Objective-Reactive hyperemia is the compensatory increase in blood flow that occurs after a period of tissue ischemia, and this response is blunted in patients with cardiovascular risk factors. Key Words: endothelium Ⅲ cardiovascular risk Ⅲ surrogate markers Ⅲ reactive hyperemia Ⅲ flow-mediated dilation R eactive hyperemia is a complex response that occurs after a period of tissue ischemia and primarily depends on local production of adenosine and other non-endothelium-dependent vasodilators that dilate tissue microvessels. 1 Studies in humans have shown that endothelium-derived nitric oxide also contributes to reactive hyperemia. 2,3 Peak brachial artery hyperemic flow velocity after 5-minute cuff occlusion of the arm relates inversely to traditional cardiovascular disease risk factors 4 and to markers of inflammation 5 in the Framingham Heart Study. Smaller scale mechanistic studies suggest that the nitric oxide-dependent component of reactive hyperemia may be particularly affected by risk factors. 3 The relation of reactive hyperemia to the incidence of cardiovascular disease events in atherosclerosis has not been previously studied.

Giant cell arteritis is a relatively common form of systemic vasculitis, best known for its predisposition to affect the extracranial branches of the carotid artery and associated potential for visual loss. Additional vascular manifestations include stroke, aortic aneurysm or dissection, and even aortic rupture. Cardiac manifestations include coronary artery disease, aortic valve insufficiency, or left ventricular dysfunction, which may occur independently from the valvular disease or hypertension. Physicians need to be vigilant for this disorder, particularly because the tragic end-organ outcomes such as visual loss can be effectively prevented with early use of corticosteroids. We review the pathophysiology and clinical manifestations of giant cell arteritis and present a rationale for diagnosis and therapy for this disease.

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