Atherosclerosis 155 (2001) 187 – 193 Endothelial function of the popliteal artery in patients with coronary artery disease Peter Angerer *, Christian Negut, Stefan Sto ¨ rk, Clemens von Schacky Medizinische Klinik, Klinikum der Uniersita ¨t Mu ¨nchen -Innenstadt, Ziemssenstraße 1, 80336 Munich, Germany Received 24 November 1999; received in revised form 19 April 2000; accepted 28 April 2000 Abstract Coronary artery disease (CAD) is associated more closely with atherosclerosis in the popliteal than in the brachial artery. This case – control study aimed at clarifying whether endothelial dysfunction of patients with CAD can be detected non-invasively in the popliteal artery by means of ischemia-induced flow-mediated dilation (FMD) and cold pressor reaction (CPR), and how it compares with the brachial artery. We further investigated a new mode of evaluation of the CPR. Eleven cases with CAD were compared with 16 matched healthy controls. Popliteal and brachial arterial diameter was monitored by ultrasound for 20 min following ischemia and cold pressor. For CPR, the difference between maximum and minimum diameter was defined as maximum vasomotion. In the popliteal artery, maximum vasomotion and FMD were significantly smaller in cases than in controls, the difference being more pronounced than in the brachial artery, where only maximum vasomotion was significantly smaller. After exclusion of current smokers, only the difference in maximum vasomotion of both arteries remained significant. We conclude that maximum vasomotion may be more sensitive for detection of endothelial dysfunction than FMD. Endothelial dysfunction in patients with CAD is more pronounced in the popliteal artery than in the brachial artery. © 2001 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Endothelial function; Vasomotion; Flow-mediated dilation; Cold pressor reaction; Coronary artery disease; Non-invasive; Ultrasound www.elsevier.com/locate/atherosclerosis 1. Introduction Coronary artery disease (CAD) is characterized by endothelial dysfunction in stenotic coronary arteries [1], in angiographically normal coronary arteries [2], and in peripheral muscular arteries [3 – 6]. Dysfunction in pe- ripheral and in coronary arteries are closely related [7,8]. Endothelial function can be studied non-inva- sively in peripheral arteries as vasomotion, i.e. change of vessel diameter in reaction to an endothelium-depen- dent stimulus. Physiological flow-mediated dilation (FMD) following occlusion of the artery for several minutes is reduced or absent in patients with CAD [3,4,9]. Immersion of the hand in iced water, termed the cold pressor test, stimulates the sympathetic system [10,11]. Dependent on endothelial function, it causes dilation of normal arteries, but constriction of atherosclerotic coronary arteries [10,12,13]. By contrast, peripheral conduit arteries of healthy persons constrict in response to cold pressor [9,14] or dilate [4], depend- ing on the time point of measurement. In a previous investigation of the brachial artery [15], we found both dilation and constriction in reaction to cold pressor during a prolonged observation period. The brachial artery is the standard vessel for non-invasive evaluation of FMD and the cold pressor reaction (CPR). The grade of atherosclerotic lesion severity in the brachial artery and coronary arteries is significantly correlated in autopsy, but clinically relevant stenosis in the brachial artery is rare [16]. By contrast, there is a strong association between clinically relevant CAD and pe- ripheral vascular disease of leg arteries, e.g. the popliteal artery [17,18]. We used a case–control design to study endothelial function of popliteal and brachial artery by FMD and CPR in patients with a high likelihood of endothelial dysfunction from documented CAD and corresponding * Corresponding author. Tel.: +49-89-51607632; fax: +49-89- 51603374. E-mail address: pangerer@medinn.med.uni-muenchen.de (P. An- gerer). 0021-9150/01/$ - see front matter © 2001 Elsevier Science Ireland Ltd. All rights reserved. PII:S0021-9150(00)00536-0