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Effects of helicobacter pylori infection on the risk of hypertension and coronary heart disease: a bidirectional Mendelian study
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Abstract
Background:
Helicobacter pylori infection (HPI) is a common gastrointestinal disease that may be associated with coronary artery disease (CAD) and its risk factor, hypertension (HTN). However, the causal relationship between HPI and CAD and HTN remains unclear.
Methods:
We used bidirectional Mendelian randomization (MR) analysis to assess the effects of HPI on CAD and HTN, as well as the effects of CAD and HTN on HPI. We used genetic instrumental variables (IVs) for HPI, CAD, and HTN extracted from publicly available large-scale genome-wide association study (GWAS) data. We employed multiple MR analysis methods, including inverse variance weighted (IVW), weighted median, Mendelian Randomization Egger regression (MR-Egger), and Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO), to examine causal relationships and evaluate the impact of heterogeneity and pleiotropy.
Results:
IVW analysis revealed no causal relationship between HPI and CAD or HTN. However, we observed a negative causal correlation between HPI and systolic blood pressure (SBP) and diastolic blood pressure (DBP), suggesting that HPI may serve as a protective factor for hypertension [SBP (Beta = -0.3509, OR, 0.7041; 95% CI, 0.5758-0.8609; P < 0.001), DBP (Beta = -0.1666, OR, 0.8463; 95% CI, 0.7537-0.9508; P = 0.007)]. Reverse MR analysis also revealed no significant effects of CAD, HTN, SBP, or DBP on HPI. Consistent results were obtained from MR-Egger and weighted median analyses, indicating minimal bias due to heterogeneity and pleiotropy.
Conclusion:
This study demonstrates that there is no causal relationship between HPI and CAD or HTN, but a negative causal relationship exists between HPI and SBP and DBP. These findings provide valuable insights for clinical practice and offer a new perspective for further exploration of the relationship between HPI and cardiovascular diseases.
Title: Effects of helicobacter pylori infection on the risk of hypertension and coronary heart disease: a bidirectional Mendelian study
Description:
Abstract
Background:
Helicobacter pylori infection (HPI) is a common gastrointestinal disease that may be associated with coronary artery disease (CAD) and its risk factor, hypertension (HTN).
However, the causal relationship between HPI and CAD and HTN remains unclear.
Methods:
We used bidirectional Mendelian randomization (MR) analysis to assess the effects of HPI on CAD and HTN, as well as the effects of CAD and HTN on HPI.
We used genetic instrumental variables (IVs) for HPI, CAD, and HTN extracted from publicly available large-scale genome-wide association study (GWAS) data.
We employed multiple MR analysis methods, including inverse variance weighted (IVW), weighted median, Mendelian Randomization Egger regression (MR-Egger), and Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO), to examine causal relationships and evaluate the impact of heterogeneity and pleiotropy.
Results:
IVW analysis revealed no causal relationship between HPI and CAD or HTN.
However, we observed a negative causal correlation between HPI and systolic blood pressure (SBP) and diastolic blood pressure (DBP), suggesting that HPI may serve as a protective factor for hypertension [SBP (Beta = -0.
3509, OR, 0.
7041; 95% CI, 0.
5758-0.
8609; P < 0.
001), DBP (Beta = -0.
1666, OR, 0.
8463; 95% CI, 0.
7537-0.
9508; P = 0.
007)].
Reverse MR analysis also revealed no significant effects of CAD, HTN, SBP, or DBP on HPI.
Consistent results were obtained from MR-Egger and weighted median analyses, indicating minimal bias due to heterogeneity and pleiotropy.
Conclusion:
This study demonstrates that there is no causal relationship between HPI and CAD or HTN, but a negative causal relationship exists between HPI and SBP and DBP.
These findings provide valuable insights for clinical practice and offer a new perspective for further exploration of the relationship between HPI and cardiovascular diseases.
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