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These basic and clinical studies suggest that localized cardiac autonomic ganglia (GPs) may play a critical role in the initiation and maintenance of AF.

These results indicate additional benefits of GP ablation to PV antrum ablation and improvement with time, particularly > or = 12 months after ablation. We postulate that this late benefit may result from destruction of the autonomic neurons in the GP that cannot regenerate.

Addition of GP ablation to PVI confers a significantly higher success rate compared with either PVI or GP alone in patients with PAF.

The autonomic nervous system regulates all aspects of normal cardiac function, and is recognized to play a critical role in the pathophysiology of many cardiovascular diseases. As such, the value of neuroscience-based cardiovascular therapeutics is increasingly evident. This White Paper reviews the current state of understanding of human cardiac neuroanatomy, neurophysiology, pathophysiology in specific disease conditions, autonomic testing, risk stratification, and neuromodulatory strategies to mitigate the progression of cardiovascular diseases.

Abstract-The National Heart, Lung, and Blood Institute convened an expert panel April 28 to 29, 2008, to identify gaps and recommend research strategies to prevent atrial fibrillation (AF). The panel reviewed the existing basic scientific, epidemiological, and clinical literature about AF and identified opportunities to advance AF prevention research. After discussion, the panel proposed the following recommendations: (1) enhance understanding of the epidemiology of AF in the population by systematically and longitudinally investigating symptomatic and asymptomatic AF in cohort studies; (2) improve detection of AF by evaluating the ability of existing and emerging methods and technologies to detect AF; (3) improve noninvasive modalities for identifying key components of cardiovascular remodeling that promote AF, including genetic, fibrotic, autonomic, structural, and electrical remodeling markers; (4) develop additional animal models reflective of the pathophysiology of human AF; (5) conduct secondary analyses of already-completed clinical trials to enhance knowledge of potentially effective methods to prevent AF and routinely include AF as an outcome in ongoing and future cardiovascular studies; and (6) conduct clinical studies focused on secondary prevention of AF recurrence, which would inform future primary prevention investigations. Key Words: atrial fibrillation Ⅲ atrium Ⅲ epidemiology Ⅲ prevention Ⅲ risk factors Ⅲ National Heart, Lung, and Blood Institute A trial fibrillation (AF) is the most common arrhythmia in the United States and other developed countries. AF is associated with significant morbidity and mortality, including a 4-to 5-fold increased risk for stroke, 1,2 a doubling of risk for dementia, 3,4 a tripling of risk for heart failure, 2 and a 40% to 90% increased risk for overall mortality. 2,5 Growth in the size of the AF population and increased recognition of the morbidity, mortality, diminished quality of life, and high healthcare costs associated with AF have spurred numerous investigations to develop more effective treatments for AF and its complications. Many risk factors for AF have been described, and some promising preventive strategies have been identified. However, although AF treatment has been studied extensively, AF prevention has received relatively little attention. Over the last 10 years, PubMed has contained almost 4 times as many citations for atrial fibrillation treatment as for atrial fibrillation prevention. When stroke was excluded from the search, citations related to treatment outnumbered those for prevention by Ϸ7-fold.

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BACKGROUND Transcutaneous low-level tragus electrical stimulation (LLTS) suppresses atrial fibrillation (AF) in canines. OBJECTIVES We examined the antiarrhythmic and anti-inflammatory effects of LLTS in humans. METHODS Patients with paroxysmal AF who presented for AF ablation, were randomized to either 1 hour of LLTS (n = 20) or sham control (n = 20). Attaching a flat metal clip onto the tragus produced LLTS (20 Hz) in the right ear (50% lower than the voltage slowing the sinus rate). Under general anesthesia, AF was induced by burst atrial pacing at baseline and after 1 hour of LLTS or sham. Blood samples from the coronary sinus and the femoral vein were collected at those time points and then analyzed for inflammatory cytokines, including tumor necrosis factor (TNF)-α and C-reactive protein (CRP), using a multiplex immunoassay. RESULTS There were no differences in baseline characteristics between the 2 groups. Pacing-induced AF duration decreased significantly by 6.3 ± 1.9 min compared to baseline in the LLTS group, but not in the controls (p = 0.002 for comparison between groups). AF cycle length increased significantly from baseline by 28.8 ± 6.5 ms in the LLTS group, but not in controls (p = 0.0002 for comparison between groups). Systemic (femoral vein) but not coronary sinus TNF-α and CRP levels decreased significantly only in the LLTS group. CONCLUSIONS LLTS suppresses AF and decreases inflammatory cytokines in patients with paroxysmal AF. Our results support the emerging paradigm of neuromodulation to treat AF.