P601Hypertrophic cardiomyopathy or athlete"s heart?

Abstract

A 17-year old male basketball player was referred to our cardiovascular magnetic resonance (CMR) unit due to a suspicion of hypertrophic cardiomyopathy. He had no history of cardiovascular or other disease and no family history of cardiac disease or premature death. During one of his training sessions he felt palpitations and an ECG was recorded. It was abnormal with QRS voltage criteria for left ventricular (LV) hypertrophy and ST segment depression with deep symmetric negative T waves in inferior and lateral precordial leads. On transthoracic echocardiography he had mildly dilated LV, other findings were normal. A standard CMR scan with cine and delayed enhancement imaging was performed. Both LV and right ventricle (RV) were mild-moderately dilated (254 and 322 mL), stroke volumes were high (150 mL), LV and RV ejection fractions were normal (58 and 50%,) and LV mass was slightly elevated (250 g). The interventricular septum was slightly thickened in the basal and mid part of the LV (12 mm) and there was a prominent 15 mm thickening of the apical lateral wall at the point of the insertion of inferomedial papillary muscle (Figure, Panel A). Other findings including RV free wall thickness, atria, valves, aorta and pericardium were normal. After gadolinium there was no late enhancement (LGE) of the myocardium (Figure, Panel A). We concluded that the patient had an athlete's heart but there remained a high suspicion of an atypical variant of localized asymmetrical apical hypertrophic cardiomyopathy. The patient was advised to stop strenuous physical activity for 6 months. During this period he had no complaints, the ECG changes persisted, the genetic testing for hypertrophic cardiomyopathy was negative. None of his first-degree relatives had similar ECG abnormalities. On a 6-month follow-up CMR scan there was a slight reduction in LV and RV cavity size (239 and 260mL, respectively). The ventricular septal thickness (maximum 11 mm) and LV mass (203 g) were reduced and the apical lateral wall was 11 mm thick with no LGE (Figure, Panel B). The findings were supportive of an athlete's heart with LV hypertrophy regression after a pause in training. The apical hypertrophy was believed to be due to an atypical papillary muscle insertion. After a multidisciplinary team consensus the patient was allowed to restart basketball training, however he will remain under close cardiological surveillance. A CMR will be repeated if needed. The presented case is an example where CMR with its high spatial resolution to assess ventricular volumes, wall thickness and with delayed enhancement imaging to allow myocardial tissue characterization offers an incremental value over other cardiovascular imaging techniques. However, it is the broad integration of clinical knowledge, multimodality cardiovascular imaging and findings of other cardiac examinations that brings us closer to the diagnosis.