Angioscopic follow-up study of coronary ruptured plaques in nonculprit lesions

被引:95
作者
Takano, M [1 ]
Inami, S [1 ]
Ishibashi, F [1 ]
Okamatsu, K [1 ]
Seimiya, K [1 ]
Ohba, T [1 ]
Sakai, S [1 ]
Mizuno, K [1 ]
机构
[1] Chiba Hokusoh Hosp, Dept Internal Med, Nippon Med Sch, Chiba 2701694, Japan
关键词
D O I
10.1016/j.jacc.2004.09.077
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVES Changes of ruptured plaques in nonculprit lesions were evaluated using coronary angioscopy. BACKGROUND The concept of multiple coronary plaque ruptures has been established. However, no detailed follow-up studies of ruptured plaques in nonculprit lesions have yet been reported. METHODS Forty-eight thrombi in 50 ruptured coronary plaques in nonculprit lesions in 30 patients were identified by angioscopy. The percent diameter stenosis (%DS) at the target plaques on quantitative coronary angiographic analysis and the serum C-reactive protein (CRP) level were measured. RESULTS The mean angioscopic follow-up period was 13 +/- 9 months. Thirty-five superimposed thrombi still remained at follow-up, and the predominant thrombus color changed from red (56%) at baseline to pinkish-white (83%) at follow-up. The healing rate increased according to the angioscopic follow-up period (23% at > 12 months vs. 55% at > 12 months, p = 0.044). The %DS at the healed plaque increased from baseline to follow-up (12.3 +/- 5.8% vs. 22.7 +/- 11.6%, respectively; p = 0.0004). The serum CRP level in patients with healed plaques (n = 10) was lower than that in those without healed plaques (n = 19; 0.07 +/- 0.03 mg/dl vs. 0.15 +/- 0.11 mg/dI, respectively, p = 0.007). CONCLUSIONS The present study demonstrated that: 1) ruptured plaques in nonculprit lesions tend to heal slowly with a progression of angiographic stenosis; and 2) the serum CRP level might reflect the disease activity of the plaque ruptures. (C) 2005 by the American College of Cardiology Foundation.
引用
收藏
页码:652 / 658
页数:7
相关论文
共 27 条
[1]   PROCOAGULANT HUMAN MONOCYTES MEDIATE TISSUE FACTOR FACTOR VIIA-DEPENDENT PLATELET-THROMBUS FORMATION WHEN EXPOSED TO FLOWING NONANTICOAGULATED HUMAN BLOOD [J].
BARSTAD, RM ;
HAMERS, MJAG ;
KIERULF, P ;
WESTVIK, AB ;
SAKARIASSEN, KS .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1995, 15 (01) :11-16
[2]  
Burke AP, 2001, CIRCULATION, V103, P934
[3]   CORONARY PLAQUE DISRUPTION [J].
FALK, E ;
SHAH, PK ;
FUSTER, V .
CIRCULATION, 1995, 92 (03) :657-671
[4]   Coronary plaque erosion without rupture into a lipid core - A frequent cause of coronary thrombosis in sudden coronary death [J].
Farb, A ;
Burke, AP ;
Tang, AL ;
Liang, YH ;
Mannan, P ;
Smialek, J ;
Virmani, R .
CIRCULATION, 1996, 93 (07) :1354-1363
[5]   How big are coronary atherosclerotic plaques that rupture? [J].
Fishbein, MC ;
Siegel, RJ .
CIRCULATION, 1996, 94 (10) :2662-2666
[6]   Intravascular ultrasound assessment of ulcerated ruptured plaques - A comparison of culprit and nonculprit lesions of patients with acute coronary syndromes and lesions in patients without acute coronary syndromes [J].
Fujii, K ;
Kobayashi, Y ;
Mintz, GS ;
Takebayashi, H ;
Dangas, G ;
Moussa, I ;
Mehran, R ;
Lansky, AJ ;
Kreps, E ;
Collins, M ;
Colombo, A ;
Stone, GW ;
Leon, MB ;
Moses, JW .
CIRCULATION, 2003, 108 (20) :2473-2478
[7]   MECHANISMS OF DISEASE - THE PATHOGENESIS OF CORONARY-ARTERY DISEASE AND THE ACUTE CORONARY SYNDROMES .1. [J].
FUSTER, V ;
BADIMON, L ;
BADIMON, JJ ;
CHESEBRO, JH .
NEW ENGLAND JOURNAL OF MEDICINE, 1992, 326 (04) :242-250
[8]  
FUSTER V, 1992, NEW ENGL J MED, V326, P310
[9]   Atherosclerosis: The road ahead [J].
Glass, CK ;
Witztum, JL .
CELL, 2001, 104 (04) :503-516
[10]   Multiple complex coronary plaques in patients with acute myocardial infarction. [J].
Goldstein, JA ;
Demetriou, D ;
Grines, CL ;
Pica, M ;
Shoukfeh, M ;
O'Neill, WW .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (13) :915-922