scholarly journals The Effect of Renin-Angiotensin-System-Inhibitor (RASI) on the Recurrence of Atrial Fibrillation (AF) after Pulmonary Vein Isolation (PVI) in Patients with Normal Left Atrium (LA)

2011 ◽  
Vol 27 (Supplement) ◽  
pp. PJ2_012
Author(s):  
Monami Ando ◽  
Masateru Takigawa ◽  
Yukihiko Yoshida ◽  
Ruka Yoshida ◽  
Akinori Sairaku ◽  
...  
2011 ◽  
Vol 12 (4) ◽  
pp. 549-556 ◽  
Author(s):  
Nurdan Papila Topal ◽  
Beste Ozben ◽  
Veysel Sabri Hancer ◽  
Azra Meryem Tanrikulu ◽  
Reyhan Diz-Kucukkaya ◽  
...  

Activation of the renin–angiotensin system (RAS) is associated with atrial fibrillation (AF). The aim of this study was to investigate the relation between AF and polymorphisms in RAS. One hundred and fifty patients with AF, 100 patients with no documented episode of AF and 100 healthy subjects were consecutively recruited into the study. The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism, and the M235T, A-20C, and G-6A polymorphisms of the angiotensinogen gene were genotyped. Patients with AF had significantly lower frequency of II genotype of ACE I/D and higher frequency of angiotensinogen M235T polymorphism T allele and TT genotype and G-6A polymorphism G allele and GG genotype compared with the controls. AF patients had significantly larger left atrium, higher left ventricular mass index (LVMI) and higher frequency of significant valvular pathology. ACE I/D polymorphism II genotype, angiotensinogen M235T polymorphism TT genotype and G allele and GG genotype of angiotensinogen G-6A polymorphism were still independently associated with AF when adjusted for left atrium, LVMI and presence of significant valvular pathology. Genetic predisposition might be underlying the prevalence of acquired AF. Patients with a specific genetic variation in the RAS genes may be more liable to develop AF.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Wen-Hao Liu ◽  
Yen-Nan Fang ◽  
Chia-Chen Wu ◽  
Mien-Cheng Chen ◽  
Jen-Ping Chang ◽  
...  

Background. Left atrial enlargement is a mortality and heart failure risk factor in primary mitral regurgitation (MR) patients. Pig models of MR have shown differential expression of genes linked to the renin-angiotensin system. Therefore, the aim of this study was to investigate the key genes of the renin-angiotensin that are expressed differentially in the left atrial myocardium in MR patients. Methods. Quantitative RT-PCR was used to compare gene expression in the renin-angiotensin system in the left atrium in MR patients, aortic valve disease patients, and normal subjects. Results. Plasma angiotensin II concentrations did not significantly differ between MR patients and aortic valve disease patients (P=0.582). Compared to normal controls, however, MR patients had significantly downregulated expressions of angiotensin-converting enzyme, angiotensin I converting enzyme 2, type 1 angiotensin II receptor, glutamyl aminopeptidase, angiotensinogen, cathepsin A (CTSA), thimet oligopeptidase 1, neurolysin, alanyl aminopeptidase, cathepsin G, leucyl/cystinyl aminopeptidase (LNPEP), neprilysin, and carboxypeptidase A3 in the left atrium. The MR patients also had significantly upregulated expressions of MAS1 oncogene (MAS1) and mineralocorticoid receptor compared to normal controls. Additionally, in comparison with aortic valve disease patients, MR patients had significantly downregulated CTSA and LNPEP expression and significantly upregulated MAS1 expression in the left atrium. Conclusions. Expressions of genes in the renin-angiotensin system, especially CTSA, LNPEP, and MAS1, in the left atrium in MR patients significantly differed from expressions of these genes in aortic valve disease patients and normal controls. Notably, differences in expression were independent of circulating angiotensin II levels. The results of this study provide a rationale for pharmacological therapies or posttranslational regulation therapies targeting genes expressed differentially in the renin-angiotensin system to remedy structural remodeling associated with atrial enlargement and heart failure progression in patients with MR.


2019 ◽  
Vol 109 (3) ◽  
pp. 324-330 ◽  
Author(s):  
Erik Holzwirth ◽  
Jelena Kornej ◽  
Sandra Erbs ◽  
Danilo Obradovic ◽  
Andreas Bollmann ◽  
...  

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