Abstract
The endothelial dysfunction has been implicated as a major event in the pathogenesis of atherosclerosis. Therefore, this study was planned to determine (a) role of endothelium-derived nitric oxide (NO) and endothelin as coronary artery disease (CAD) risk markers and (b) intergenotypic variation of endothelial nitric oxide synthase (eNOS) Glu298Asp polymorphism in CAD.The endothelin, NO and eNOS genotypes were determined in 60 patients with documented history of CAD. These were compared with 50 age- and sex- matched healthy controls. The genotype frequencies for eNOS gene polymorphism were determined by PCR and RFLP. The plasma endothelin in CAD patients was significantly higher (p< 0.001) whereas, the NO level in CAD group was significantly lower (p< 0.001) than the control group. The genotype frequencies for Glu298/Asp (Glu/Glu and Glu/Asp) genotypes were 75% and 25% in CAD subjects and 88% and 12% in control subjects, respectively. No Asp/Asp was found in any of the groups. The genotype frequencies differed significantly (p< 0.05) between the controls and cases. In conclusion, endothelin and NO may be used as markers of endothelial dysfunction in CAD. Asp allele might be a risk factor for CAD in the North Indian population.
Highlights
Coronary artery disease (CAD) is described as our modern “epidemic”
The nitric oxide (NO) level was found out to be significantly lower in the CAD group than in the control group (p < 0.001) whereas endothelin was significantly higher in the CAD patients as compared to the healthy controls (p < 0.001)
We attempted to investigate the frequency of endothelial nitric oxide synthase (eNOS) Glu298Asp polymorphism along with usefulness of some novel biomarkers in patients of CAD
Summary
Coronary artery disease (CAD) is described as our modern “epidemic”. Studies suggest that most CAD event rates are noted in individuals with one or more CAD risk factors [2]. At least 25 percent of coronary patients have sudden death or myocardial infarction without prior symptoms [3]. There is a need to focus attention on additional markers to predict coronary risk. It is well accepted that endothelial dysfunction occurs in response to cardiovascular risk factors and precedes the development of atherosclerosis [4]. In this study, we have investigated some of the factors which are considered to play a pivotal role in the maintaining endothelial homeostasis – nitric oxide (NO), endothelium derived bioactive peptide endothelin and G894T variant of endothelial nitric oxide synthase (eNOS) gene polymorphism
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