Abstract 14961: Atrial Structural Remodeling is Progressive Following Exposure to Nicotine: Implications for Atrial Fibrillation.
Introduction: Smoking has been implicated as one of the new risk factors accounting for the burgeoning epidemic of atrial fibrillation (AF). Structural remodeling is recognized as an important element forming the AF substrate. We investigated whether nicotine, an important element in cigarette smoking, causes atrial structural remodeling.
Methods: 36 adult male Sprague Dawley rats were studied in 3 equal groups: high dose nicotine (6mg/kg/day); low dose nicotine (0.6mg/kg/day); and saline, infused via subcutaneous osmotic pumps. Atria were harvested at 7 or 14 days for histological analysis. Sections (6μm) were stained for fibrosis (Picro Sirius Red), glycogen and mast cells (Periodic Acid Schiff counterstained with Toluidine Blue). A plasma level of cotinine, the primary metabolite of nicotine, was measured by ELISA.
Results: The table presents the data for each element evaluated at 7 and 14 days in each group. Nicotine treatment resulted in a dose dependent increases in the levels of collagen (r2=0.809), glycogen (r2=0.789) and mast cell infiltrates (r2=0.722) with the levels of each being correlated with plasma cotinine levels (P<0.001).
Conclusions: Nicotine exposure results in a dose dependent, progressive atrial structural remodeling characterized by increased collagen and glycogen deposits and inflammatory cell infiltrates. These abnormalities may account for the association between cigarette smoking and AF. In addition, it raises concern of the potential detrimental effects of nicotine replacement therapies.
- © 2010 by American Heart Association, Inc.