This review highlights the mechanisms of atrial remodeling and fibrosis in permanent atrial fibrillation and discusses potential pharmacological strategies to counteract these processes.
May guide mechanistic AF research; leaves open whether anti-fibrotic strategies reduce recurrence in prospective trials.
Atrial fibrillation (AF), the most prevalent rhythm disorder in clinical practice, is currently significantly contributing morbidity and mortality of the ageing population. In the past decades, a tremendous amount of research resulted in insights into AF pathophysiology, with a primary focus on atrial remodeling. Defined as a persistent change atrial function and structure, remodeling has the intrinsic properties to enhance the probability of focal (ectopic) /or re-entrant pursuits, thus supporting AF persistence. The hallmark of structural remodeling is represented by fibrosis, a multifactorial process involving an interaction between neurohormonal and cellular mediators. This provides a brief summary of the recent knowledge with respect to electrical and structural remodeling and insights into the pathogenesis of atrial fibrosis. Since current drug options for AF treatment are far from being we also discuss the therapeutic principles and current alternatives for counteracting atrial fibrosis, and thus arrhythmia recurrence.
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Muntean et al. (2013) studied this question.
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