Ethan J. Rowin, Konstantinos C. Siontis, Anjali Owens, Iacopo Olivotto, Farid-Moussavi Harami, Michelle Michels, Steve R. Ommen, Pablo Garcia-Pavia, Babak Nazer, Jonathan S. Silver, Timothy C. Wong, N.A.Mark Estes, Daniele Massera, Hisham Ahamed, Martin S. Maron, Ahmad Masri
Atrial fibrillation (AF) is the most common sustained arrhythmia in hypertrophic cardiomyopathy (HCM) occurring in 20%-25% of patients and associated with significant morbidity including stroke risk and worsening heart failure. AF in HCM (HCM-AF) arises from disease-specific mechanisms distinct from non-HCM-AF, including HCM-related atrial structural changes (dilation/fibrosis), biophysical abnormalities (within ion-channels), and atrial dysfunction that culminate in an HCM-specific atrial myopathy. Although the adoption of contemporary AF therapies have been associated with improved clinical outcomes in non-HCM-AF populations, outcomes in HCM-AF remain worse, including lower rates of rhythm control success with catheter ablation and antiarrhythmic medications. In this context, we provide support that HCM-AF is a distinct clinical entity, highlighting gaps in knowledge and care, and represents an area of need for dedicated investigation as the effectiveness of applying therapeutics from AF populations without HCM to populations with HCM is unclear.