Key result
Genetically predicted aspirin consumption was associated with a significantly increased risk of heart failure (OR 1.085; 95% CI 1.015-1.161; P=0.017).
Why the study?
The study aimed to investigate whether there is a causal association between aspirin consumption and the risk of heart failure.
Does aspirin consumption increase the risk of heart failure?
Observational (n=218,208)
Does aspirin consumption increase the risk of heart failure?
Odds Ratio: 1.085 (95% CI 1.015–1.161)
p-value: p=0.017
Mendelian randomization analysis suggests a potential causal relationship between aspirin consumption and an increased risk of heart failure.
MR suggests aspirin may causally raise HF risk; leaves open confirmation by RCTs before practice change.
AIMS: This study aimed to investigate the causal association of aspirin consumption with the risk of heart failure. METHODS: Our study included a total of 218 208 individuals, with 23 397 cases of heart failure. Genetic summary data on the association between single-nucleotide polymorphisms (SNPs) and aspirin consumption were obtained from a large-scale genome-wide association study involving 462 933 individuals, of which 61 702 people were taking aspirin. After the exclusion of critical confounding factors, we assessed the final and independent association between the aspirin consumption and the risk of heart failure using 3 two-sample Mendelian randomization (MR) methods-inverse variance weighted (IVW), weighted-median, and MR-Egger regression. Sensitivity analyses and directionality test were employed to further validate the stability of the results. RESULTS: After excluding the SNPs that exhibited associations with potential confounders and harmonizing the data, a total of 32 SNPs were finally selected for MR analysis from the initially identified 60 SNPs that displayed strong associations with the exposure. The results of the main method (IVW) showed a significant positive association between aspirin use and the occurrence of heart failure (OR [odds ratio]: 1.085; 95% CI [confidence interval]: 1.015-1.161; P = 0.017), although other methods did not showed statistically significant results (MR-Egger, OR: 1.211, 95% CI: 0.842-1.21, P = 0.896; weighted-median, OR: 1.087, 95% CI: 0.983-1.202, P = 0.105). Heterogeneity test, the MR-Egger intercept, and the funnel plot did not reveal any evidence of heterogeneity (Cochran's Q statistic = 29.263; P = 0.556) or horizontal pleiotropy (intercept = 0.007; P = 0.319). The 'leave-one-out' analysis indicated that no individual SNP exerted a dominant influence on the main estimate. Directionality test confirmed the accuracy of the causal relationship between exposure and outcome direction in our data. CONCLUSIONS: Our results support a potential positive causal relationship between aspirin consumption and the occurrence of heart failure.
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Cai et al. (2023) conducted an observational in Heart failure (n=218,208). Aspirin consumption vs. No aspirin consumption was evaluated on Occurrence of heart failure (OR 1.085, 95% CI 1.015-1.161, p=0.017). Genetically predicted aspirin consumption was associated with a significantly increased risk of heart failure (OR 1.085; 95% CI 1.015-1.161; P=0.017).
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