title: Increased plasminogen activator inhibitor-1 and apolipoprotein (a) in coronary atherectomy specimens in acute coronary syndromes.
abstract: BACKGROUND
  Although increased tissue factor expression is known in vulnerable plaques, there is no reported study to compare plaque fibrinolysis in stable and unstable plaques. This study investigates the extent of plasminogen activator inhibitor-1 (PAI-1) and apolipoprotein (a) [apo(a)] in the plaques of different types of coronary artery disease as well as the correlation between these molecules and infiltration of macrophages to plaques.
  
  
  METHODS
  Using immunohistochemical staining, we examined PAI-1 expression and apo(a) deposition in coronary atherosclerotic specimens obtained by directional coronary atherectomy from 19 patients with acute myocardial infarction (AMI), 12 with unstable angina pectoris (UAP), and 13 with stable angina pectoris (SAP). The percentages of the total areas of specimens stained with PAI-1 or apo(a) were estimated by an NIH image program. The proportion of 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 specimens stained with PAI-1 in AMI (25.5 +/- 8.6%, P < 0.001) and UAP (22.2 +/- 10.4%, P < 0.005) than in SAP (9.5 +/- 5.0%), as well as with apo(a) (AMI; 11.7 +/- 7.1%, P < 0.005, UAP; 11.1 +/- 5.5%, P < 0.01 versus SAP; 3.9 +/- 1.5%). Linear regression analysis of all the samples showed a correlation between PAI-1 or apo(a) and macrophage density (PAI-1: r = 0.75, 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 including impaired fibrinolysis.
authors.affiliation: First Department of Internal Medicine, Fukushima Medical University, Fukushima, 960-1295, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Shindo
authors.forename: T
authors.initials: T
authors.lastname: Ishibashi
authors.forename: M
authors.initials: M
authors.lastname: Kijima
authors.forename: K
authors.initials: K
authors.lastname: Nakazato
authors.forename: K
authors.initials: K
authors.lastname: Nagata
authors.forename: K
authors.initials: K
authors.lastname: Yokoyama
authors.forename: A
authors.initials: A
authors.lastname: Hirosaka
authors.forename: E
authors.initials: E
authors.lastname: Sato
authors.forename: H
authors.initials: H
authors.lastname: Kunii
authors.forename: N
authors.initials: N
authors.lastname: Yamaguchi
authors.forename: N
authors.initials: N
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Saito
authors.forename: K
authors.initials: K
authors.lastname: Maehara
authors.forename: Y
authors.initials: Y
authors.lastname: Maruyama
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000378:metabolism*; D000789:Angina, Unstable / Q000378:metabolism; D001053:Apolipoproteins / Q000032:analysis*; D053241:Apoprotein(a); D017225:Atherectomy, Coronary; D003331:Coronary Vessels / Q000737:chemistry*; D005260:Female; D006651:Histocytochemistry; D006801:Humans; D017270:Lipoprotein(a) / Q000032:analysis*; D008264:Macrophages / Q000737:chemistry; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism*; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis*
chemical_list: D001053:Apolipoproteins; D017270:Lipoprotein(a); D017395:Plasminogen Activator Inhibitor 1; D053241:Apoprotein(a)