Influence of menopause on biochemical markers of endothelial dysfunction—A case–control pilot study in North Indian population

ObjectiveMenopause, an estrogen deficient state, is known to increase the cardiovascular risk. Lipid changes accompanying menopause account for only few cases of coronary artery disease (CAD). Endothelium-dependent nitric oxide-mediated vasodilatory mechanisms are also known to play a role in development of coronary artery disease, but studies in menopausal women are very few. This study was hence undertaken to see if nitric oxide (NO)–cyclic guanidine monophosphate (c-GMP) pathway is influenced by menopause.DesignThis study was a hospital-based case–control study involving 100 women in age group 40–55 years. Of these, 50 women were postmenopausal and 50 were premenopausal. Women with known risk factors for CAD were excluded. Fasting blood samples from these women were collected and analyzed for estradiol levels, lipid profile, apolipoprotein B, plasma nitric oxide, c-GMP and platelet nitric oxide using standard kits and reagents. Statistical analysis was done on SPSS and two-tailed p-value <0.05 was considered significant.ResultPostmenopausal women had significantly lower estradiol, plasma NO, and c-GMP levels as compared to premenopausal women (p < 0.05). Cholesterol, low-density lipoprotein (LDL) cholesterol and apolipoprotein B (apo-B) levels were higher and HDL levels were lower in postmenopausal as compared to premenopausal women (p < 0.05). Plasma NO showed a significant positive correlation with estradiol, HDL levels and negative correlation with apo-B levels.ConclusionMenopause tends to downregulate NO–c-GMP pathway resulting in endothelial dysfunction. The mechanism may be directly through estrogen receptors or indirectly through potentiation of dyslipidemia.