AFib and HCM: Setting the Stage for Safety

Atrial fibrillation (AFib) has long shadowed hypertrophic cardiomyopathy (HCM), but the arrival of cardiac myosin inhibitor (CMI) therapy has sharpened the question of what that relationship really means. As real-world experience with mavacamten and aficamten accumulates alongside pivotal trial data and new adolescent findings from SCOUT-HCM, clinicians are working to reconcile a safety signal that looks different depending on where they look.

This is the first installment of a 9-part video series in which 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, unpack how the AFib safety signal reported with CMI therapy compares against pivotal trial data, adolescent findings, and the latest real-world evidence, including data presented at the American College of Cardiology (ACC) meeting.

Harper and MacNamara open by grounding the discussion in how common AFib already is in HCM, independent of any specific therapy. MacNamara notes that reported incidence varies widely by study, ranging as high as 20% and, in some series, as high as 50%. He adds that the more clinicians look for AFib in this population, the more they find it, a theme that recurs throughout the conversation.

Harper points out that background AFib rates in more recent literature have climbed well past the historical range of roughly 15% to 20%, and that AFib and HCM appear closely linked, with AFib often poorly tolerated in these patients. MacNamara underscores the clinical stakes: patients with HCM who develop AFib do not fit standard population-level stroke risk classification systems, meaning many are committed to long-term anticoagulation, and most AFib studies evaluating de-escalation of anticoagulation exclude patients with HCM altogether.

The 2 also discuss how overlapping symptoms complicate detection. HCM itself produces vague symptoms, chest pain, dyspnea, dizziness, and palpitations, that mirror those of AFib, making it difficult to know which condition is driving a given complaint without active surveillance. Both report aggressive annual rhythm monitoring in their own practices, particularly in older patients, specifically to catch paroxysmal AFib that would otherwise go undetected between visits. Harper notes that many referred patients have never had a monitor placed despite guideline recommendations, underscoring a persistent gap in screening consistency across practices.

References:

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