Introduction. Asymmetric dimethylarginine (ADMA) is a nonselective nitric oxide (NO) synthase inhibitor associated with cardiovascular and metabolic disorders. ADMA plays an important role in the regulation of vascular tone by acting as an endogenous inhibitor of NO synthesis. Objectives. This study aimed to investigate ADMA with respect to diabetes and its clinical relevance as an independent predictor of CAD (Coronary Artery Disease). Methodology. The present case control study includes two hundred and forty patients selected randomly. Serum ADMA was analyzed by using enzyme immunoassay for the quantitative determination of endogenous ADMA, and serum nitric oxide was estimated by the method of Cortes. Results. Elevated NO level levels was a strong predictor and significantly ( : 9.86, ) associated with occurrence of CAD. Increased ADMA level was found to be another strong predictor and associated significantly ( : 8.02, ) with CAD. On intra group analysis, the relationship between ADMA and NO in diseased group, is significant negative correlation ( ). (0.001) was found between ADMA and NO. Conclusion. ADMA level was found to be one of the strong predictors for CAD. ADMA is an emerging independent risk marker for future CVD (cardiovascular disease) events. 1. Introduction Cardiovascular disease (CVD) is the major cause of morbidity and mortality in patients with diabetes mellitus (DM). Diabetes is at high risk for several cardiovascular disorders: coronary heart disease, stroke, peripheral arterial disease, cardiomyopathy, and congestive heart failure [1–3]. Endothelial dysfunction is a common feature in diabetic patients and may contribute to cardiovascular morbidity [4–6]. Mechanisms of diabetes-induced endothelial dysfunction include the production of prostanoid vasoconstrictors and the increased oxidative degradation of NO [7, 8]. Deficiency of NO increases vascular resistance and promotes atherogenesis [9]. Nitric oxide (NO) is a very active but short lived, a molecule that is released into the circulation from endothelial cells. It is a potent vasodilator that regulates vascular resistance and tissue blood flow. In addition, NO inhibits key processes of atherosclerosis, such as monocyte endo-thelial adhesion, platelet aggregation, and vascular smooth muscle cell proliferation. Hence, endothelial dysfunction due to reduced NO availability is an early step in the course of atherosclerotic vascular disease [10]. NO is synthesized by stereospecific oxidation of the terminal guanidino nitrogen of the amino acid, L-arginine, by the action of a family
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