Key result
Apical HCM shows no difference in lethal arrhythmias versus non-apical HCM, but disease-causing variants increase risk.
Why the study?
Apical hypertrophic cardiomyopathy is often considered to have a benign prognosis, but its clinical characteristics and genetic predisposition compared to non-apical HCM needed evaluation.
Does apical hypertrophic cardiomyopathy alter the risk of lethal arrhythmic events and MACE compared to non-apical hypertrophic cardiomyopathy in patients with HCM?
Cohort (n=195)
Yes
Does apical hypertrophic cardiomyopathy alter the risk of lethal arrhythmic events and MACE compared to non-apical hypertrophic cardiomyopathy in patients with HCM?
Effect estimate: HR 0.62 (95% CI 0.36-1.08)
Although apical HCM is associated with a lower risk of MACE and a lower genetic yield than non-apical HCM, it carries a similar risk of lethal arrhythmic events, which are independently predicted by the presence of disease-causing variants.
Apical HCM warrants similar arrhythmic vigilance as non-apical forms; leaves open whether variants refine LAE risk beyond phenotype in prospective cohorts.
Background Apical hypertrophic cardiomyopathy (HCM) is a rare variant of HCM, often considered to have a benign prognosis. This study aimed to compare the clinical characteristics and genetic predisposition of apical HCM with non-apical HCM. Methods We included 195 patients with HCM who underwent next-generation sequencing at two tertiary centres in South Korea (2017–2024). The primary outcome was a composite of lethal arrhythmic events (LAE), including death, ventricular arrhythmia, implantable cardioverter defibrillator (ICD) implantation and appropriate ICD shock. Secondary outcomes included major adverse cardiovascular events (MACE), such as new-onset atrial fibrillation, ischaemic stroke, heart failure hospitalisation, septal reduction therapy or heart transplant. Results Of the 195 patients, 67 (34.4%) had apical HCM. Patients with apical HCM were older at diagnosis and had lower maximal left ventricular wall thickness compared with non-apical HCM. Disease-causing variants were less frequent in apical HCM (20.9% vs 46.9%, p<0.001). MYBPC3 and MYH7 variants were less common in apical HCM (50.0%) than in non-apical HCM (75.0%). MACE occurred less frequently in apical HCM (HR 0.38, 95% CI 0.19 to 0.75), but no difference was observed in LAE (HR 0.62, 95% CI 0.36 to 1.08). The presence of disease-causing variants was independently associated with LAE (adjusted HR 2.50, 95% CI 1.44 to 4.35). Conclusions Although apical HCM is associated with less hypertrophy and lower genetic yield, it is not entirely benign. The presence of disease-causing variants is an important predictor of arrhythmic risk, underscoring the value of genetic testing in all HCM patients, regardless of phenotype.
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Jeong et al. (2025) conducted a cohort in Hypertrophic cardiomyopathy (n=195). Apical hypertrophic cardiomyopathy vs. Non-apical hypertrophic cardiomyopathy was evaluated on Composite of lethal arrhythmic events (LAE), including death, ventricular arrhythmia, ICD implantation and appropriate ICD shock (HR 0.62, 95% CI 0.36-1.08). Apical HCM showed no significant difference in lethal arrhythmic events compared with non-apical HCM (HR 0.62; 95% CI 0.36-1.08), while disease-causing variants independently increased this risk.
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