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Angiotensin-Converting Enzyme and Endothelial Nitric Oxide Synthase Polymorphisms in Patients with Atrial Fibrillation
Authors:FRANCESCA GENSINI  LUIGI PADELETTI†  CINZIA FATINI‡  ELENA STICCHI  GIAN FRANCO GENSINI†  ANTONIO MICHELUCCI†
Institution:From the Department of Clinical Physiopathology, Unit of Medical Genetics, University of Florence, Italy;, Department of Medical and Surgical Critical Care, Section of Clinical Medicine and Cardiology, University of Florence, Italy;, and the Thrombosis Center, Azienda Ospedaliera Careggi, Florence, Italy
Abstract:GENSINI, F., et al. ; Angiotensin-Converting Enzyme and Endothelial Nitric Oxide Synthase Polymorphisms in Patients with Atrial Fibrillation. Experimental studies have shown a significant increase in angiotensin-converting enzyme (ACE) expression in atrial tissue of AF patients. ACE regulates the synthesis of endothelial nitric oxide (NO), which modulates autonomic nervous activity involved in the development of AF. The aim of the study was to evaluate the prevalence of ACE insertion/deletion and endothelial NO synthase (eNOS) T-786C, G894T, and 4a/4b polymorphisms in 148 patients with persistent AF, compared with 210 control subjects. ACE insertion/deletion 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 = 3.24, P < 0.0001)   . Analysis of eNOS polymorphisms showed no significant difference in genotype distribution and allele frequency between patients and controls. The results suggest a possible role of ACE DD genotype as a predisposing factor to AF and a pathophysiological mechanism of ACE inhibition in reducing the incidence of AF in patients with left ventricular dysfunction. (PACE 2003; 26Pt. II]:295–298)
Keywords:angiotensin-converting enzyme                                              endothelial nitric oxide synthase                                              genetic polymorphism                                              atrial fibrillation
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