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Thanyasiri, Panuratn, David S. Celermajer, and Mark R. Adams. Endothelial dysfunction occurs in peripheral circulation in patients with acute and stable coronary artery disease. Am J Physiol Heart Circ Physiol 289: H513-H517, 2005; doi:10.1152/ajpheart.01086.2004.-Atherosclerosis is a diffuse, systemic process. In addition, acute coronary syndromes (ACS) are associated with inflammatory marker elevations that are hypothesized to affect the function of nonculprit coronary as well as peripheral vessels. We investigated whether femoral vascular reactivity and/or fibrinolytic capacity are impaired in ACS patients over and above any dysfunction associated with stable coronary artery disease. Patients undergoing diagnostic coronary angiography (n ϭ 42 total, 14 patients/group) were recruited into three groups as follows: 1) stable coronary syndromes (SAP group), 2) ACS as defined by rest angina with ECG changes and troponin rise (ACS group), and 3) angiographically normal coronary arteries (control group). After diagnostic coronary angiography, femoral artery endothelial and smooth muscle function were assessed by infusing acetylcholine (ACh) and nitroglycerin (GTN), and tissue-type plasminogen activator (t-PA) release across the femoral circulation was measured as the difference between arterial and venous concentrations before and after ACh and GTN stimulation. There were no significant differences between groups in relevant baseline characteristics apart from significantly higher C-reactive protein levels and reduced net t-PA release in the ACS group at baseline (P Ͻ 0.05). The ACS and SAP groups had equivalent angiographic severity of coronary artery disease. Endothelium-dependent dilatation was significantly higher in control individuals (14.9 Ϯ 9.1%; P Ͻ 0.001) compared with either stable patients (2.3 Ϯ 8.1%) or those with unstable syndromes (2.6 Ϯ 8.9%, who were similar to each other; P ϭ not significant). Although baseline t-PA release was impaired in the ACS patients (0.09 Ϯ 0.06 compared with 0.39 Ϯ 0.33 and 0.49 Ϯ 0.56 ng/ml; P ϭ 0.03), stimulation of t-PA release by ACh and GTN occurred only in the control subjects and not in the ACS or SAP patients. Coronary artery disease is associated with impaired endothelium-dependent dilatation and impaired stimulation of t-PA release in the systemic circulation. These aspects of endothelial dysfunction, however, were equally severe in acute and chronic coronary syndrome patients.tissue-type plasminogen activator; nitroglycerin; acetylcholine; cardiac inflammation; thromboresistance; vasodilation ACUTE CORONARY SYNDROMES OCCUR when coronary atherosclerotic plaques become unstable with lesion rupture and/or subsequent thrombosis (12). In recent years, it has become apparent that this process is largely an inflammatory one that involves the interaction of leukocytes, cytokines, and endothelium (13). It has been hypothesized that this inflammatory activation with systemic cytokine release may lead to distant endothelial dysfunction in nonculprit coronary as well as per...

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FMD occurs in human coronary arteries following restoration of flow. The magnitude of FMD appears related to vascular risk factors and their treatment.