Does the Nitric Oxide Synthase T786C Gene Polymorphism Influence Arterial Stiffness in Patients with Metabolic Syndrome?

Abstract

Background: Endothelial Nitric Oxide Synthase (eNOS) is responsible for Nitric Oxide (NO) bioavailability at endothelial level. Aging (even in healthy people) is involved in arterial stiffness increases. Materials and Methods: We investigated (in the service of Cardiology, 4th Medical Clinic) 100 patients, 55 with metabolic syndrome (MS), mean age 56.91 ± 14.39 years, 66% women. Identification of the T786C polymorphism was performed by enzymatic digestion of the fragment obtained by polymerase chain reaction (PCR) amplification. Evaluation of arterial parameters (aortic pulse wave velocity (PWV), as a measure of arterial stiffness and aortic [AixAo] and brachial [Aixb] augmentation index) was performed with the TensioMed ™ Arteriograph. Results: Regarding T786C polymorphism, the distribution was the following: 57% did not have the mutation (TT), 30% were heterozygous, 13% were homozygous (CC). Patients with MS more frequently had C allele (54.5% vs. 28.9% in those without MS) and CC state (16.4% vs. 8.9%, p-NS). Significant differences (p = 0.005) regarding PWV were found in TT patients vs. heterozygous CT vs. homozygous CC: 9.75 ± 1.75 m/s vs. 9.86 ± 1.56 m/s vs. 11.65 ± 1.87 m/s. In case of the other parameters, no significant differences were found (AixAo, p = 0.35; Aixb, p = 0.22; pulse pressure, p = 0.14), but CC patients presented higher values. Conclusion: Arterial stiffness is influenced by eNOS gene polymorphisms, being a possible link between the increase in cardiovascular risk and presence of metabolic syndrome in these patients.