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Titolo:
Increased plasminogen activator inhibitor-1 and apolipoprotein (a) in coronary atherectomy specimens in acute coronary syndromes
Autore:
Shindo, J; Ishibashi, T; Kijima, M; Nakazato, K; Nagata, K; Yokoyama, K; Hirosaka, A; Sato, E; Kunii, H; Yamaguchi, N; Watanabe, N; Saito, T; Maehara, K; Maruyama, Y;
Indirizzi:
Fukushima Med Univ, Dept Internal Med 1, Fukushima 9601295, Japan Fukushima Med Univ Fukushima Japan 9601295 d 1, Fukushima 9601295, Japan Hoshi Gen Hosp, Div Pathol, Koriyama, Fukushima 9638501, Japan Hoshi Gen Hosp Koriyama Fukushima Japan 9638501 Fukushima 9638501, Japan Hoshi Gen Hosp, Ctr Cardiovasc, Koriyama, Fukushima 9638501, Japan Hoshi Gen Hosp Koriyama Fukushima Japan 9638501 Fukushima 9638501, Japan
Titolo Testata:
CORONARY ARTERY DISEASE
fascicolo: 7, volume: 12, anno: 2001,
pagine: 573 - 579
SICI:
0954-6928(200111)12:7<573:IPAIAA>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN ATHEROSCLEROTIC LESIONS; SMOOTH-MUSCLE CELLS; TISSUE-FACTOR; MYOCARDIAL-INFARCTION; UNSTABLE ANGINA; PLAQUE RUPTURE; HEART-DISEASE; EXPRESSION; LIPOPROTEIN(A); MACROPHAGES;
Keywords:
acute coronary syndromes; plasminogen activator inhibitor-1; apolipoprotein (a); macrophages; smooth muscle cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Maruyama, Y Fukushima Med Univ, Dept Internal Med 1, 1 Hikarigaoka, Fukushima 9601295,Japan Fukushima Med Univ 1 Hikarigaoka Fukushima Japan 9601295apan
Citazione:
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

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<plus/minus>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=0.75, P<0.001 and apo(a): r=0.56, P<0.001). Conclusions Our results suggest a possible contribution of increased PAI-1and apo(a) in plaques to the pathogenesis of acute coronary syndromes including impaired fibrinolysis. Coronary Artery Dis 12:573-579 (C) 2001 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 00:33:14