Abstract
ObjectiveThis meta-analysis aims to evaluate the relationships between seven functional polymorphisms in the CETP gene and myocardial infarction (MI) risk.MethodThe PubMed, CISCOM, CINAHL, Web of Science, Google Scholar, EBSCO, Cochrane Library, and CBM databases were searched for relevant articles published before March 1st, 2013 without any language restrictions. Meta-analysis was conducted using the STATA 12.0 software.ResultsNine case-control studies with a total 8,623 MI cases and 8,564 healthy subjects met the inclusion criteria. The results of our meta-analysis suggested that CETP rs708272 (C>T) polymorphism might be correlated with an increased risk of MI, especially among Caucasians. Furthermore, we observed that CETP rs1800775 (C>A) polymorphism might increase the risk of MI. Nevertheless, no similar findings were found for CETP rs5882 (A>G), rs2303790 (A>G), rs1800776 (C>A), rs12149545 (G>A), and rs4783961 (G>A) polymorphisms.ConclusionThe current meta-analysis suggests that CETP rs708272 (C>T) and rs1800775 (C>A) polymorphisms may contribute to MI susceptibility, especially among Caucasians. Thus, CETP rs708272 and rs1800775 polymorphisms may be promising and potential biomarkers for early diagnosis of MI.
Highlights
Myocardial infarction (MI) remains the leading cause of death and disability worldwide, accounting for up to 40% of all deaths [1]
Atherogenic dyslipidemia is usually characterized by three lipid abnormalities: increases in plasma triglyceride, small low density cholesterol (LDL-C) and very low density lipoprotein cholesterol (VLDL-C) levels, and decreased high-density lipoprotein cholesterol (HDL-C) levels [8,9,10]
Selection criteria The included studies must meet all four of the following criteria: (1) the study design must be clinical cohort or case-control study that focused on the relationships of Cholesteryl ester transfer protein (CETP) genetic polymorphisms with the risk of MI; (2) all patients met the diagnostic criteria for MI; (3) the genotype frequencies of healthy controls should follow the Hardy-Weinberg equilibrium (HWE); (4) the study must provide sufficient information about the genotype frequencies
Summary
Myocardial infarction (MI) remains the leading cause of death and disability worldwide, accounting for up to 40% of all deaths [1]. Due to high mortality and disability rates, MI is becoming a global epidemiological health concern [2]. Atherogenic dyslipidemia is usually characterized by three lipid abnormalities: increases in plasma triglyceride, small low density cholesterol (LDL-C) and very low density lipoprotein cholesterol (VLDL-C) levels, and decreased high-density lipoprotein cholesterol (HDL-C) levels [8,9,10]. The exact cellular and molecular mechanisms leading to the development of MI remain unclear, it is believed that functionally relevant mutations in the dyslipidemia-related genes may contribute to increased susceptibility to MI [11]
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