Dataset Information

The association between heme oxygenase-1 gene promoter polymorphism and the outcomes of catheter ablation of atrial fibrillation.

ABSTRACT: A length polymorphism of GT repeats in the promoter region of the human heme oxygenase-1 (HO-1) gene modulates its gene transcription to protect against myocardial injury. The present study investigated the association between HO-1 promoter polymorphisms and the outcomes of catheter ablation of atrial fibrillation (AF). The allelic frequencies of GT repeats in the HO-1 gene promoter were screened in 205 random individuals who underwent catheter ablation for drug refractory AF.In the patients who received catheter ablation, those with AF recurrence had fewer GT repeats (53.4±7.1 vs. 56.1±6.5, p = 0.004), a lower incidence of hyperlipidemia, more non-paroxysmal AF, and a larger left atrial diameter. After conducting a multivariate logistic analysis, the number of GT repeats (Odds ratio: 0.94, 95% CI 0.90-0.99, p = 0.01) and the diameter of the left atrium (Odds ratio: 1.08, 95% CI 1.02-1.15, p = 0.01) remained independent predictors. The carriers of GT repeats, which were <29 in both alleles, were associated with a lower sinus maintenance rate after catheter ablation (38.5% vs. 60.1%, p = 0.003). The patients were divided into paroxysmal and non-paroxysmal AF groups; the number of GT repeats was associated with AF recurrence only in the patients with paroxysmal AF. The number of GT repeats, combined with LAD, was significant for predicting AF recurrence after catheter ablation (p = 0.01). The number of GT repeats was not found to be associated with differences in the left atrial diameter, the biatrial voltage, or the levels of bilirubin, ferritin, iron, C-reactive protein, or von-Willibrand factor. In conclusions, HO-1 gene promoter polymorphisms were associated with AF recurrence after catheter ablation.

SUBMITTER: Hu YF

PROVIDER: S-EPMC3577889 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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The association between heme oxygenase-1 gene promoter polymorphism and the outcomes of catheter ablation of atrial fibrillation.

Hu Yu-Feng YF Lee Kun-Tai KT Wang Hsueh-Hsiao HH Ueng Kwo-Chang KC Yeh Hung-I HI Chao Tze-Fan TF Liao Jo-Nan JN Lin Yenn-Jiang YJ Chang Shih-Lin SL Lo Li-Wei LW Tuan Ta-Chuan TC Li Cheng-Hung CH Chung Fa-Po FP Hsu Chiao-Po CP Chang Hsiao-Huang HH Huang Cheng-Hsiung CH Chen Shih-Ann SA

PloS one 20130220 2

A length polymorphism of GT repeats in the promoter region of the human heme oxygenase-1 (HO-1) gene modulates its gene transcription to protect against myocardial injury. The present study investigated the association between HO-1 promoter polymorphisms and the outcomes of catheter ablation of atrial fibrillation (AF). The allelic frequencies of GT repeats in the HO-1 gene promoter were screened in 205 random individuals who underwent catheter ablation for drug refractory AF.In the patients who ...[more]

PMID: 23437133

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Project description:ObjectivesTo determine whether Gal-3 mediates sustained atrial fibrillation (AF)-induced atrial structural and electrical remodeling and contributes to AF perpetuation.BackgroundGalectin-3 (Gal-3) mediates extracellular matrix remodeling in heart failure, but its role in AF progression remains unexplored.MethodsWe examined intracardiac blood samples from patients with AF (N=55) to identify potential biomarkers of AF recurrence. In a sheep model of tachypacing-induced AF (N=20), we tested the effects of Gal-3 inhibition during AF progression.ResultsIn patients, intracardiac serum Gal-3 levels were greater in persistent than paroxysmal AF and independently predicted atrial tachyarrhythmia recurrences after a single ablation procedure. In the sheep model, both Gal-3 and TGF-β1 were elevated in the atria of persistent AF animals. The Gal-3 inhibitor GM-CT-01 (GMCT) reduced both Gal-3 and TGF-β1-induced sheep atrial fibroblast migration and proliferation in vitro. GMCT (12 mg/kg twice/week) prevented the increase in serum procollagen type III N-terminal peptide seen during progression to persistent AF, and also mitigated atrial dilatation, myocyte hypertrophy, fibrosis, and the expected increase in dominant frequency of excitation. Atria of GMCT-treated animals had significantly less TGF-β1-Smad2/3 signaling pathway activation and expression of α-smooth muscle actin and collagen than saline-treated animals. Ex-vivo hearts from GMCT-treated animals had significantly longer action potential durations and fewer rotors and wavebreaks during AF, and myocytes had lower functional expression of inward rectifier K+ channel (Kir2.3) than saline-treated animals. Importantly, GMCT increased the probability of spontaneous AF termination, decreased AF inducibility and reduced overall AF burden.ConclusionsInhibiting Gal-3 during AF progression might be useful as an adjuvant treatment to improve outcomes of catheter ablation for persistent AF. Gal-3 inhibition may be a potential new upstream therapy for prevention of AF progression.

Project description:AF is a heterogeneous rhythm disorder that is related to a wide spectrum of etiologies and has broad clinical presentations. Mechanisms underlying AF are complex and remain incompletely understood despite extensive research. They associate interactions between triggers, substrate and modulators including ionic and anatomic remodeling, genetic predisposition and neuro-humoral contributors. The pulmonary veins play a key role in the pathogenesis of AF and their isolation is associated to high rates of AF freedom in patients with paroxysmal AF. However, ablation of persistent AF remains less effective, mainly limited by the difficulty to identify the sources sustaining AF. Many theories were advanced to explain the perpetuation of this form of AF, ranging from a single localized focal and reentrant source to diffuse bi-atrial multiple wavelets. Translating these mechanisms to the clinical practice remains challenging and limited by the spatio-temporal resolution of the mapping techniques. AF is driven by focal or reentrant activities that are initially clustered in a relatively limited atrial surface then disseminate everywhere in both atria. Evidence for structural remodeling, mainly represented by atrial fibrosis suggests that reentrant activities using anatomical substrate are the key mechanism sustaining AF. These reentries can be endocardial, epicardial, and intramural which makes them less accessible for mapping and for ablation. Subsequently, early interventions before irreversible remodeling are of major importance. Circumferential pulmonary vein isolation remains the cornerstone of the treatment of AF, regardless of the AF form and of the AF duration. No ablation strategy consistently demonstrated superiority to pulmonary vein isolation in preventing long term recurrences of atrial arrhythmias. Further research that allows accurate identification of the mechanisms underlying AF and efficient ablation should improve the results of PsAF ablation.

Dataset Information

The association between heme oxygenase-1 gene promoter polymorphism and the outcomes of catheter ablation of atrial fibrillation.

Publications

The association between heme oxygenase-1 gene promoter polymorphism and the outcomes of catheter ablation of atrial fibrillation.

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