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Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
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Apolipoprotein and peripheral artery disease: Mendelian randomization analysis.

Chen-Xin Wan1, Yu-Shu Gong2, Tao Xu3

  • 1Pu'ai Hospital, Huazhong University of Science and Technology, Tongji Medical College, Wuhan City, China.

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|December 17, 2024
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Summary

Elevated apolipoprotein B/A1 ratio significantly increases peripheral arterial disease (PAD) risk. Hypertension, myocardial infarction, and ischemic stroke mediate this association, explaining 81% of the causal effect.

Keywords:
Peripheral arterial diseaseapolipoproteinmediationmendelian randomization

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Area of Science:

  • Cardiovascular Science
  • Genetics
  • Epidemiology

Background:

  • Peripheral arterial disease (PAD) prevalence is increasing globally, associated with poor clinical outcomes.
  • Investigating the link between apolipoprotein levels and PAD is crucial for understanding disease mechanisms.

Purpose of the Study:

  • To determine the causal relationship between apolipoprotein B/A1 ratio and PAD risk.
  • To evaluate the mediating roles of smoking, diabetes, hypertension, myocardial infarction, and ischemic stroke in this association.

Main Methods:

  • Two-sample Mendelian randomization (TSMR) was utilized to assess causal effects.
  • Multivariate Mendelian randomization (MVMR) was employed to quantify mediation pathways.

Main Results:

  • A one standard deviation increase in apolipoprotein B/A1 ratio was associated with a 46% increased risk of PAD.
  • Hypertension, myocardial infarction, and ischemic stroke were identified as significant mediators, collectively explaining 81% of the causal effect.

Conclusions:

  • Elevated apolipoprotein B/A1 ratio is a causal risk factor for PAD.
  • Hypertension, myocardial infarction, and ischemic stroke are key mediators in the pathway from apolipoprotein levels to PAD.