An ACE-dependent increase in the amounts of activated Erk1/Erk2 in atrial interstitial cells may contribute as a molecular mechanism for the development of atrial fibrosis in patients with AF.
We genotyped the insertion/ deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene in 138 HCM patients (26 with AF, 112 with sinus rhythm).
In a study in a Japanese population, it was reported that the angiotensin-converting enzyme insertion/deletion polymorphism was not associated with atrial fibrillation.
This study demonstrates the association of RAS gene polymorphisms with nonfamilial structural AF and may provide the rationale for clinical trials to investigate the use of ACE inhibitor or angiotensin II antagonist in the treatment of structural AF.
Although activation of the renin-angiotensin-aldosterone system (RAAS) now appears to play a role in the pathophysiology of atrial fibrillation (AF), it remains to be determined if ACE genotype impacts response to conventional AAD therapy in patients with AF.
The aim of this study was to investigate the role of the ACE I/D polymorphism in relation to the different clinical forms of AF, lone and secondary nonvalvular atrial fibrillation (NVAF).
This study suggests that the presence of the D allele in hypertensive patients with AF is associated with attenuation of type-I collagen degradation, and that therapy with ACE inhibitors increases degradation of collagen type I.
The purpose of this study was to investigate whether response to antiarrhythmic drug (AAD) therapy in patients with AF is modulated by the ACE I/D polymorphism.
It was recently suggested that the angiotensin-converting enzyme insertion/insertion genotype, which is considered to be protective against cardiovascular disease, was a significant risk factor for atrial fibrillation (AF) in patients with hypertrophic cardiomyopathy (HCM).
Our study suggests that ACE I/D polymorphism is associated with AF and the DD genotype may be an independent predictive factor for AF in patients with hypertensive heart disease.
Our study suggests that ACE I/D polymorphism is associated with AF and the DD genotype may be an independent predictive factor for AF in patients with hypertensive heart disease.
The T allele carriers (TT + CT) had significantly increased risk of AF compared with the CC homozygotes (OR 1.94, 95% CI 1.20-3.14; adjusted P=0.006) in a logistic regression model after controlling age, left atrial dimension, and the use of angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers.
We investigated the association between polymorphism in angiotensinogen (AGT) and angiotensin-converting enzyme gene and risk of acquired AF in a pair-matched case-control study conducted in Chinese Hans.
This article reviews clinical trials on the use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) for the prevention of AF.
We identified 21 SNPs and the angiotensin-converting enzyme insertion/deletion polymorphism that were reported to be associated with AF in the literature.
The aim of the present study was to investigate the association of the angiotensin-converting enzyme2350 G/A polymorphism with atrial fibrillation in Han Chinese patients with essential hypertension.