Are We Nearly There Yet? Progress in the Prevention of Sudden Cardiac Death in the Young

cular diseases subsequently discussed. On the contrary, many ICVD show age-related clinical expression and/or have late-onset forms. The main difference is that IHD overshadows ICVD as a cause of SCD in the older population [1] . Prior to commencing the fellowship, my clinical training had left me with a perception of ICVD that was dominated by the heritable risk factors for IHD. Disorders with archetypal physical signs had also received attention, particularly Marfan’s syndrome and obstructive hypertrophic cardiomyopathy (HCM). Patients with HCM came to attention in the presence of debilitating symptoms from resting left-ventricular outflow-tract obstruction or atrial fibrillation. That HCM was a familial disease associated with SCD was tacitly acknowledged, but had limited impact on clinical practice. There was little awareness of available guidelines or impetus to risk stratify HCM cases and offer assessment to relatives. The genetic contribution to dilated cardiomyopathy (DCM) was not even recognised; instead, DCM was presumed viral, although the requisite viral serology seldom shed light on its aetiology. ARVC was still termed ‘dysplasia’, overlooking its genetic basis; it was the main differential diagnosis The Context