This editorial refers to ‘The new antiarrhythmic drug Vernakalant: ex vivo study of human atrial tissue from sinus rhythm and chronic atrial fibrillation’ by Wettwer et al ., pp. 145–154, this issue, and to ‘Atrial selectivity in Na+ channel blockade by acute amiodarone’ by Suzuki et al. pp. 136–144, this issue. Atrial fibrillation (AF) is the most common arrhythmia and one of the most vexing cardiovascular conditions for patients and the physicians who care for them. AF is a primary cause of cardioembolic stroke and may account for more than 20% of all stroke cases in older individuals.1 While AF can easily be diagnosed by electrocardiography, many cases of AF are undetected due to the lack of symptoms. Lifetime risk for developing AF after an age of 40 years is ∼25% for both men and women. The prevalence of AF has been increasing, due to both ageing of the population and an increased prevalence of risk factors such as obesity and sedentary lifestyle. The personal and societal economic consequences of AF are staggering. Given the scope of the problem, efforts to better diagnose and manage AF are urgently needed. Although many cardiovascular conditions (hypertension, heart failure, etc.) can be managed with drugs, pharmacotherapy for the management of AF remains inadequate. Many of the available antiarrhythmic drugs have the potential for life-threatening ventricular proarrhythmia, coupled with a limited efficacy in maintaining sinus rhythm. Other drugs have less proarrhythmia, but are associated with systemic toxicity when used for long periods. From this perspective, it seems clear that additional efforts to develop drugs that safely and effectively treat AF are urgently needed. To achieve this goal, fundamental studies are needed to better understand the pathophysiology of AF, to identify the differences between atrial and ventricular physiology, and then to selectively target the atrial …
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