Genetic and non-genetic risk factors associated with atrial fibrillation

Young, Lindsay J.; Antwi-Boasiako, Steve; Ferrall, Joel; Wold, Loren E.; Mohler, Peter J.; Refaey, Mona El

doi:10.1016/j.lfs.2022.120529

Cited by 14 publications

(30 citation statements)

References 178 publications

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“…In attempt to outline a pathophysiology of COVID-19-related AF, several putative mechanisms have been proposed. They include a reduced availability of angiotensin-converting enzyme (ACE) 2, binding of viral spike protein to CD147 or sialic acid, enhancement of inflammatory signaling culminating in cytokine storm, endothelial damage and increased adrenergic drive ( 38 ; Figure 2 ).…”

Section: The Outline Of Af Pathophysiologymentioning

confidence: 99%

“…There is a causal link between activation of the NLRP3 inflammasome in atrial cardiomyocytes and AF development. The mechanisms underlying the pro-arrhythmic effects of NLRP3 inflammasome take account of abnormal diastolic RyR2-mediated sarcoplasmic reticulum Ca 2+ release with generation of pro-arrhythmic delayed afterdepolarizations (DADs), continued activation of ultra-rapid delayed rectifier K + current with action potential abbreviation, and atrial hypertrophy and fibrosis ( 27 , 38 , 78 ).…”

Section: The Outline Of Af Pathophysiologymentioning

confidence: 99%

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COVID-19 and atrial fibrillation: Intercepting lines

Donniacuo

Angelis

Rafaniello

et al. 2023

Front. Cardiovasc. Med.

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Almost 20% of COVID-19 patients have a history of atrial fibrillation (AF), but also a new-onset AF represents a frequent complication in COVID-19. Clinical evidence demonstrates that COVID-19, by promoting the evolution of a prothrombotic state, increases the susceptibility to arrhythmic events during the infective stages and presumably during post-recovery. AF itself is the most frequent form of arrhythmia and is associated with substantial morbidity and mortality. One of the molecular factors involved in COVID-19-related AF episodes is the angiotensin-converting enzyme (ACE) 2 availability. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses ACE2 to enter and infect multiple cells. Atrial ACE2 internalization after binding to SARS-CoV-2 results in a raise of angiotensin (Ang) II, and in a suppression of cardioprotective Ang(1–7) formation, and thereby promoting cardiac hypertrophy, fibrosis and oxidative stress. Furthermore, several pharmacological agents used in COVID-19 patients may have a higher risk of inducing electrophysiological changes and cardiac dysfunction. Azithromycin, lopinavir/ritonavir, ibrutinib, and remdesivir, used in the treatment of COVID-19, may predispose to an increased risk of cardiac arrhythmia. In this review, putative mechanisms involved in COVID-19-related AF episodes and the cardiovascular safety profile of drugs used for the treatment of COVID-19 are summarized.

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Section: The Outline Of Af Pathophysiologymentioning

confidence: 99%

Section: The Outline Of Af Pathophysiologymentioning

confidence: 99%

COVID-19 and atrial fibrillation: Intercepting lines

Donniacuo

Angelis

Rafaniello

et al. 2023

Front. Cardiovasc. Med.

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“…Previous studies have implicated the genetic basis of AF and found that both common and rare variants in ion-channel genes, gap junction and transcription factor genes, or structural genes are likely associated with AF pathogenesis ( 16 , 17 ).…”

Section: Cardiomyopathy Gene Variants and Early-onset Afmentioning

confidence: 99%

“…It has been postulated that GATA4 and GATA5, cardiac transcription factors involved in myocardial development, directly coregulate SCN5A. GATA4, GATA5 and GATA6 are linked to decreased transcriptional activity and may play a role in reducing the levels of NKX2.5 and other target proteins, which could have further downstream effects on cardiac development and function or electrical activity ( 16 , 17 ). The LMNA gene variants interact with the NUP155 gene, encoding lamin A/C and nucleoporin 155.…”

Section: Cardiomyopathy Gene Variants and Early-onset Afmentioning

confidence: 99%

Genetic variants, pathophysiological pathways, and oral anticoagulation in patients with hypertrophic cardiomyopathy and atrial fibrillation

Wang

Chen

Liu

et al. 2023

Front. Cardiovasc. Med.

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Atrial fibrillation (AF) is commonly prevalent in patients with hypertrophic cardiomyopathy (HCM). However, whether the prevalence and incidence of AF are different between genotype-positive vs. genotype-negative patients with HCM remains controversial. Recent evidence has indicated that AF is often the first presentation of genetic HCM patients in the absence of a cardiomyopathy phenotype, implying the importance of genetic testing in this population with early-onset AF. However, the association of the identified sarcomere gene variants with HCM occurrence in the future remains unclear. How the identification of these cardiomyopathy gene variants should influence the use of anticoagulation therapy for a patient with early-onset AF is still undefined. In this review, we sought to assess the genetic variants, pathophysiological pathways, and oral anticoagulation in patients with HCM and AF.

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“…AF is associated with poor life quality and increasing morbidity and mortality ( Staerk et al, 2017 ; Virani et al, 2021 ), resulting in a heavy socioeconomic burden ( Chugh et al, 2014 ). AF is a multifactorial complex disease involving modifiable risk factors (e.g., smoking, obesity, and hypertension) and unmodifiable risk factors (e.g., genetics, age, and male) ( Young et al, 2022 ). Despite incomplete understanding of the pathogenesis, inflammation is a well-established core process contributing to not only atrium electronic and structural remodeling but also thrombogenesis, increasing the vulnerability to AF.…”

Section: Introductionmentioning

confidence: 99%

Exploring the causality between ankylosing spondylitis and atrial fibrillation: A two-sample Mendelian randomization study

et al. 2022

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Objective: To study whether ankylosing spondylitis (AS) has a causal effect on the risk of atrial fibrillation (AF) using two-sample Mendelian randomization (MR) analysis.Methods: Single nucleotide polymorphisms (SNPs) were selected as independent instrumental variables (IVs) from a GWAS study of AS. Summary data from a large-scale GWAS meta-analysis of AF was utilized as the outcome dataset. Inverse-variance weighted (IVW) model was used for the primary analysis. Multiple sensitivity and heterogeneity tests were conducted to confirm the robustness of the results.Results: In total, 18 SNPs were identified as IVs for MR analysis. Five MR methods consistently found that ankylosing spondylitis was not causally associated with atrial fibrillation (IVW: OR = 0.983 (0.894, 1.080), p = 0.718; MR-Egger: OR = 1.190 (0.973, 1.456), p = 0.109; Simple mode: OR = 0.888 (0.718, 1.098), p = 0.287; Weighted mode: OR = 0.989 (0.854, 1.147), p = 0.890; Weight median: OR = 0.963 (0.852, 1.088), p = 0.545). Leave-one-out analysis supported the stability of MR results. Both the MR-Egger intercept and MR-PRESSO method revealed the absence of horizontal pleiotropy.Conclusion: The two-sample MR analysis did not support a causal relationship between AS and the risk of AF.

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Genetic and non-genetic risk factors associated with atrial fibrillation

Cited by 14 publications

References 178 publications

COVID-19 and atrial fibrillation: Intercepting lines

COVID-19 and atrial fibrillation: Intercepting lines

Genetic variants, pathophysiological pathways, and oral anticoagulation in patients with hypertrophic cardiomyopathy and atrial fibrillation

Exploring the causality between ankylosing spondylitis and atrial fibrillation: A two-sample Mendelian randomization study

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