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

被引:49
作者
Gensini, F
Padeletti, L
Fatini, C
Sticchi, E
Gensini, GF
Michelucci, A
机构
[1] Univ Florence, Dipartimento Fisiopatol Clin, Sez Genet Med, Unit Med Genet, I-50139 Florence, Italy
[2] Univ Florence, Dept Med & Surg Crit Care, Sect Clin Med & Cardiol, I-50121 Florence, Italy
[3] Azienda Osped Careggi, Thrombosis Ctr, Florence, Italy
来源
PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY | 2003年 / 26卷 / 01期
关键词
angiotensin-converting enzyme; endothelial nitric oxide synthase; genetic polymorphism; atrial fibrillation;
D O I
10.1046/j.1460-9592.2003.00036.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Experimental studies have shown a significant increase in angiotensin-converting enzyme (ACE) expression in atria] tissue of AF patients. ACE regulates the synthesis of endothelial nitric oxide (NO), which modulates autonomic nervous activity involved in the development of AR 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 path ophysiological mechanism of ACE inhibition in reducing the incidence of AF in patients with left ventricular dysfunction. (PACE 2003; 26[Pt. II]:295-298).
引用
收藏
页码:295 / 298
页数:4
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