Abstract

G20210A polymorphism (rs1799963) within the prothrombin gene is associated with a higher circulation level of prothrombin, thus increasing the likelihood of developing myocardial infarction (MI). Opinions differ regarding the correlation between prothrombin G20210A genotype and MI risk, which prompted us to conduct a meta-analysis to determine this association. PubMed, EMBASE, Web of Science and CNKI were searched for pertinent reports. A total of 34 studies involving 14 611 MI cases and 84 358 controls were analyzed in this quantitative analysis. We found a statistically significant association between prothrombin G20210A polymorphism and MI in the allele model (A vs. G, OR = 1.43, 95%CI: 1.18–1.72), heterozygote model (GA vs. GG, OR = 1.41, 95%CI: 1.16–1.72) and dominant model (GA + AA vs. GG, OR = 1.41, 95%CI: 1.15–1.72). The association remains significant in Caucasians but not in non-Caucasians. Moreover, prothrombin G20210A polymorphism increases MI risk in an age-related manner. A further significant association was found in a subpopulation younger than 55 years (allele model, OR = 1.76, 95%CI: 1.32–2.35; heterozygote model, OR = 1.70, 95%CI: 1.24–2.33; dominant model, OR = 1.70, 95%CI: 1.24–2.34). Sensitivity analysis and publication bias analysis revealed stable and statistically robust results. Our meta-analysis demonstrated that prothrombin G20210A polymorphism may represent a risk factor for MI.

Highlights

  • Myocardial infarction (MI) is a highly lethal disease in developed countries, usually caused by pathological coronary artery occlusion

  • Myocardial infarction is pathologically caused by coronary thrombotic occlusion following rupture of atherosclerotic plaques

  • The prothrombin G20210A single-nucleotide polymorphisms (SNPs) has been correlated with increased levels of prothrombin in circulation and is clearly associated with an increased risk of venous thrombosis[2]

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Summary

Introduction

Myocardial infarction (MI) is a highly lethal disease in developed countries, usually caused by pathological coronary artery occlusion. Coronary thrombosis involving platelet adhesion, coagulation cascade activation and subsequent thrombus formation plays a fundamental role in the clinical progression to MI. Over-activated procoagulation, acquired from complex patterns of inheritance or environmental risk factors, has more propensity to induce localized coronary occlusion. The detrimental role of prothrombin G20210A is controversial in MI7,8. The reason for this confounding phenomenon may be diversity of the ages of patients recruited in the previous studies. To draw a conclusion about the clinical impact of the prothrombin G20210A with regard to MI risk within a given age stratum, we gathered data from a number of published studies and performed a meta-analysis

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