Increased plasminogen activator inhibitor-1 and apolipoprotein (a) in coronary atherectomy specimens in acute coronary syndromes

Citation
J. Shindo et al., Increased plasminogen activator inhibitor-1 and apolipoprotein (a) in coronary atherectomy specimens in acute coronary syndromes, CORON ART D, 12(7), 2001, pp. 573-579
Citations number
42
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
CORONARY ARTERY DISEASE
ISSN journal
0954-6928 → ACNP
Volume
12
Issue
7
Year of publication
2001
Pages
573 - 579
Database
ISI
SICI code
0954-6928(200111)12:7<573:IPAIAA>2.0.ZU;2-T
Abstract
Background Although increased tissue factor expression is known in vulnerab le plaques, there is no reported study to compare plaque fibrinolysis in st able and unstable plaques. This study investigates the extent of plasminoge n activator inhibitor-1 (PAI-1) and apolipoprotein (a) [apo(a)] in the plaq ues of different types of coronary artery disease as well as the correlatio n between these molecules and infiltration of macrophages to plaques. Methods Using immunohistochemical staining, we examined PAI-1 expression an d apo(a) deposition in coronary atherosclerotic specimens obtained by direc tional coronary atherectomy from 19 patients with acute myocardial infarcti on (AMI), 12 with unstable angina pectoris (UAP), and 13 with stable angina pectoris (SAP). The percentages of the total areas of specimens stained wi th PAI-1 or apo(a) were estimated by an NIH image program. The proportion o f macrophages as a percentage of all cells in plaques was calculated as the macrophage density. Results We found significantly higher percentages of total areas of specime ns stained with PAI-1 in AMI (25.5 +/-8.6%, P<0.001) and UAP (22.2<plus/min us>10.4%, P<0.005) than in SAP (9.5<plus/minus>5.0), as well as with apo(a) (AMI; 11.7 +/-7.1%, P<0.005, UAP; 11.1<plus/minus>5.5%, P<0.01 versus SAP; 3.9<plus/minus>1.5%). Linear regression analysis of all the samples showed a correlation between PAI-1 or apo(a) and macrophage density (PAI-1: r=0.7 5, P<0.001 and apo(a): r=0.56, P<0.001). Conclusions Our results suggest a possible contribution of increased PAI-1 and apo(a) in plaques to the pathogenesis of acute coronary syndromes inclu ding impaired fibrinolysis. Coronary Artery Dis 12:573-579 (C) 2001 Lippinc ott Williams & Wilkins.