Abstract

Atrial fibrillation (AF), the most common sustained arrhythmia associated with substantial cardiovascular morbidity and mortality with stroke being the most critical complication. Most frequently, AF occurs in conjunction with other cardiovascular disease, such as hypertension, ischemic heart disease, valve disease or cardiac failure. Role of atrial remodeling has emerged as the new pathophysiological mechanism of atrial fibrillation. Experimental and clinical studies point at two major mechanisms involved in the intrinsically progressive nature of AF. The first consists of a change in the electrical properties of the atrium, notably a shortening of the AERP and a loss of rate adaptation, and hence was named electrical remodeling. Furthermore, based on data from is experimental models, it has been considered that AF is also associated with elaborate adaptive and maladaptive changes in tissue and cellular architecture. By parallel, this type of change was denominated structural remodeling. Together, these mechanisms will increase the probability of generating multiple atrial wavelets by enabling rapid atrial activation and dispersion of refractoriness.

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