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.
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 identified 21 SNPs and the angiotensin-converting enzyme insertion/deletion polymorphism that were reported to be associated with AF in the literature.
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.
However, the effects of angiotensin-converting-enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) on thrombogenicity in AF remain incompletely elucidated.
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 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.
Classic RAS blockers such as angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) may prevent AF by affecting the accumulation of the EAT, representing a useful therapeutic strategy for preventing AF especially in patients with heart failure and known left ventricular dysfunction.
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.
Furthermore, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers and statins were of statistical significance for stroke risks.The majority of AF patients post-RFAs was of high stroke risk and received warfarin thromboprophylaxis in accordance with national guidelines.
Additional treatment options in selected patients with persistent HF associated with reduced left ventricular ejection fraction include switching the angiotensin-converting enzyme inhibitor to an angiotensin receptor neprilysin inhibitor; ivabradine; implantable cardioverter defibrillators; cardiac resynchronisation therapy; and atrial fibrillation ablation.
After optimal up-titration of BBs and angiotensin converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs), mean HR in patients with AF was 73 ± 15 beats/minute (bpm), 36% had resting HR ≤65 bpm.
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 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).
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).
Blockade of the renin-angiotensin-aldosterone system (RAAS) with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARB) has been shown to decrease incident atrial fibrillation (AF).
Our study is to investigate whether treatment with ACE inhibitors (ACEIs) or angiotensin-receptor blockers (ARBs) could lower the risk of new AF in 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.