Cholesteryl ester transfer protein gene polymorphism (I405V) and premature coronary artery disease in an Iranian population

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Abstract

The effect of human cholesteryl ester transfer protein ( CETP) expression on atherogenesis is still under debate. The rs5882 (I405V) polymorphism affect CETP function. We aimed to examine the relationship between the rs5882 polymorphism and the risk of angiographically determined coronary artery disease (CAD). To define premature CAD (PCAD), an age cutoff of 55 years for women and 45 years for men was used. An age- and sex-matched case-control study was conducted in 560 patients with newly diagnosed angiographically documented PCAD (≥50% luminal stenosis of any coronary vessel) and an equal number of control patients with normal coronary arteries (no luminal stenosis at coronary arteries). The severity of CAD was determined by vessel score and Gensini score. A real-time polymerase chain reaction (PCR) and high resolution melting analysis were used to distinguish between genotypes. The I405V genotype distributions were not statistically different in CAD and non-CAD groups in univariate and multivariable-adjusted logistic regression analyzes. The median and inter-quartile range for Gensini score was not significantly different among the AA (43, 24 to 73), AG (40, 20 to 66), and GG (45, 25 to 72) genotypes ( p = 0.097). Furthermore, the distribution of vessel score did not statistically differ between these genotypes ( p = 0.691). Our results suggest that there is no significant association between CETP I405V polymorphism and the risk of PCAD presence and severity. Larger prospective studies are needed to investigate such associations in different populations.

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Cholesteryl ester transfer protein TaqIB variant, high-density lipoprotein cholesterol levels, cardiovascular risk, and efficacy of pravastatin treatment: individual patient meta-analysis of 13,677 subjects.

Alex Shepherd, Kai M Savolainen, V Gudnason … (2005)

Several studies have reported that the cholesteryl ester transfer protein (CETP) TaqIB gene polymorphism is associated with HDL cholesterol (HDL-C) levels and the risk of coronary artery disease (CAD), but the results are inconsistent. In addition, an interaction has been implicated between this genetic variant and pravastatin treatment, but this has not been confirmed. A meta-analysis was performed on individual patient data from 7 large, population-based studies (each >500 individuals) and 3 randomized, placebo-controlled, pravastatin trials. Linear and logistic regression models were used to assess the relation between TaqIB genotype and HDL-C levels and CAD risk. After adjustment for study, age, sex, smoking, body mass index (BMI), diabetes, LDL-C, use of alcohol, and prevalence of CAD, TaqIB genotype exhibited a highly significant association with HDL-C levels, such that B2B2 individuals had 0.11 mmol/L (0.10 to 0.12, P<0.0001) higher HDL-C levels than did B1B1 individuals. Second, after adjustment for study, sex, age, smoking, BMI, diabetes, systolic blood pressure, LDL-C, and use of alcohol, TaqIB genotype was significantly associated with the risk of CAD (odds ratio=0.78 [0.66 to 0.93]) in B2B2 individuals compared with B1B1 individuals (P for linearity=0.008). Additional adjustment for HDL-C levels rendered a loss of statistical significance (P=0.4). Last, no pharmacogenetic interaction between TaqIB genotype and pravastatin treatment could be demonstrated. The CETP TaqIB variant is firmly associated with HDL-C plasma levels and as a result, with the risk of CAD. Importantly, this CETP variant does not influence the response to pravastatin therapy.

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Isolated low HDL cholesterol as a risk factor for coronary heart disease mortality. A 21-year follow-up of 8000 men.

S Yaari, J Medalie, U Goldbourt (1996)

For the purpose of screening individuals at high risk for coronary heart disease (CHD), serum total cholesterol (TC) of 5.2 mmol/L, has been set as a value dividing "desirable" from intermediate high or elevated levels, and HDL cholesterol (HDL-C) 0.9 mmol/L was contained in the high-density fraction. In men with TC > 5.2 mmol/L, abnormally low HDL-C was associated with a virtually identical CHD mortality risk ratio, 38%. These findings persisted after adjustment for multiple CHD risk factors. The excess CHD risk associated with isolated low HDL-C appeared particularly increased in men with diabetes mellitus, whose death rate was 65% higher than in diabetics with HDL-C > 0.9 mmol/L. A second subgroup result was consistent with equal CHD mortality risk among men in the "desirable" TC range, with or without low HDL-C, if systolic blood pressure was > 160 mm Hg. These are post hoc findings, and hypotheses arising from these observations would require independent examination. Total mortality was not increased in men with isolated low HDL-C compared with men who had HDL-C 5.2 mmol/L at baseline. These results indicate that an increased risk of CHD death is associated with abnormally low HDL-C for cholesterol ranges both below and above 5.2 mmol/L. For the individual, therefore, the risk is multiplied by the same amount regardless of TC. Quitting smoking, increasing physical activity, and decreasing body weight would all contribute to raise HDL-C in individuals of most or all age groups. When examined from a community perspective, the results are consistent with a relatively low population-attributable fraction among CHD-free men. This would tend to support the recommended practice of considering a TC level of 5.2 mmol/L (200 mg/dL) as a threshold for further evaluation in screened individuals without manifest CHD.

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Common genetic variation in multiple metabolic pathways influences susceptibility to low HDL-cholesterol and coronary heart disease.

E Schaefer, Dorothea Collins, Laura B. Gabriel … (2010)

A low level of HDL-C is the most common plasma lipid abnormality observed in men with established coronary heart disease (CHD). To identify allelic variants associated with susceptibility to low HDL-C and CHD, we examined 60 candidate genes with key roles in HDL metabolism, insulin resistance, and inflammation using samples from the Veterans Affairs HDL Intervention Trial (VA-HIT; cases, n = 699) and the Framingham Offspring Study (FOS; controls, n = 705). VA-HIT was designed to examine the benefits of HDL-raising with gemfibrozil in men with low HDL-C (≤40 mg/dl) and established CHD. After adjustment for multiple testing within each gene, single-nucleotide polymorphisms (SNP) significantly associated with case status were identified in the genes encoding LIPC (rs4775065, P < 0.0001); CETP (rs5882, P = 0.0002); RXRA (rs11185660, P = 0.0021); ABCA1 (rs2249891, P = 0.0126); ABCC6 (rs150468, P = 0.0206; rs212077, P = 0.0443); CUBN (rs7893395, P = 0.0246); APOA2 (rs3813627, P = 0.0324); SELP (rs732314, P = 0.0376); and APOC4 (rs10413089, P = 0.0425). Included among the novel findings of this study are the identification of susceptibility alleles for low HDL-C/CHD risk in the genes encoding CUBN and RXRA, and the observation that genetic variation in SELP may influence CHD risk through its effects on HDL.

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Author and article information

Journal

Journal ID (nlm-ta): Bosn J Basic Med Sci

Journal ID (iso-abbrev): Bosn J Basic Med Sci

Title: Bosnian Journal of Basic Medical Sciences

Publisher: Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina (Bosnia )

ISSN (Print): 1512-8601

ISSN (Electronic): 1840-4812

Publication date (Print): May 2016

Volume: 16

Issue: 2

Pages: 114-120

Affiliations

[1 ]Department of Cardiac Research, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran

[2 ]Department of Molecular Pathology, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran

[3 ]Department of Genetics, School of Biological Sciences, Tarbiat Modares University, Tehran, Iran

Author notes

[* ]Corresponding authors: Mohammadali Boroumand, Tehran Heart Center, North Karegar Ave. and Jalal-Al-Ahmad Cross, Tehran, Iran. E-mail: maboroumand@ 123456yahoo.com .

Mehrdad Behmanesh, Tarbiat Modares University, No.7, Jalal-Al-Ahmad Highway, Tehran, Iran. P.O. Box: 14115-154. E-mail: behmanesh@ 123456modares.ac.ir

Article

Publisher ID: BJBMS-16-114

DOI: 10.17305/bjbms.2015.942

PMC ID: 4852992

PubMed ID: 26773179

SO-VID: f19d75b2-48fa-487d-a074-633098c48d7e

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This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Cholesteryl ester transfer protein gene polymorphism (I405V) and premature coronary artery disease in an Iranian population

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Most cited references 31

Cholesteryl ester transfer protein TaqIB variant, high-density lipoprotein cholesterol levels, cardiovascular risk, and efficacy of pravastatin treatment: individual patient meta-analysis of 13,677 subjects.

Isolated low HDL cholesterol as a risk factor for coronary heart disease mortality. A 21-year follow-up of 8000 men.

Common genetic variation in multiple metabolic pathways influences susceptibility to low HDL-cholesterol and coronary heart disease.

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