Abstract
Management of atrial tachyarrhythmias, especially atrial fibrillation (AF), in patients with congestive heart failure (CHF) remains a major challenge. It is widely recognized that CHF promotes AF and that AF worsens CHF. An individual with either condition who develops the other has higher morbidity and poorer prognosis. The prevalence of AF and CHF is expected to increase as the population ages. Therefore, it remains just as likely as it was more than a decade ago that the emerging epidemic of AF and CHF will continue to be both a challenge and an opportunity. Article p 93 Current antiarrhythmic drugs (AADs) for AF prevention in patients with CHF remain unsatisfactory, with limited efficacy and considerable potential for adverse effects. Preliminary results from a large trial examining whether a rhythm-control strategy is superior to a rate-control strategy in patients with AF and CHF do not suggest a benefit in cardiovascular mortality rate, CHF, or stroke by attempting to maintain sinus rhythm with current AAD therapy (primarily amiodarone).1 Newer nonpharmacological therapies, including pulmonary vein (PV) isolation and cardiac resynchronization therapy, are generating considerable interest; however, their rates of efficacy in patients with AF and CHF have not been established definitively. Thus, continued progress toward an enhanced understanding of upstream mechanisms that promote AF and contractile dysfunction in CHF and development of innovative therapeutic approaches based on fundamental, mechanistic insights is of paramount importance. In this context, the study by Yeh et al2 in this issue of Circulation: Arrhythmia and Electrophysiology provides important new insights into the role of atrial calcium dysregulation in promoting atrial arrhythmias and contractile dysfunction in the CHF substrate. This report comes from the Nattel laboratory, which has been a major driving force in improving our understanding of arrhythmogenic mechanisms in a variety of AF substrates, including CHF. …
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