Molecular basis of atrial fibrillation: a dream or a reality?

Abstract

AF is a difficult disease to treat because of the numerous (ischemic, metabolic, inflammatory, structural) mechanisms contributing to its etiology. AF persistence requires both an adequate tissue substrate for reentrant activity and triggers to initiate the arrhythmia. In a few interesting instances, AF may have a monogenic cause. Although there are common electrophysiologic characteristics of myocytes from a variety of AF models and clinical presentations, it is unrealistic to expect that all patients will respond equally to the same interventions. Thus, patients with AF of an inflammatory etiology may respond better to anti-inflammatory therapies, whereas those with enlarged atria secondary to valvular disease may require surgery. Some may respond better to ablation than others. However, the heterogeneity of the substrate does not negate the value of searching for the underlying molecular mechanisms. As we begin to comprehend these mechanisms in greater detail, the dream of using individualized rational therapies will come closer to reality.