The Athletic Heart on Echocardiography

Structure

Regular training increases LV mass, with the pattern determined in part by the type of training undertaken by the athlete, as described earlier. For the echocardiographer trying to differentiate physiologic remodeling from cardiac pathology, the key issue is whether the echocardiographic findings fall inside or outside the expected range for the type and intensity of exercise undertaken by the athlete being examined. Most studies that have determined normal ranges for LV structure have used M-mode to measure LV internal diameter at end-diastole and end-systole, septal wall thickness, and posterior wall thickness at end-diastole, with these values used to determine relative wall thickness and often mass. Others have reported LV volume measurements obtained by echocardiography or cardiac magnetic resonance imaging (MRI).

In pure dynamic exercise, LV mass, volume, dimensions, and wall thickness are all increased ; however, the extent of chamber enlargement and the increase in wall thickness tends to be in balance, such that relative wall thickness is similar to that in nonathletes in many studies. In pure static exercise training, LV dimensions are normal or mildly increased with normal or increased wall thickness. The commonly held view that a concentric pattern of hypertrophy is seen as a result of strength training is incorrect, and a smaller than normal LV cavity should raise the possibility of HCM.

The most profound changes are seen in athletes undertaking endurance and strength training, such as cyclists and rowers. Most studies have found these athletes to have the greatest LV mass and largest dimensions. Many studies are carried out in recreational athletes, and the changes seen in elite and professional athletes can be quite profound when compared with the ranges presented in many cross-sectional studies ( Fig. 35.1 ).

The parameters of cardiac structure most commonly used to differentiate healthy athletes from those with inherited cardiac disease such as HCM have been measures of LV wall thickness and relative wall thickness. Wall thickness less than 13 mm in males or less than 11 mm in females is considered to be normal for an athlete ( Fig. 35.2 ). Wall thicknesses greater than 15 mm in a black male athlete, 14 mm in a white male athlete, and 13 mm in a female athlete are considered to be abnormal. This leaves a “gray zone” between these values where differentiation of physiology from pathology may be necessary.

It is clear that gender, age, and race have effects on the athlete’s heart phenotype. Although the direction of change with training is similar, dimensions, wall thickness, and LV mass are lower in females than in males, even when indexing for body surface area (BSA) is performed. However, published data on cardiac dimensions in female athletes, particularly elite female endurance athletes, are sparse. Whether female athletes undertaking high intensities and volumes of exercise similar to those of male athletes may develop similarly profound adaptations is a question that requires further research. Different normal ranges are employed for female athletes (see Table 35.2 ).

Adolescent athletes tend to have less developed changes of athlete’s heart that become more pronounced during maturation, leading to different published normal ranges for younger athletes (see Table 35.2 ). Whether these differences are truly attributable to cardiac maturation or simply to the lower volume of training exposure compared with adults is unknown. Adolescent cohorts in these publications have been largely subelite nonendurance athletes; data are lacking on the cardiac adaptations in populations of elite adolescent athletes, who may have already undergone 3 to 4 years of intensive endurance training.

Athletes of Afro-Caribbean background have increased wall thickness compared with white athletes, and different ranges are used to define normality. For example, the upper limit of normal wall thickness in a white male athlete is 12 mm, but it may be up to 15 mm in healthy Afro-Caribbean male athletes (see Fig. 35.2 ). Wall thickness in black female athletes is also greater than in their white counterparts. Wall thickness greater than 11 mm is unusual in white female athletes, but wall thickness up to 13 mm is seen in black female athletes.

Determining the impact of performance-enhancing drugs on cardiac structure and function is difficult because most athletes are reluctant to admit to their use. Studies using cardiac MRI and echocardiography have shown that strength-trained athletes who do not use anabolic steroids have LV wall thicknesses, ventricular volumes, and left ventricular ejection fractions (LVEFs) similar to those of nonathletes. In contrast, users of anabolic steroids have larger LV volumes, thicker walls, and lower LVEFs compared with nonathletes and with strength-trained athletes not using steroids. Echocardiographic studies have also suggested that anabolic steroid use produces abnormalities in Doppler measures of LV systolic function and diastolic function. It is therefore likely that pure strength training is not truly associated with significant changes in measures of LV structure and that published normal cardiac findings for purely strength-trained athletes have been affected by undeclared use of anabolic steroids.

Systolic Function

Two large meta-analyses reported similar LVEF values for athletes and the general population. ^, However, lower than normal resting LVEF with preserved stroke volumes can be observed in healthy elite endurance athletes, in whom profound increases in volumes affect all four cardiac chambers. In other words, a healthy enlarged LV needs less vigorous contraction and a lower LVEF to maintain normal cardiac output at rest ( Fig. 35.3 ). The same finding has been observed in elite athletes with nondilated ventricles. In cases of uncertainty, imaging of the heart during exercise may be helpful to differentiate a dilated athlete’s heart from a dilated cardiomyopathy (DCM) (see Technical Considerations and Physiologic Differences).

Less is known about the effect of athletic activity on direct measures of myocardial function, such as tissue velocity, strain, and strain rate. Most studies have reported normal or supranormal LV myocardial systolic velocities at rest in athletes. ^, A cutoff value of 9 cm/s of systolic peak velocity ( s ′, averaged over four mitral annular sites) has been proposed as an accurate discriminator between pathologic LVH and athlete’s heart. However, athletes with HCM may have preserved myocardial velocities. Therefore, when there is a clinical suspicion of HCM, normal systolic myocardial velocities should not be used as a discriminator between HCM and athlete’s heart.

Resting global longitudinal strain measures have been reported to be lower in athletic cohorts compared with nonathletic controls. In much the same way as LVEF may appear reduced at rest in healthy endurance athletes, these observations likely reflect the inadequacy of resting measures to assess functional reserve; lower strain velocities may be required at rest to maintain normal stroke volumes in physiologically enlarged hearts. This has been eloquently demonstrated in the right ventricle (RV), with lower RV strain rates at rest in endurance athletes than in controls but normal augmentation of these indices with exercise. In the absence of normative values in large populations of athletes from a spectrum of sporting disciplines, these measures are not currently considered routine in the assessment of the athlete’s heart but may prove to be useful in the future, particularly in the assessment of cardiac reserve with stress echocardiography ( Fig. 35.4 ).

Diastolic Function

Resting measures of LV diastolic function are typically normal or supranormal in athletes, who demonstrate higher LV chamber compliance than sedentary controls. ^, Increases in measures of early diastolic function (i.e., peak transmitral E-wave and E′ tissue velocities) and late diastolic indices (i.e., peak transmitral A-wave and A′ velocity) appear to be most marked in endurance athletes. Although cutoffs for diastolic parameters (e.g., E/ e ′ > 7.3) have been proposed for discrimination between athlete’s heart and pathologic LVH, normal diastolic parameters may be observed in athletes with HCM. Although abnormal diastolic filling detected by echocardiography in an athlete is likely to reflect myocardial disease, diastolic filling in the normal range for nonathletes does not exclude disease.

Structure

During exercise, the RV is subjected to the same volume load as the LV, but wall stress increases more in the RV due to increases in pulmonary artery pressure that parallel the increased cardiac output. Compared with nonathletes, athletes have increased RV volume, increased RV linear dimensions, and increased wall thickness. The magnitude of the increase in RV volume with training is similar to the increase in LV volume, and some reports suggest that it is slightly greater. This has been seen with both strength- and endurance-trained athletes. The degree of RV remodeling increases with duration of training, with more profound changes seen in older athletes with longer participation.

At a practical level, the use of a focused RV view is important for examining the RV, identifying the free wall and the trabeculae, and quantifying dimensions and area ( Fig. 35.5 ).