Angiotensin converting enzyme and endothelial nitric oxide synthase polymorphisms in patients with atrial fibrillation

Abstract number: P0504

Gensini^* F., Padeletti^* L., Fatini† C., Sticchi† E., Colella† A., Pieragnoli† P., Giuello† A., Musilli† N., Porciani† M. C., Abbate† R., Gensini† G. F., Michelucci† A.

†Italy ^*University of Florence, Italy;

Experimental studies show a significant increase in angiotensin-converting enzyme (ACE) expression in atrial tissue of patients with atrial fibrillation (AF). ACE regulates the synthesis of endothelial nitric oxide (NO), which modulates autonomic nervous activity involved in the development of AF. The aim of our study was to evaluate the prevalence of ACE insertion/deletion and endothelial nitric oxide synthase (eNOS) T-786C, G894T and 4a/4b polymorphisms in 239 patients with persistent AF, compared to 210 control subjects. ACE I/D polymorphism genotype distribution and allele frequency were significantly different between patients and controls (P < 0.0001 and P < 0.0001, respectively). ACE DD genotype was significantly associated with the risk of AF (OR DD/ID + II = 2.31, P < 0.0001). Analysis of eNOS polymorphisms showed no significant difference in genotype distribution and allele frequency between patients and controls. As far as idiopathic and secondary AF are considered, no significant difference in genotype distribution and allele frequency in ACE and eNOS polymorphisms was observed. Our results suggest a possible role of ACE DD genotype as a predisposing factor to AF and a pathophysiologic mechanism through which ACE inhibition could reduce the incidence of AF in patients with left ventricular dysfunction.