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Published on: February 26, 2013
Corticosteroid Use and Atrial Fibrillation: Exploring Underlying Mechanisms, FAERS Disproportionality Analysis, and a
Harri Hardi1, Agian Jeffilano Barinda2,3, Ananda Pipphali Vidya4
1Clinical Pharmacology Specialist Study Program, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia.
Insights
Corticosteroid use significantly increases the risk of atrial fibrillation by 1.74 times. This risk is dose- and duration-dependent, affecting various administration routes and potentially impacting cardiac health.
Area of Science:
- Cardiology
- Pharmacology
- Epidemiology
Background:
- Corticosteroids exhibit proarrhythmic properties, yet their impact on atrial fibrillation (AF) incidence post-cardiac surgery remains debated.
- Existing research presents inconsistent findings regarding the association between steroid use and AF, necessitating further investigation.
Purpose of the Study:
- To systematically review and elucidate the association between corticosteroid usage and the risk of developing atrial fibrillation.
- To analyze the dose- and duration-dependent effects of corticosteroids on AF risk.
Main Methods:
- A systematic review and meta-analysis of 23 studies involving 679,330 participants.
- Keywords 'corticosteroids' and 'atrial fibrillation' were used across major scientific databases.
- Disproportionality and Bayesian analyses were performed on FDA FAERS data, complemented by a narrative review for mechanistic insights.
Main Results:
- Exogenous steroid use was associated with a 1.74-fold increased risk of atrial fibrillation (95% CI: 1.55-1.96, p < 0.0001).
- Intravenous, oral, and inhaled corticosteroids increased AF risk by 2.02, 1.95, and 1.67 times, respectively.
- Higher doses and longer durations of corticosteroid administration correlated with elevated AF risk, supported by FDA FAERS data.
Conclusions:
- Corticosteroids significantly elevate the risk of atrial fibrillation, with effects varying by administration route, dose, and duration.
- Mechanisms include cardiomyocyte remodeling, senescence, and exacerbation of conditions like hypertension and diabetes.
- Inflammation should be considered a potential confounding factor in future research.
Abstract:
Steroids are known to have proarrhythmogenic properties, even though they have been demonstrated to lower the incidence of atrial fibrillation following heart surgery. According to the American Heart Association (AHA), this negative impact was still inconsistent. Therefore, this study aims to elucidate the association between corticosteroid usage and atrial fibrillation.This systematic review employed the keywords "corticosteroids" and "atrial fibrillation," collected from PubMed, Scopus, Web of Science, and Google Scholar. Meta-analysis was performed using a random effects model through Mantel-Haenszel analysis. Disproportionality analysis and Bayesian analysis were conducted utilizing the United States Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) datasets. A narrative review was conducted to obtain mechanistic insights into corticosteroid-induced atrial fibrillation. The meta-analysis of 23 studies involving 679,330 individuals indicated that exogenous steroids elevated the risk of atrial fibrillation by 1.74 times (95% CI = 1.55 to 1.96, p < 0.0001). Intravenous, oral, and inhaled corticosteroids elevated the risk of atrial fibrillation by 2.02, 1.95, and 1.67 times, respectively. The risk of atrial fibrillation was elevated with the administration of corticosteroids at higher doses and for longer durations. Disproportionality analysis from FAERS indicated that some corticosteroids exhibited a significant reported odds ratio (ROR). Corticosteroids can induce mechanical and electrical remodeling of cardiomyocytes, as well as cardiomyocyte senescence, cardiac hypertrophy, hypertension, and diabetes mellitus, all of which may collectively increase susceptibility to atrial fibrillation. Corticosteroids might increase the risk of atrial fibrillation in a dose- and duration-dependent fashion. Inflammation should be regarded as a confounding factor in this conclusion.
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