However, existing data also demonstrates that a small proportion of athletes (< 2%) exhibit increased left ventricular wall thickness (LVWT) ranging between 13-16 mm, which overlaps with morphologically mild HCM.ĭeaths from HCM are predominantly confined to intermittent 'start-stop' sports such as American football, basketball and soccer, with few cases reported in endurance sports. Hypertrophic cardiomyopathy (HCM), defined by the presence of increased ventricular wall thickness or mass in the absence of loading conditions (hypertension, valve disease, etc) sufficient to cause the observed abnormality, is the leading cause of SCD in the young and accounts for one third of all sudden cardiac deaths in young competitive athletes. Approximately 80% of non-traumatic sudden deaths in young athletes (< 35 years) are caused by inherited or congenital structural and functional cardiovascular abnormalities, which provide a substrate for arrhythmias predisposing to SCD. Differentiating a physiological or pathological remodelling mechanism is important, as significant cardiac enlargement may be an expression of underlying cardiac disease, placing the athlete at a greater risk of sudden cardiac death (SCD).
Regular physical exercise is associated with physiological increases in cardiac dimensions which may be reflected on the electrocardiogram (ECG).
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