Hypertrophic Cardiomyopathy vs. Athlete’s Heart

ABSTRACT & COMMENTARY

Synopsis: Early myocardial Doppler velocity gradients can accurately separate HCM from athletes in the 18-45 age group.

Source: Palka P, et al. J Am Coll Cardiol 1997;30: 760-768.

Although left ventricular hypertrophy (LVH) can be readily detected by echocardiography, its cause is often difficult to determine. Thus, Palka and associates studied 158 subjects divided into groups based upon age (I = 18-45 yrs; II = 46-70 yrs) and diagnosis (hypertrophic cardiomyopathy [HCM], athletes, normals, and hypertensives). In addition to traditional M-mode and two-dimensional echocardiographic measurements, myocardial velocity gradients (MVG) across the posterior wall were determined by phased array ultrasound during three phases of the cardiac cycle (systole, early diastole, late diastole). MVG in systole was reduced in HCM patients compared to athletes, normals, and hypertensives (P < 0.01). In early diastole, MVG was lower in HCM patients and hypertensives compared to normals and athletes (P < 0.05). In late diastole, MVG in HCM patients was lower than hypertensives and normals in group II but not athletes or group I normals. Early diastolic measurements were the most discriminant between HCM and athletes with an MVG less than 7S-1 exhibiting a positive predictive value of 0.96 and negative PV of 0.94. Diastolic MVG was independent of other clinical and echo variables by multivariate analysis. MVG at any cardiac cycle phase was less accurate in separating older hypertensives from HCM patients. Palka et al conclude that MVG is lower in HCM patients than in athletes, hypertensives, or normals, and early diastolic measurements can accurately separate HCM from athletes in the 18-45 age group.

COMMENT BY MICHAEL H. CRAWFORD, MD

Previous reports have suggested that diastolic function measurements by echo-Doppler or radionuclide angiography can distinguish pathologic hypertrophy due to hypertension from the physiologic hypertrophy of athletes. However, hypertensive LV hypertrophy is usually easy to diagnose with current or previous blood pressure measurements. The differentiation of the athletes heart from HCM would seem equally easy because of the history of athletic activity, but since both conditions are more frequently encountered in young adults, an athletic history may be less helpful, and the occurrence of HCM in an athlete presents a serious risk to their well-being. Also, echo wall thickness values overlap between HCM and athletes, especially in men. Thus, this report is of interest.

MVG provides similar information as does digitized M-mode echo recordings of the posterior wall, but it is less dependent on accurately identifying endo and epicardial borders. Presumably, this is why MVG was superior in this study. Also, MVG was superior to mitral Doppler inflow measures that have been reported to be abnormal in HCM and normal in athletic LVH. In addition, other standard M-mode and 2-D echo measures of the posterior wall and the intraventricular septum were not as discriminant as MVG. One reason for the superiority of MVG may be that the investigators eliminated patients with obvious HCM (high out-flow tract gradients, marked symptoms, wall thickness > 2 cm, and major mitral valve systolic anterior motion). Standard measurements may perform well in patient groups with more obvious HCM, whereas MVG had superior accuracy in more difficult cases. This raises the issue of what was the gold standard for the diagnosis of HCM? In this study, it was the whole clinical picture. All had a positive family history of HCM and an abnormal ECG in addition to suggestive standard echo-Doppler measures. Thus, there is some uncertainty about how well MVG would perform in less clear cut cases.

MVG was less valuable in older patients since it decreases with age. In those older than 45 years, it could not accurately distinguish HCM from hypertensive LV hypertrophy. The best discriminant in the young subjects was early diastolic MVG, which would reflect passive LV properties better than late diastolic or systolic measures. Of course, HCM is characterized by myofiber disarray that is thought to impair passive relaxation. Hypertensive patients progressively develop increased myocardial fibrosis in association with LVH, which also results in impaired relaxation. This probably explains why diastolic dysfunction measures are not discriminant in older hypertensives vs. HCM.

Since the ability to measure MVG is not readily available in all echocardiography laboratories, it is worth noting some of the other echo features that were statistically different between HCM and athletes: heart rate was slower in athletes; the septum was relatively thicker in HCM; LV end diastolic diameter was larger in athletes; and ejection fraction was higher in HCM.