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
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.