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STATE-OF-THE-ART PAPER

Structural and Functional Remodeling of the Left Atrium

Clinical and Therapeutic Implications for Atrial Fibrillation

Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minnesota.

Manuscript received August 30, 2007; accepted September 26, 2007.

^_* Reprint requests and correspondence: Dr. Teresa S. M. Tsang, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55901. (Email: tsang.teresa{at}mayo.edu).

Left atrial (LA) structural and functional remodeling reflects a spectrum of pathophysiological changes that have occurred in response to specific stressors. These changes include alterations at the levels of ionic channels, cellular energy balance, neurohormonal expression, inflammatory response, and physiologic adaptations. There is convincing evidence demonstrating an important pathophysiological association between LA remodeling and atrial fibrillation (AF). Measures that will prevent, attenuate, or halt these processes of LA remodeling may have a major public health impact with respect to the epidemic of AF. In this review, we describe the mechanisms involved in LA remodeling and highlight the existing and potential therapeutic options for its reversal, and implications for AF development.

Abbreviations and Acronyms   ACE = angiotensin-converting enzyme   AF = atrial fibrillation   ALT-711 = alagebrium chloride   Ang-II = angiotensin II   ANP = atrial natriuretic peptide   BNP = brain natriuretic peptide   CRP = C-reactive protein   LA = left atrium/atrial   LV = left ventricle/ventricular   MMP = matrix metalloproteinase   TIMP = tissue inhibitor of metalloproteinase

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