title: Angiotensin II type 1 receptor blockers do not promote coronary collateral circulation in patients with coronary artery disease.
abstract: We previously reported that angiotensin-converting enzyme inhibitors (ACE-Is) promote collateral circulation in patients with coronary artery disease (CAD). There have been many reports on the beneficial effects of angiotensin II type 1 receptor blockers (ARBs) on the cardiac microvasculature. Therefore, the following studies were performed to evaluate the association between treatment with an ARB and the enhancement of coronary collateral circulation as assessed by the Rentrop Score (RS) (Study 1) and to compare these results to those obtained with an ACE-I (Study 2). The subjects were 456 patients with angina who underwent coronary angiography. Study 1: Those who had one (1-V), two (2-V) or three significantly stenosed vessels (3-V) and who received only an ARB without any other anti-hypertensive medication were defined as the ARB group (n=81), and age-, sex- and body mass index-matched subjects (n=146) were selected as a comparative group. There were no significant differences in the percentage of patients with RS>or=1 between the two groups. Study 2: Those who received an ACE-I as the only anti-hypertensive treatment were defined as the ACE-I group (n=67), which was matched to the ARB group in Study 1. The percentage of patients with RS>or=1 in the ACE-I group was significantly higher than that in the ARB group as assessed by a Cochran-Mantel-Haenszel analysis. In addition, patients with 3-V disease who were treated with an ACE-I, but not an ARB, were most likely (odds ratio [confidence Interval]): 27.7 [4.8-161.0]) to show enhanced collateral circulation, as assessed by a multiple logistic regression analysis. These results suggest that treatment with an ACE-I, but not treatment with an ARB, was associated with the enhancement of collateral circulation in patients with CAD.
authors.affiliation: Department of Cardiology, Fukuoka University School of Medicine, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Imaizumi
authors.forename: Shin-ichiro
authors.initials: S
authors.lastname: Miura
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Nishikawa
authors.forename: Atsushi
authors.initials: A
authors.lastname: Iwata
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.forename: Akira
authors.initials: A
authors.lastname: Kawamura
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Tsuchiya
authors.forename: Koichiro
authors.initials: K
authors.lastname: Kumagai
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Matsuo
authors.forename: Keijiro
authors.initials: K
authors.lastname: Saku
mesh_terms: D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology* / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D003097:Collateral Circulation / Q000187:drug effects*; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000503:physiopathology; D003326:Coronary Circulation / Q000187:drug effects*; D023921:Coronary Stenosis / Q000188:drug therapy / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D012189:Retrospective Studies
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors