Genetic liability between COVID-19 and heart failure: Evidence from a bidirectional mendelian randomization study

Authors

Huachen Wang
Zheng Guo, Edith Cowan UniversityFollow
Yulu Zheng, Edith Cowan UniversityFollow
Bing Chen

Document Type

Journal Article

Publication Title

BMC Cardiovascular Disorders

Volume

22

Issue

1

PubMed ID

35690714

Publisher

Springer

School

Centre for Precision Health / School of Medical and Health Sciences

RAS ID

52020

Comments

Wang, H., Guo, Z., Zheng, Y., & Chen, B. (2022). Genetic liability between COVID-19 and heart failure: evidence from a bidirectional Mendelian randomization study. BMC cardiovascular disorders, 22(1), 1-9. https://doi.org/10.1186/s12872-022-02702-w

Abstract

Background: Previous studies have observed inconsistent associations between coronavirus disease 2019 (COVID-19) and heart failure (HF), but these studies were prone to bias based on reverse causality and residual confounding factors. We aimed to investigate genetic liability between COVID-19 and heart failure using a bidirectional Mendelian randomization study. Methods: The causal relationship between COVID-19 (including COVID-19, hospitalized COVID-19 compared with the general population, and severe COVID-19) and HF are determined by using a bidirectional Mendelian randomization analysis. We drew on summary statistics from the largest HF genome-wide association study (GWAS) meta-analysis on individuals of European ancestry, which included 47,309 HF patients and 930,014 controls. The inverse variance weighted (IVW), an adaption of the Egger regression (MR-Egger), the weighted median, and weighted model were conducted for the Mendelian randomization analysis to estimate a causal effect. To confirm the stability, we performed a “leave-one-out” approach for the sensitivity analysis. Results: Genetically predicted severe COVID-19 was not significantly associated with the risk of HF [odds ratio (OR), 1.003; 95% confidence interval (CI), 0.969–1.037; p = 0.867]. The IVW demonstrated that there was no association between genetically hospitalized COVID-19 infection and HF risk [OR, 1.009; 95% CI, 0.939–1.085; p = 0.797]. There was no evidence to support the association between genetically determined COVID-19 and the risk of HF [OR, 1.066; 95% CI, 0.955–1.190; p = 0.253]. In addition, genetically predicted HF was also not causally associated with COVID-19 [OR, 1.162; 95% CI, 0.824–1.639; p = 0.393]. MR-Egger analysis indicated no evidence of directional pleiotropy. Conclusion: The current bidirectional Mendelian randomization analysis overcomes the limitations of observational studies. Our findings indicated that there is no causal association between COVID-19 and HF.

DOI

10.1186/s12872-022-02702-w

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 License.