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Sudden cardiac death from hypertrophic cardiomyopathy (HCM) is well recognised. 1, 2 The death of some high profile athletes from HCM in the past few years has galvanised some sporting authorities to implement cardiovascular screening in all recruits before selection. However, cardiovascular adaptation to intense physical training itself can cause significant left ventricular hypertrophy (LVH) that may mimic HCM. 3, 4 A common and challenging scenario involves the differentiation of physiological LVH ("athlete's heart") from HCM.
CASE REPORT
A 17 year old elite male swimmer was referred with an abnormal 12 lead electrocardiogram (ECG) during cardiovascular screening. The athlete trained for about 14 hours and swam 16 miles a week. He was asymptomatic. There was no history of illicit drug abuse or a family history of premature sudden cardiac death. Blood pressure measured 110/70 mm Hg, and cardiovascular examination was normal.
The 12 lead ECG showed voltage criteria for left ventricular hypertrophy and deep T wave inversions (>0.2 mV) in the inferior and lateral leads (fig 1). A two dimensional echocardiogram revealed significant concentric LVH with a maximal left ventricular wall thickness of 14 mm. The left ventricular cavity size was normal measuring 48 mm in end diastole. Indices of systolic and diastolic functions were normal (E wave 0.9 m/s; A wave 0.36 m/s; E/A 2.63; E deceleration time 226 milliseconds). The valves and right ventricle appeared normal.
A 12 lead electrocardiogram from a 17 year old swimmer showing sinus rhythm with deep T wave inversion (>0.2 mV) in inferior and lateral leads and isolated Sokolow voltage criterion for left ventricular hypertrophy.
The differential diagnosis was between HCM and athlete's heart. The distinction between the two entities is crucial as a false diagnosis of HCM in an athlete calls for disqualification from competitive sport, conversely a false diagnosis of athlete's heart could jeopardise a young life.
A cardiac magnetic resonance imaging scan excluded apical HCM. A 12 lead ECG and echocardiography performed on both parents and two siblings were normal. Although this excluded familial HCM, it did not rule out the possibility of a sporadic disease causing mutation.
During a cardiopulmonary exercise stress test, the athlete achieved a peak oxygen consumption of 68 ml/kg/min (141% of predicted). The blood pressure response to exercise was normal...