Dataset Information

Atrial fibrillation and risk of major arrhythmic events in Brugada syndrome: A meta-analysis.

ABSTRACT:

Background

Brugada syndrome (BrS) is a common cause of sudden cardiac death (SCD). There is recent evidence that atrial fibrillation (AF) is associated with increased risk of SCD in general population. However, whether AF increases a risk of major arrhythmic events (MAE) in patients with BrS is still unclear. We performed a systematic review and meta-analysis to explore the effect of AF on MAE in BrS population.

Methods

We searched the databases of MEDLINE and EMBASE from inception to March 2019. Included studies were published cohort studies reporting rates of MAE (ventricular fibrillation, sustained ventricular tachycardia, SCD, or sudden cardiac arrest) in BrS patients, with and without previous documented AF. Data from each study were combined using the random-effects model.

Results

Six studies from 1,703 patients were included. There was a significant association between AF and an increased risk of MAE in patients with BrS (pooled OR = 2.37, 95% CI = 1.36-4.13, p-value = .002, I² = 40.3%).

Conclusions

Our meta-analysis demonstrated that AF is associated with an increased risk of MAE in patients with BrS.

SUBMITTER: Kewcharoen J

PROVIDER: S-EPMC6931417 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature

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Publications

Atrial fibrillation and risk of major arrhythmic events in Brugada syndrome: A meta-analysis.

Kewcharoen Jakrin J Rattanawong Pattara P Kanitsoraphan Chanavuth C Mekritthikrai Raktham R Prasitlumkum Narut N Putthapiban Prapaipan P Mekraksakit Poemlarp P Pattison Robert J RJ Vutthikraivit Wasawat W

Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc 20190729 6

<h4>Background</h4>Brugada syndrome (BrS) is a common cause of sudden cardiac death (SCD). There is recent evidence that atrial fibrillation (AF) is associated with increased risk of SCD in general population. However, whether AF increases a risk of major arrhythmic events (MAE) in patients with BrS is still unclear. We performed a systematic review and meta-analysis to explore the effect of AF on MAE in BrS population.<h4>Methods</h4>We searched the databases of MEDLINE and EMBASE from inceptio ...[more]

PMID: 31353765

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Project description:Background: Atrial fibrillation (AF) is associated with calcium (Ca2+) handling remodeling and increased spontaneous calcium release events (SCaEs). Nevertheless, its exact mechanism remains unclear, resulting in suboptimal primary and secondary preventative strategies. Methods: We searched the PubMed database for studies that investigated the relationship between SCaEs and AF and/or its risk factors. Meta-analysis was used to examine the Ca2+ mechanisms involved in the primary and secondary AF preventative groups. Results: We included a total of 74 studies, out of the identified 446 publications from inception (1982) until March 31, 2020. Forty-five were primary and 29 were secondary prevention studies for AF. The main Ca2+ release events, calcium transient (standardized mean difference (SMD) = 0.49; I 2 = 35%; confidence interval (CI) = 0.33-0.66; p < 0.0001), and spark amplitude (SMD = 0.48; I 2 = 0%; CI = -0.98-1.93; p = 0.054) were enhanced in the primary diseased group, while calcium transient frequency was increased in the secondary group. Calcium spark frequency was elevated in both the primary diseased and secondary AF groups. One of the key cardiac currents, the L-type calcium current (ICaL) was significantly downregulated in primary diseased (SMD = -1.07; I 2 = 88%; CI = -1.94 to -0.20; p < 0.0001) and secondary AF groups (SMD = -1.28; I 2 = 91%; CI = -2.04 to -0.52; p < 0.0001). Furthermore, the sodium-calcium exchanger (INCX) and NCX1 protein expression were significantly enhanced in the primary diseased group, while only NCX1 protein expression was shown to increase in the secondary AF studies. The phosphorylation of the ryanodine receptor at S2808 (pRyR-S2808) was significantly elevated in both the primary and secondary groups. It was increased in the primary diseased and proarrhythmic subgroups (SMD = 0.95; I 2 = 64%; CI = 0.12-1.79; p = 0.074) and secondary AF group (SMD = 0.66; I 2 = 63%; CI = 0.01-1.31; p < 0.0001). Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) expression was elevated in the primary diseased and proarrhythmic drug subgroups but substantially reduced in the secondary paroxysmal AF subgroup. Conclusions: Our study identified that ICaL is reduced in both the primary and secondary diseased groups. Furthermore, pRyR-S2808 and NCX1 protein expression are enhanced. The remodeling leads to elevated Ca2+ functional activities, such as increased frequencies or amplitude of Ca2+ spark and Ca2+ transient. The main difference identified between the primary and secondary diseased groups is SERCA expression, which is elevated in the primary diseased group and substantially reduced in the secondary paroxysmal AF subgroup. We believe our study will add new evidence to AF mechanisms and treatment targets.

Project description:Genetic polymorphisms associated with common aetiologically complex diseases have recently been identified through genome-wide association studies. Direct-to-consumer genetic testing for such polymorphisms, with provision of absolute genetic risk estimates, is marketed by several commercial companies. Polymorphisms associated with atrial fibrillation (AF) have shown relatively large risk estimates, but the robustness of such estimates across populations and study designs has not been investigated.A systematic literature review with meta-analysis and assessment of between-study heterogeneity was carried out for single-nucleotide polymorphisms (SNPs) in the six genetic regions associated with AF in genome-wide or candidate gene studies.Data were identified from 18 samples of European ancestry (n=12,100 cases, 115,702 controls) for the single-nucleotide polymorphisms (SNP) on chromosome 4q25 (rs220733), from 16 samples (n=12,694 cases, 132,602 controls) for the SNP on 16q22 (rs2106261) and from four samples (n=5272 cases, 59,725 controls) for the SNP in KCNH2 (rs1805123). Only the publications in which the associations were initially reported were identified for SNPs on 1q21 and in GJA5 and IL6R, why meta-analyses were not performed for those SNPs. In overall random-effects meta-analyses, association with AF was observed for both SNPs on chromosomes 4q25 [odds ratio (OR), 1.67; 95% CI, 1.50-1.86, P=2×10(-21)] and 16q22 (OR, 1.21; 95% CI, 1.13-1.29, P=1×10(-8)) from genome-wide studies, but not the SNP in KCNH2 from candidate gene studies (P=0.15). There was substantial effect heterogeneity across case-control and cross-sectional studies for both polymorphisms (I(2)=0.50-0.78, P<0.05), but not across prospective cohort studies (I(2)=0.39, P=0.15). Both polymorphisms were robustly associated with AF for each study design individually (P<0.05).In meta-analyses including up to 150,000 individuals, polymorphisms in two genetic regions were robustly associated with AF across all study designs but with substantial context-dependency of risk estimates.

Dataset Information

Atrial fibrillation and risk of major arrhythmic events in Brugada syndrome: A meta-analysis.

Background

Methods

Results

Conclusions

Publications

Atrial fibrillation and risk of major arrhythmic events in Brugada syndrome: A meta-analysis.

Similar Datasets

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