from the mitral valve and spreading into the left atrium or originating from the tricuspid valve and spreading into the right atrium during systole. Aortic regurgitation and PR were considered to be present if red, yellow, or mosaic signals (blue in the parasternal long axis) were seen to originate from the aortic valve and to spread into the left ventricle or to originate from the pulmonary valve and to spread into the right ventricle during diastole. Valvular regurgitation was assessed qualitatively with semiquantitative guidelines and graded as none, trace, mild, moderate, or severe,10,18 according to the US Food and Drug Administration case definition.19 For statistical analysis, a score was used: cases with no regurgitation received a score of 0; cases with trace regurgitation received a score of 1; cases with mild regurgitation received a score of 2; cases with moderate regurgitation received a score of 3; and cases with severe regurgitation received a score of 4. The mean value ± SD of all scores was calculated. Subjects were excluded if they met any of the following criteria: a technically poor echocardiogram (ie, color Doppler signals of insufficient quality to accurately assess the severity of regurgitation), mild or more severe mitral stenosis, mild or more severe aortic stenosis, or pathologic hypertrophy of other causes.
Statistics
Characteristics of Subjects All 5124 subjects were included (4046 male and 1078 female). Anthropometric data, heart frequency, blood pressure, and hemoglobin and hematocrit values showed no significant differences in both male and female subjects in the nonparametric analysis (Man-U; Table 1  ). During the ergometer, the test maximum lactate concentration and maximum heart frequency were not significantly different (Man-U). The maximum oxygen consumption (VO2max) increased with the RHV from 48.4 to 62.4 mL/(kg · min) in male subjects and from 45.7 to 61.7 mL/(kg · min) in female subjects (Man-U).
Echocardiographic Data The AHV and RHV were highly significantly increased from the CS to the VEHG in male subjects (Man-U; Table 2 ). The LVIDd, left ventricular PWTd, and IVSTd were significantly higher in VEHG male subjects than in MEHG and CS male subjects. In female subjects, nearly the same significant differences were found. Because of their smaller body dimensions, the absolute values for LVIDd, PWTd, and IVSTd were lower.
Doppler Sonographic Data In male subjects, MR and AR decreased in severity and frequency with increasing heart volume (Table 3 ). For TR, higher regurgitation with increasing heart size was observed in male and female subjects. In contrast, TR and PR showed a slight increase in frequency and severity from the CS to the VEHG.
To quantify and summarize the effect of the increasing physiological heart size on the regurgitation status, a score was calculated. In male and female subjects, MR and AR occurred less frequently and was less severe than TR and PR independent of heart size (Tables 4 and 5 and Figures 1 and 2). For both, male and female subjects, the MR and AR regurgitation scores decreased with increasing heart size; TR and PR scores increased.
Chronic endurance training leads to improved aerobic capacity. If endurance training exceeds individual limits, harmonic enlargement and hypertrophy of the heart result. The thicknesses of both the septum and posterior wall of the left ventricle increase to the same extent as the inner volume. The mass-volume ratio of the left ventricle remains constant, in contrast to pathologic forms of hypertrophy. There is less valid information about the right heart. In general, the physiologically hypertrophied heart is considered to have very high performance and enables the heart to increase its maximum cardiac output and oxygen uptake.
Our data illustrate this relationship between the RHV and maximum oxygen uptake in male as well as female subjects. No differences between the groups could be seen in anthropometric data, heart rate behavior, blood pressure, and the red blood parameters hemoglobin and hematocrit (Table 1 On the other hand, it is unclear whether physiologic enlargement affects the frequency and severity of valve regurgitation, as observed in pathologic forms of hypertrophy.9–12 For healthy subjects, prevalence rates of 24% to 96% for TR, 10% to 80% for MR, and 0% to 33% for AR have been reported.20–23 The discrepancies in prevalence rates can be explained by the fact that earlier studies were limited to small numbers of subjects and varied in their definitions of regurgitation.11 Additionally, previous studies have shown that the prevalence of MR, TR, PR, and AR increase with age, which is consistent with earlier Doppler studies.11–13 However, although left-sided valves (aortic and mitral valves) are exposed to high pressures and are likely to undergo degenerative changes earlier than right-sided valves, the relationships of the prevalence rates of all valves were comparable for all ages. The prevalence rates of MR, PR, TR, and AR (as defined according to US Food and Drug Administration criteria) in our control group were nearly the same as those found in other studies.11,24,25 The occurrence of severe valvular regurgitation in our control group is also consistent with the findings in those epidemiologic studies. Some clinicians consider the classification of physiologic (trace) and mild MR as "abnormal" inappropriate. Both occur frequently and are clinically irrelevant. However, AR is something different. Our study and others have found that less than 5% of the population have mild or greater AR,16 the usual cutoff for clinical significance.
The main findings of our study are that a high and moderate physiological increase of the RHV reduces the frequency and severity of MR and AR and increases PR and TR. Some differences were found between male and female subjects. According to Table 4 Douglas et al15 showed that in highly trained athletes, prolonged exercise causes different responses from the right and left ventricles. They postulated that the differences in regurgitation levels may be due to changes in function, shape, or compliance in the right ventricle.15 This thesis is supported by radiologic findings of a pronounced right ventricle and an increase in the incomplete right bundle branch block of an athlete’s heart. On the other hand, noninvasive studies, in particular, echocardiographic studies, have shown that right and left ventricular function remains unchanged in the athlete’s heart.17 These observations were confirmed by Scharhag et al9 in their magnetic resonance imaging study, which showed that the athlete’s heart is a balanced, enlarged heart. Another explanation for the difference of left-and right-sided regurgitation could be that connective tissues in the left side of the heart are very stable because of the higher pressure and hypertrophy in the left heart. It is thought that the remodeling effect is higher in the left side of the heart than in the right-side, where the connective tissues are less stable and more vulnerable to changes in the remodeling process. Lonati et al26 showed that in patients with essential hypertension, physiologic regurgitant jets were present in 1 or more cardiac valves; moreover, they found that regurgitation of the mitral and aortic valves was more frequent than in the normotensive control group. Their data suggest that the afterload of the left ventricle may play an important role in the pathogenesis of even a minor degree of insufficiency of the cardiac valves.26 However, in our groups, there were no differences in heart frequency or blood pressure. As a limitation, it should be mentioned that the cross-sectional nature of this study and the findings could be explained by the possibility that athletes with mitral or aortic regurgitation could have been less able to exercise and therefore less able to induce cardiac hypertrophy. In conclusion, the cause of the different behavior of the left-sided valves compared with the right-sided valves is unclear. This study shows that exercising individuals with concomitant adaptive cardiac hypertrophy have less left-sided and more right-sided regurgitation than physically active healthy subjects with smaller hearts. The increases in the frequency and severity of TR and PR regurgitation should be kept in mind when examining athletes with physiologic hypertrophy.
Received June 18, 2007, from the 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.). Revision requested July 22, 2007. Revised manuscript accepted for publication August 20, 2007.
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Abstract
Introduction
