
Screening and Management Approaches for AFib in HCM
Atrial fibrillation (AFib) is common in patients with hypertrophic cardiomyopathy (HCM) and, once identified, raises immediate questions about how aggressively to pursue rhythm control. In this segment, Mariko Harper, MD, MS, FACC, director of the Hypertrophic Cardiomyopathy Center of Excellence at Virginia Mason Franciscan Health, and James MacNamara, MD, a non-invasive cardiologist and HCM specialist at UVA Health, compare their screening habits and management philosophies before turning to what the pivotal cardiac myosin inhibitor (CMI) trials showed about AFib risk.
Episodes in this series
Atrial fibrillation (AFib) is common in patients with hypertrophic cardiomyopathy (HCM) and, once identified, raises immediate questions about how aggressively to pursue rhythm control. In this segment, Mariko Harper, MD, MS, FACC, director of the Hypertrophic Cardiomyopathy Center of Excellence at Virginia Mason Franciscan Health, and James MacNamara, MD, a non-invasive cardiologist and HCM specialist at UVA Health, compare their screening habits and management philosophies before turning to what the pivotal cardiac myosin inhibitor (CMI) trials showed about AFib risk.
Harper opens by asking what data shows about AFib as a driver of morbidity and mortality, noting that longer time spent in AFib appears to carry independent risk in older studies, which is why detection remains the first step toward treatment. She then turns the conversation to management style, asking MacNamara whether he favors early rhythm control or a more conservative beta-blocker-first approach.
MacNamara describes himself as an aggressive early rhythm control adopter. His practice pursues initial cardioversion to restore sinus rhythm and works closely with electrophysiology colleagues, not only for defibrillator placement but for catheter ablation. Pharmacologic rhythm control is used less often than procedural options in his experience. MacNamara says he does everything possible to avoid leaving a patient with HCM in persistent AFib, since prolonged AFib becomes progressively harder to reverse.
Harper agrees, noting that before CMI therapy existed, there was little favorable atrial remodeling to counterbalance the progressive enlargement of the left atrium and accumulating atrial fibrosis seen in HCM. She observes that AFib compounds those structural changes, driving both symptoms and worse prognosis. With pulsed field ablation now available and offering a faster, safer procedural option, Harper says she encourages early electrophysiology consultation and shared decision-making, adding that she rarely encounters a truly asymptomatic AFib patient who does not feel better after ablation or cardioversion.
The discussion then shifts to the first cardiac myosin inhibitor approved, mavacamten, and roughly 5 years of accumulated long-term data. Harper asks MacNamara for his interpretation of the AFib signal seen in the pivotal EXPLORER-HCM and VALOR-HCM trials. MacNamara recalls that AFib was not viewed as a major concern in those earlier randomized trials since some background AFib would be expected in any HCM population. EXPLORER-HCM showed no increased incidence of AFib relative to placebo, at about 8% over the trial course, while VALOR-HCM saw AFib in about 10% of patients over a longer follow-up period, again with no significant difference between the treatment and placebo arms.
Harper notes that real-world data carries its own caveats since patients seen in clinical practice do not always mirror trial populations. She points out that the VALOR-HCM cohort was exclusively New York Heart Association (NYHA) class III and IV patients already being considered for septal reduction therapy, a sicker population that would be expected to carry higher background AFib rates.
References:
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- Maurizi N, Jensen D, Vischer AS, Stämpfli SF, Monney P, Gruner C. Real-world effectiveness, response patterns and clinical implementation of mavacamten in obstructive hypertrophic cardiomyopathy: insights from the SWISS-MAVA cohort. Int J Cardiol. 2026;462:134689. doi:10.1016/j.ijcard.2026.134689
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