Association of PvuII polymorphism in the lipoprotein lipase gene with the coronary artery disease in Macedonian population

Abstract

In the etiology of coronary artery disease there are many factors involved as a result of the complex interaction between genetic predisposition and environmental influences. The lipoprotein lipase (LPL) plays a very important role in lipid metabolism. It hydrolyzes the triglycerides in hylomicrones and very low density lipoproteins - VLDL. PvuII polymorphism in the LPL gene is a frequent variant and it increases triglyceride levels and the risk of the appearance of coronary arterial disease. Aim: The aim of this work is to show LPL-PvuII polymorphism as an independent risk factor and also as a predictor of coronary arterial disease in the Macedonian population. Material and methods: The study included 109 randomized patients with coronary artery disease (CAD) (83 males, 26 females), treated at the Cardiology Clinic. The stenosis of coronary arteries greater than 70% of the artery lumen was angiographically documented in the CAD group. The control group consisted of 32 patients (25 males, 7 females) with documented normal coronarographic findings. The patients' age ranged from 50 to 59; the mean age in the CAD group was 59.4 and the mean age in the control group was 57.9. LPL-PvuII polymorphism in the intron 6 in the CAD and control group was detected by PCR amplification and restriction enzyme digestion. Results: A statistically significant association between CAD and the control group was found regarding the presence of hyperlipidaemia (p < 0.001), diabetes (p < 0.05) and the use of antilipidaemic drugs (p < 0.049). The presence of LPL-PvuII polymorphism in both investigated groups does not represent a statistically significant risk factor for the appearance of coronary artery disease (p = 0.816). The PvuII + allele frequency of 0.495 and 0,469 was obtained in both the angiographically confirmed CAD and the control groups, respectively. This finding indicates no significant differences between the prevalence of the LPL-PvuII genotypes in both study groups, suggesting a lack of association of LPL-PvuII polymorphism with CAD. However, the homozygous genotype (PvuII +/+) was more prevalent in the CAD group (22.9%) in comparison with the control group (15.6%). Conclusion: In our study LPL-PvuII polymorphism was not identified as an independent risk factor for the appearance of CAD.