Patients with diabetes mellitus are known to be at increased risk for coronary artery disease and myocardial infarction, and have worse outcomes after coronary interventions such as stenting. 1 The mechanisms for this increased risk are not fully known, but are thought to reflect vascular abnormalities of inflammation, hypertension, dyslipidemia, and hypercoagulability. 2 In turn, these vascular abnormalities may be the result of hyperglycemia, insulin resistance, and advanced glycation products seen in diabetes. 3, 4 However, the precise molecular links between the metabolic abnormalities seen in diabetes, and the resulting vascular changes that increase propensity for atherosclerosis are not clearly understood.

One such link is endothelial dysfunction, seen in diabetes, obesity, hypertension, hyperlipidemia, smoking, and aging. 5, 6 Endothelial dysfunction is characterized by defects in the normal vascular relaxation response to mediators such as acetylcholine, or to increased blood flow. This can be clinically measured by ultrasound studies of forearm blood flow responses. The basis for endothelial dysfunction may involve a reduction in the amount of bioavailable nitric oxide (NO) in the vasculature. NO is necessary for vascular relaxation and endothelium dependent relaxing factor (EDRF) activity. 7, 8 NO also serves to suppress atherosclerosis by reducing endothelial cell activation, smooth muscle proliferation, leukocyte activation and leukocyte-endothelial interactions, and platelet aggregation and adhesion. 9–12 Therefore, reduction in the amount of bioavailable NO would result in a proatherogenic state.