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Atrial fibrillation (AF) is a well-recognised comorbidity in patients with hypertrophic cardiomyopathy (HCM), occurring in about 25% of patients.1 It is associated with increased mortality and worse heart failure symptoms, especially if there is concomitant outflow tract obstruction,2 and can be markedly debilitating in some individuals. The loss of atrial kick can reduce preload and worsen or unmask outflow obstruction, and higher ventricular rates can decrease cardiac outputs by reducing left ventricular (LV) filling time in the setting of diastolic dysfunction and reduced LV compliance.
Rhythm control strategies are indicated with symptomatic AF, but the current antiarrhythmic choices are suboptimal. Patients with HCM have a propensity for both atrial and ventricular arrhythmias, and there is little data on the safety of antiarrhythmic therapies in this population. Disopyramide is perhaps the best studied agent and may concurrently help to mitigate outflow obstruction through its negative inotropic properties. However, its use is limited by anticholinergic effects and breakthrough AF is common. Amiodarone is more efficacious, but has well described toxicities and should be used cautiously in young individuals. Sotalol, dofetilide and dronedarone may also be considered, but there is less data supporting their use, and there must be caution in monitoring the QT interval with the first two agents and heart failure symptoms with the latter.3 ,4
In this setting, the use of an AF ablation strategy for rhythm control is quite attractive. HCM may manifest as progressive fibrosis and stiffening and any interventions that can slow AF progression would be beneficial, but evidence for the efficacy of AF ablation in HCM is also lacking.
In their Heart publication, Providencia et al report a systematic review and meta-analysis of AF ablation in …
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