Physiologic LV remodeling in young trained athletes as a consequence of chronic training can occasionally mimic certain pathologic conditions associated with sudden death, such as HCM. A small but important subset of elite male athletes may show a borderline increased LV wall thickness of 13 to 15 mm, which defines a gray zone of overlap between the extreme expressions of athlete's heart and a mild HCM phenotype. Such diagnostic ambiguity can be resolved by using the paradigm of noninvasive parameters including testing with echocardiography (and, more recently, with CMR): left atrial and LV chamber dimensions and shape, brief periods of deconditioning to alter LV mass, measurement of oxygen consumption and diastolic filling, and recognition of familial occurrence of HCM or a pathogenic HCM-causing sarcomere mutation. Such distinctions between physiologic/benign athlete's heart and HCM, the most common cause of sudden death in the young in the United States, can be crucial. The recognition of HCM leads to disqualification from intense competitive sports to reduce sudden death risk and, when appropriate, permits initiation of therapeutic interventions.
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