Prolonged and intensive endurance training is associated with a pattern of functional and structural changes to the cardiovascular system that often results in ventricular hypertrophy and has been termed an athlete’s heart. Conversely, hypertrophic cardiomyopathy (HCM) is a genetic disorder that also results in hypertrophy of the cardiac ventricular muscle. Thus, identification of HCM in athletes can be problematic because of the substantial left ventricular hypertrophy associated with intense physical training (4,7,12,17). Because HCM is frequently associated with sudden cardiac death, the need to differentiate between athlete’s heart and HCM exists. Currently, mechanisms are available to assist in diagnosing HCM and to identify the prognostic implications associated with the disease. This article explores the athlete’s heart and HCM and evaluates the use of clinical testing to differentiate between these conditions.
HCM VERSUS THE ATHLETE’S HEART
Because exercise can induce functional and structural changes in the cardiovascular system, and because of the significant association between HCM and sudden cardiac death, detection of structural heart disease in athletes is important (5). The athlete’s heart develops as regular dynamic exercise increases the aerobic capacity and the oxygen consumption of skeletal muscles, which ultimately mitigates the response of the cardiovascular system to catecholamines at rest and with exercise (5). These changes lead to an increased diastolic filling and stroke volume, which produces a rise in maximum cardiac output and peak oxygen consumption (5). Morphological changes associated with endurance-trained hearts, including an increase in chamber size and moderate increase in wall thickness, are termed eccentric hypertrophy of the ventricles. When an athlete’s heart results from prolonged strength training, typically from the large transient hypertension that develops during the training, a concentric hypertrophy develops (14).
Conversely, HCM is an inherited condition in which the heart muscle becomes thick, making it more difficult for the heart to pump blood. It is the most common genetic disorder of the cardiovascular system, affecting approximately 1 in 500 people (8). Hypertrophic cardiomyopathy can be associated with left ventricular outflow tract obstruction (11). This obstruction can lead to significant outflow tract gradients, which put patients with HCM at greater risk of death (13). In contrast to the hypertrophy associated with the athlete’s heart, hypertrophy of the left ventricle in HCM is asymmetrical and usually involves the interventricular septum (5). The hypertrophied left ventricle often is characterized by diastolic dysfunction that results in a reduced ventricular filling and increased left ventricular end-diastolic and left atrial pressure. These resulting changes promote the occurrence of atrial fibrillation that further deteriorates the left ventricular filling during diastole (5).
Symptoms and conditions frequently associated with HCM can be seen in the Table. In addition to these symptoms, HCM can be associated with significant cardiac arrhythmias, including ventricular tachycardia, atrial fibrillation, and incomplete or complete heart block, as well as an attenuated or hypotensive systolic blood pressure response that could ultimately lead to sudden cardiac death (9).
CLINICAL TESTING TO DIFFERENTIATE HCM FROM ATHLETE’S HEART
Various noninvasive testing procedures can be used to provide information on the underlying cause of a hypertrophied heart. Although an electrocardiogram (ECG) has limitations and cannot fully distinguish an athlete’s heart from HCM, some preliminary information can be derived to determine the need for additional testing. The ECG pattern demonstrated in an athlete’s heart often depicts prolonged conduction intervals and also may include the presence of an incomplete right bundle branch block or high T-waves (5). In situations where the ECG demonstrates deep Q-waves and negative T-waves, the presence of HCM should be considered because these physiological changes are not typical after prolonged training programs (5).
However, echocardiography can provide significant clinical information to differentiate an athlete’s heart from HCM. An athlete’s heart is typically characterized by proportional increases in ventricular diameters and wall thickness, leading to left and right heart walls that are symmetrically affected (5). In HCM, asymmetric left ventricular hypertrophy is present, primarily affecting the interventricular septum. In fact, septal thickness exceeding 15 mm has been clearly linked to HCM (5). Lastly, serial echocardiography could be used to further differentiate between HCM and athlete’s heart by demonstrating evidence of detraining. During this period, marked reduction in the morphological changes associated with training will be noted in the athlete’s heart, where no changes in structural abnormalities will be noted in those with HCM (5).
Although recent recommendations from the American College of Cardiology Foundation (ACC)/American Heart Association list the presence of HCM as a relative contraindication to exercise testing (3), researchers have identified a relatively low incidence of significant cardiovascular complications during testing in this patient population (1,16). Additionally, according to the ACC/European Society of Cardiology, a risk factor for sudden death that often is associated with HCM includes an abnormal systolic blood pressure response to exercise (9). Thus, it seems that exercise testing has a role in distinguishing between HCM and an athlete’s heart, particularly when adjunctive echocardiography or oxygen consumption measures are used. Maron et al. (10) recommend that exercise echocardiography be used to evaluate for outflow track obstruction (a narrowing caused by the thickened ventricle walls that can block or reduce the blood flow from the left ventricle to the aorta) in patients with suspected HCM. Exercise testing also can identify hypotensive or attenuated blood pressure responses that are indicative of HCM but not typically seen with an athlete’s heart (2,6,9,15). Lastly, when concomitant oxygen consumption measures are used during the exercise test, those with an athlete’s heart will demonstrate significantly higher peak oxygen consumption as compared with those with hypertrophy caused by HCM (16). In fact, given available data, it is postulated that oxygen consumption measures below 50 ml/kg per minute in an athlete with diagnosed cardiac hypertrophy can be used to identify probable HCM versus an athletic heart (16).
IMPLICATIONS FOR THE EXERCISE PHYSIOLOGIST
Identification of potentially dangerous clinical conditions is imperative for the exercise physiologist who works in an exercise testing laboratory or in a clinical rehabilitation center. Abnormal ECG findings may elicit the need for further clinical testing that may be beneficial in clarifying questionable clinical status. When working as part of a team of health professionals and by recognizing the signs and symptoms of HCM, the risks of sudden cardiac death during exercise in this clinical population can be reduced. In addition, recognizing that persistent aerobic and strength training exercise can alter cardiac morphology, which may require alternative clinical testing or adjunctive imaging modalities during exercise testing, improvements in testing processes can be identified and discussed in an effort to better diagnose or rule out the presence of cardiac ischemia and HCM.
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