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Published on: September 20, 2024
COVID-19 and the risk of acute cardiovascular diseases: a two-sample Mendelian randomization study
Yuling Li1,2, Dongliang Yang3, Jian Kang2
1Department of Surgical Oncology and General Surgery, The First Hospital of China Medical University, 155 North Nanjing Street, Heping District, Shenyang, 110001, China.
Insights
This study found no causal link between COVID-19 and cardiovascular diseases (CVDs). Mendelian randomization analysis suggests that COVID-19 does not increase the risk of conditions like heart failure or heart attack.
Area of Science:
- Epidemiology
- Genetics
- Cardiology
Background:
- Emerging evidence suggests a link between COVID-19 and cardiovascular diseases (CVDs), but causality remains unclear.
- Inconsistent findings necessitate robust investigation into the potential causal relationship between SARS-CoV-2 infection and CVD risk.
Purpose of the Study:
- To investigate the potential causal relationship between COVID-19 and various cardiovascular diseases using a two-sample Mendelian randomization (MR) approach.
- To clarify whether genetic predisposition to COVID-19 influences the risk of developing specific cardiovascular conditions.
Main Methods:
- Utilized summary-level data from the IEU OpenGWAS project for COVID-19 and cardiovascular diseases (myocarditis, heart failure, acute myocardial infarction, arrhythmia, venous thromboembolism).
- Employed five complementary MR methods, including inverse variance weighted (IVW) as the primary approach, with single nucleotide polymorphisms (SNPs) as instrumental variables.
- Conducted sensitivity analyses (Cochran's Q test, MR-Egger intercept, leave-one-out) to ensure the robustness and reliability of the causal estimates.
Main Results:
- The primary IVW analysis indicated no statistically significant causal relationship between genetically predicted COVID-19 and an increased risk of myocarditis, heart failure, acute myocardial infarction, arrhythmia, or venous thromboembolism.
- Supplementary MR methods yielded consistent results, further supporting the absence of a causal link.
- Sensitivity analyses confirmed the robustness of the findings, with no evidence of pleiotropy or other biases affecting the causal estimates.
Conclusions:
- This two-sample Mendelian randomization study found insufficient evidence to support a causal relationship between COVID-19 and the risk of acute cardiovascular diseases.
- These findings may inform strategies for the prevention and management of cardiovascular complications in patients with COVID-19.
Background:
Evidence suggests that coronavirus disease 2019 (COVID-19) is associated with the risk of cardiovascular diseases (CVDs). However, the results are inconsistent, and the causality remains to be established. We aimed to investigate the potential causal relationship between COVID-19 and CVDs by using two-sample Mendelian randomization (MR) analysis.
Methods:
Summary-level data for COVID-19 and CVDs including myocarditis, heart failure (HF), acute myocardial infarction (AMI), arrhythmia and venous thromboembolism (VTE) were obtained from the IEU OpenGWAS project, a public genome-wide association study (GWAS). Single nucleotide polymorphisms (SNPs) were used as instrumental variables. Five complementary MR methods were performed, including inverse variance weighted (IVW), MR-Egger, weighted median, weighted mode and simple mode methods. IVW method was considered as the primary approach. Besides, sensitivity analyses, including Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis, were performed to evaluate the robustness of the results.
Results:
According to the IVW results, our MR study indicated that genetically predicted COVID-19 was not causally connected with the risk of CVDs [myocarditis: odds ratio (OR) = 1.407, 95% confidence interval (CI) = 0.761-2.602, p-value = 0.277; HF: OR = 1.180, 95% CI = 0.980-1.420, p-value = 0.080; AMI: OR = 1.002, 95% CI = 0.998-1.005, p-value = 0.241; arrhythmia: OR = 0.865, 95% CI = 0.717-1.044, p-value = 0.132; VTE: OR = 1.013, 95% CI = 0.997-1.028, p-value = 0.115]. The supplementary MR methods showed similar results. Sensitivity analyses suggested that the causal estimates were robust.
Conclusion:
This two-sample MR analysis did not provide sufficient evidence for a causal relationship between COVID-19 and the risk of acute CVDs, which may provide new insights into the prevention of acute CVDs in COVID-19 patients.
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