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Aim: Nitroglycerin-mediated vasodilatation (NMD) provides insight into the NTG-induced bioactivity of smooth muscle. It is plausible that in dysfunctional smooth muscle cells, the response to nitroglycerin may become blunted. The relationship between impaired brachial artery NMD and subsequent cardiovascular events is not well established. Methods: We examined brachial artery flow-mediated dilatation (FMD) and NMD using ultrasound in 93 subjects (71 7 years, including 26 with peripheral artery disease (PAD), 37 with aortic aneurysms, 10 with PAD complicated with aneurysms, and 20 without evident arterial disease). Brachial artery responses to hyperemia and nitroglycerin were measured every minute after cuff deflation and nitroglycerin administration. Time courses of vasodilatation were assessed and maximal FMD and NMD were measured. Results: The time courses in response to NTG were sigmoidal and maximal diameter reached 7.2 1.6 minutes after NTG was administered sublingually. The mean FMD was 2.3±2.0% and the mean NMD was 17.6 7.1%. Subjects were prospectively followed for an average of 47 13 months. Eighteen subjects had an event during follow-up; events included myocardial infarction (five), unstable angina pectoris (four), stroke (two), aortic dissection (one), ruptured aortic aneurysm (three), symptomatic abdominal aortic aneurysm (two), and lower limb ischemia requiring revascularization (one). NMD and FMD were significantly lower in subjects with events than in those without an event. In a Cox proportional-hazards model, lower FMD as well as lower NMD independently predicted future cardiovascular events. Conclusion: Brachial artery nitroglycerin-mediated vasodilatation may add information to conventional risk stratification.