Association of vaspin rs2236242 gene variants and circulating serum vaspin concentrations with coronary artery disease in a Turkish population.

Coronary artery disease (CAD) is the primary cause of death worldwide. Vaspin was a recently described adipokine, playing a protective role in many metabolic and cardiovascular diseases. This study aimed to assess the relation of serum vaspin levels and vaspin rs2236242 polymorphisms with CAD. The study included 105 healthy subjects and 105 CAD patients. Serum vaspin concentrations and vaspin rs2236242 polymorphisms were determined by enzyme-linked immunosorbent assay and polymerase chain reaction, respectively. There was a statistically significant difference between the genotypes of CAD patients (TT 26.7%, TA 71.4%, and AA 1.9%) and controls (TT 70.5%, TA 28.6%, and AA 1%; χ2 = 40.3; df = 2; p = .000). The TA genotype increased the risk of CAD (odds ratio [OR] = 6.60; 95% confidence interval [CI] = 3.60-12.1; p = .000) as compared to the TT genotype. There was a statistically significant difference between the allelic distribution of CAD patients (T 62.4% and A 37.6%) and controls (T 84.8% and A 15.2%; χ2 = 27.0; df = 1; p = .000). Those carrying the A allele had a higher risk of CAD compared to those with the T allele (OR = 3.35; 95% CI = 2.10-5.36; p = .000). The serum vaspin concentrations of the patients with TT, TA, and AA genotypes were 30.4 ± 1.72, 28.4 ± 2.89, and 36.4 ± 6.38 pg/ml, respectively, and there was no significant difference between the serum vaspin levels and vaspin genotypes (p = .696). All of the above suggested that the vaspin rs2236242 polymorphism was associated with CAD in the Turkish population.

APJ receptor A445C gene polymorphism in Turkish patients with coronary artery disease.

Coronary artery disease (CAD) is a disease in which a waxy substance called plaque builds up inside the coronary arteries. Apelin is a novel endogenous peptide with inotropic and vasodilatory properties and is the ligand for the angiotensin receptor-like 1 (APJ) receptor. We aimed to determine genotype and allele frequencies of APJ receptor A445C gene polymorphism in Turkish patients with CAD and healthy controls by RFLP-PCR. This study was performed on 159 unrelated CAD patients and 62 healthy controls. We obtained AA, AC and CC genotype frequencies in CAD patients as 41.5%, 49.1% and 9.4%, respectively. In the control group, frequencies of genotypes were found as 35.5% for AA, 48.4% for AC and 16.1% for CC. We did not observe difference in APJ receptor A445C polymorphism between CAD patients and healthy controls (χ(2) = 2.178; df = 2; P = 0.336). The A allele was encountered in 66% (210) of the CAD and 59.7% (74) of the controls. The C allele was seen in 34% (108) of the CAD and 40.3% (50) of the controls. Allele frequencies of interested genes were not significantly different between groups (χ(2) = 1.57; df = 1; p = 0.225). The frequencies of APJ receptor A445C genotype were not significantly different between control and patients. None of the three APJ receptor A445C genotypes, AA, AC and CC displayed significant difference in CAD patients. We did not find any difference in the clinical parameters except for weight and diastolic blood pressure levels in the AA, AC and CC genotypes of patients. Individuals with CC genotypes had significantly higher weight, systolic and diastolic blood pressure levels and systolic blood pressure than other genotypes, P ≤ 0.05. In addition, HDL-C level was found decreased, but this reduction was not statistically significant. Contrarily, the low levels of weight, SBP, DBP and TC were statistically significant in the subjects with AA genotype in CAD. In conclusion, CC genotype carriers may have more risk than other genotypes in the development of hypertension in CAD, but not AAgenotype carriers. We suggest that this polymorphism may not be a marker of CAD, but it may cause useful in function of the apelin/APJ system and may be a genetic predisposing factor for diagnostic processes and can be helpfull in finding new treatment strategies. We think that it is required to further comprehensive studies in order to make clear this situation in CAD.

Characterization of the apelin -1860T>C polymorphism in Turkish coronary artery disease patients and healthy individuals.

To evaluate the association between the apelin -1860T>C polymorphism and plasma apelin levels in Turkish patients with coronary artery disease (CAD). A total of 276 individuals were enrolled in the present study, including 158 patients with CAD and 118 individuals without CAD as controls. The presence of the apelin -1860T>C gene polymorphism and plasma apelin levels were determined using polymerase chain reaction/restriction fragment length polymorphism and enzyme-linked immunosorbent assay, respectively. Significance was set at p≤0.05 for all statistical analyses. The genotype and allele frequencies of interested genes were significantly different between groups (χ(2)=10.2; df=2; p=0.006 and χ(2)=13.4; df=1; p=0.000, respectively). Frequency of CC genotype and the C allele of -1860T>C site was significantly higher in CAD patients compared to healthy controls. We found that individuals with the TC and CC genotypes were associated with an increased risk of CAD when compared with the TT genotype in CAD patients, and the adjusted ORs (95% CI) were 6.50 (1.27-33.0) and 6.39 (1.77-23.0), respectively. Plasma apelin levels were significantly lower in CAD patients compared to control group. Apelin level of CAD patient group having CC genotype of -1860T>C site was significantly lower compared to those having TT genotypes, but it was not statistically significant (p > 0.05). The homozygous CC genotype of apelin gene is associated with high risk of CAD. Apelin gene polymorphism -1860T>C is a significant predictor of predisposition to CAD in in Turkish population.