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Angioscopic follow-up study of coronary ruptured plaques in nonculprit lesions
Masamichi Takano1, Shigenobu Inami, Fumiyuki Ishibashi
1Department of Internal Medicine, Chiba-Hokusoh Hospital, Nippon Medical School, Chiba, Japan.
Insights
Coronary plaque ruptures in nonculprit lesions heal slowly, often worsening stenosis. Lower C-reactive protein (CRP) levels indicate better plaque healing, suggesting CRP reflects disease activity.
Area of Science:
- Cardiology
- Vascular Biology
- Interventional Cardiology
Background:
- Multiple coronary plaque ruptures are recognized, but follow-up of nonculprit lesions is limited.
- Understanding the natural history of ruptured plaques in nonculprit lesions is crucial for managing coronary artery disease.
Purpose of the Study:
- To evaluate changes in ruptured plaques within nonculprit coronary lesions using angioscopy.
- To investigate the relationship between plaque healing, angiographic progression, and serum C-reactive protein (CRP) levels.
Main Methods:
- Coronary angioscopy identified 48 thrombi in 50 ruptured plaques in nonculprit lesions from 30 patients.
- Quantitative coronary angiography assessed percent diameter stenosis (%DS), and serum CRP levels were measured.
Main Results:
- Over a mean 13-month follow-up, 35 thrombi persisted, with color changing from red to pinkish-white, indicating healing.
- Healing rates increased with follow-up duration (23% at ≤12 months vs. 55% at >12 months).
- Healed plaques showed increased %DS (12.3% to 22.7%), and lower CRP levels were observed in patients with healed plaques.
Conclusions:
- Ruptured plaques in nonculprit lesions exhibit slow healing and may progress in stenosis.
- Serum CRP levels appear to correlate with the activity and healing status of coronary plaque ruptures.
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, 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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