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J Am Coll Cardiol, 2005; 45:652-658, doi:10.1016/j.jacc.2004.09.077 © 2005 by the American College of Cardiology Foundation |
Department of Internal Medicine, Chiba-Hokusoh Hospital, Nippon Medical School, Chiba, Japan
Manuscript received June 3, 2004; revised manuscript received September 8, 2004, accepted September 13, 2004.
* Reprint requests and correspondence: Dr. Kyoichi Mizuno, Department of Internal Medicine, Chiba-Hokusoh Hospital, Nippon Medical School, 1715 Kamakari, Imba, Chiba, Japan 270-1694 (Email: mizunok{at}nms.ac.jp).
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/dl, 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.
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