The role of endothelin-1 and nitric oxide affecting endothelial dysfunction in the etiopathogenesis of ischaemic heart disease

Abstract

Introduction: Endothelial dysfunction is an imbalance in bioavailability of endothelium-derived relaxing (Nitric Oxide) and contracting factors (Endothelin). Studies have shown that NO has antiatherogenic property as it inhibits vascular smooth muscle contraction and proliferation, platelet aggregation and leukocyte adhesion. On the other hand, Endothelin-1 causes proliferation and vasoconstriction of myocytes resulting in elevated vascular tone thereby contributing to endothelial dysfunction. This dysfunction is a well-established response to cardiovascular risk factors and precedes the development of atherosclerosis. As a result, status of an endothelial dysfunction may reflect the propensity to develop atherosclerotic disease and may serve as a marker of an unfavourable cardiovascular prognosis. Materials and Methods: 50 cases of angiographically proven ischemic heart disease and 50 age and sex matched patients with no evidence of ischaemic heart disease on angiography were selected from G.B Pant Hospital, New Delhi, India. Serum levels of Endothelin were estimated by sandwich ELISA and nitric oxide levels by modified Griess reaction. Results: Serum levels of Endothelin were raised while nitric oxide levels were significantly reduced (p=0.049) in the cases as compared to controls. The mean plasma nitric oxide level in the study group (cases) was 23.51±13.48 µM and in the control group was 29.35±15.73 µM. The difference between the two was significant (p=0.049*). The mean plasma endothelin level in the study group was 3.04±1.37fmol/ml and in the control group was 2.95±1.70 fmol/ml. The difference between the two was not significant (p = 0.764). Conclusion: Higher Endothelin-1 and lower NO levels in cases suggest their role in causing endothelial dysfunction in ischemic heart disease patients. However, larger sample size is required to assess the role of Endothelin as a biomarker of endothelial dysfunction in patients of ischemic heart disease.