Lcat gene polymorphism and related inflammatory biomarkers in coronary artery disease

Coronary artery disease (CAD) is one of the leading causes of death both in our country and worldwide. The enzyme Lecithin Cholesterol Acyltransferase (LCAT) is an essential protein and changes in the activity of this protein are implicated in the development of CAD. Cytokines such as interleukin-6 (IL-6) and acute phase reactants such as high-sensitivity C-reactive protein (hsCRP) appear to be strong predictors in CAD. The aim of present study was to identify role of LCAT gene polymorphism in patients with CAD and to investigate relationship between LCAT gene polymorphism and inflammatory biomarkers found to be important in the etiology of disease. The study included 200 patients aged 18-80 years who were diagnosed as CAD based on angiography and 100 healthy subjects who were proven to have no CAD by angiography. Serum IL-6, LCAT and hsCRP levels were measured by ELISA method. In DNA samples isolated from patients in the study population, LCAT gene polymorphism (608 C/T and 4886 C/T) were studied by PCR using appropriate oligonucleotide primers. Tryglyceride, hsCRP and IL-6 levels were found to be significantly higher while HDL and LCAT levels were found to be significantly lower in CAD group when compared to control group. When LCAT 4886 C/T gene polymorphism was assessed, there was homozygous genotype in 55, heterozygous genotype in 33 and mutant genotype in 12 of the controls, while there was homozygous genotype in 23, heterozygous genotype in 30 and mutant genotype in 17 of 70 patients with single-vessel disease. However, there was homozygous genotype in 35, heterozygous genotype in 60 and mutant genotype in 35 of 130 patients with multi-vessel disease. In conclusion, lower serum LCAT levels and higher frequency of TT genotype, the mutant genotype in LCAT 4886 position, in CAD indicate the role of LCAT in CAD pathogenesis.