Atrial fibrillation (AF) affects millions of individuals worldwide and is associated with significant morbidity and mortality.1 Despite the relatively high prevalence and incidence of this condition, our understanding of its pathobiology and precipitants remains superficial. The diagnosis of AF relies on a standard 12-lead electrocardiogram or rhythm monitor. Once confirmed, details related to arrhythmia burden and symptoms are assessed. Distinctions are created between paroxysmal, persistent, and permanent AF; however, the implications of these stratifications on long-term morbidity are unknown. Further, fundamental questions about AF remain unanswered: why are some patients symptomatic and others not; why do some develop rapid ventricular rates that increase the risk for heart failure; and why do some respond better to antiarrhythmic drugs or ablation therapies? The heterogeneity of AF is not accounted for in most clinical trials evaluating novel therapies and interventions. As a result, treatment strategies remain relatively monolithic. Other comorbidities, such as heart failure, hypertension, diabetes, prior stroke, and vascular disease, and demographics, such as age and sex, inform the physician’s decision to anticoagulate a patient much more than the etiology, characteristics, and associated conditions of the underlying arrhythmia.
Hyman MC, Deo R. Proteomics of Atrial Fibrillation: Evolving From a Coarse Understanding to a Fine Phenotype. JAMA Cardiol. 2017;2(5):474–475. doi:10.1001/jamacardio.2017.0292
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