Current guidelines have emphasized the central role of catheter ablation in the management of patients with atrial fibrillation (AF). Recent advances in catheter and mapping technology and in the understanding of lesion formation have resulted in manifest progress, predominantly in the durability of ablation lesion sets and in the reduction of complications, translating into better procedural, and follow-up results.
Patients presenting with AF, however, encompass a disparate population who experience different outcomes post-ablation. At one end of the spectrum, ‘healthy, normal heart’ patients with paroxysmal AF have the best prognosis after ablation. At the other end are those with structural heart disease in whom ongoing atrial structural remodelling secondary to underlying cardiac pathology renders management of AF significantly more challenging. In these patient populations, multiple procedures may be needed with modest success rates, particularly in the case of persistent AF.
Within the spectrum of structural heart disease, hypertrophic cardiomyopathy (HCM) is strongly associated with the development of AF, with a prevalence of over 20%,[1] and successful management and ablation remains a significant challenge for the electrophysiologist. It is a disease with multiple components, genotypes, and structural phenotypes with increased left ventricular (LV) wall thickness and diastolic dysfunction a universal feature. Consequent increased left atrial pressure, left atrial dilatation and fibrosis create an ongoing milieu for atrial arrhythmia in these patients. Moreover, HCM often tends to progress over time and the associated evolution of the arrhythmia substrate can result in multiple recurrences of atrial arrhythmia even after apparent successful catheter ablation.
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