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Apical hypertrophic cardiomyopathy (HCM) was first described in 1976 by Sakamoto and colleagues as a novel cardiac condition characterised by a spade-shaped left ventricular cavity, apical hypertrophy and giant negative T waves.1 Contemporary reports of apical HCM describe it as a phenotypic variant of HCM in which hypertrophy is localised to the left ventricular apex with or without midsegment involvement. Apical HCM is observed worldwide, although it is traditionally reported more frequently in Asian countries (20%–40% of all HCMs) compared with Western countries (3%–11% of all HCMs). In general, patients with apical HCM exhibit mild symptoms and follow a more benign course with a lower mortality rate compared with other forms of HCM. However, numerous case reports and studies suggest considerable overlap between apical hypertrophy, midventricular obstruction and apical aneurysm. Further, our prior study and a report by Maron and colleagues demonstrated a largely unfavourable clinical course for patients with HCM with midventricular obstruction and/or apical aneurysm.2 3 Thus, the clinical course of patients with apical HCM may not always be benign, and the risk stratification of these patients is of great interest.
In this issue of Heart, Lee and colleagues report the clinical impact of atrial fibrillation (AF) in patients with apical HCM (n=306).4 They showed that AF occurred in 25.2% of patients with apical HCM (annual incidence of 4.6%) and was independently predicted by an older age and enlarged left atrial diameter (>45 mm). During a follow-up of 5.5 years, patients with AF had a higher incidence of death and stroke, and those with AF still had an increased …
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