Abstract

Objective CS promotes endothelial dysfunction and atherosclerosis in the vascular bed. The impact of smoking on atrial myocardium is not defined in humans. In the present study we aimed to determine the effect of cigarette smoking (CS) on the development of interstitial fibrosis in atrial myocardium.

Design Case-control study

Patients 95 patients (46 smokers and 49 non-smokers) undergoing coronary artery bypass grafting (CAGB).

Main outcome measures Amount of atrial fibrosis, collagen I, III and IV expression pattern, and quantitative RT-PCR. Occurrence of postoperative atrial fibrillation (AF).

Results In the study population, patient age correlated significantly with the amount of atrial fibrosis (r=0.18; p<0.05). Nicotine abuse (pack years) was identified as the only factor related to atrial fibrosis in smokers (r=0.31; p<0.05). The amount of fibrosis was higher in patients with postoperative AF (22.9±6.2% vs. 27.0±8.2%; p<0.05). To demonstrate a causal relationship between CS and atrial fibrosis, atrial tissue slices from NS (n=8) were cultured in the presence of nicotine base (185 and 740 nmol/l). Nicotine base induced in a concentration dependent manner mRNA expression of collagen III (up to 10 fold) resembling the immunohistologic collagen expression pattern observed in CS.

Conclusion CS contributes via nicotine to the development of atrial fibrosis. Atrial fibrosis per se has been shown to provide an arrhythmogenic substrate, which may increase the likelihood for the occurrence of atrial arrhythmias, including postoperative AF.