Background Vulnerable plaque is defined as a lesion with thin-cap fibrous atheroma (TCFA) and responsible for acute coronary syndrome (ACS).
Objectives We sought evaluate that tissue characterization and inflammation were related with the development of ACS in patients with TCFA.
Methods Study subjects consisted of 136 consecutive patients (95 males (69.9%), mean 61.4±12.7 years old) who have TCFA at culprit lesion evaluated with intravascular ultrasound- virtual histology (IVUS-VH) study. TCFA was defined as culprit lesion with at least 3 consecutive frames that have necrotic core > 10% without overlying fibrous tissue and percent atheroma area > 40% at minimal luminal area. We divided the subjects into two groups: patient with ACS (n=80) and patients with stable angina (n=56).
Results Patients with ACS had higher hs-CRP level (3.76±3.57mg/L vs. 2.40±2.87mg/L, p= 0.018), higher blood sugar (136.7±55.3mg/dL vs. 113.8±54.7mg/dL, p=0.018) and more smoker (47.5% vs. 23.2%, p=0.004) than patients with stable angina. Age, LDL-cholesterol level and frequency of male gender, hypertension, diabetes and prior myocardial infarction were no differences between two groups. With IVUS-VH analysis, patients with ACS had more plaque volume (208.9±116.6㎣ vs. 146.6±72㎣, p=0.001), longer lesion length (20.2±7.7㎜ vs. 17.3±7.4㎜, p=0.027) more fibrous volume (78.5±53.9㎣ vs. 48.4±26.0㎣, p<0.001), more fibro-fatty volume (16.0±17.1㎣ vs. 9.8±9.1㎣, p=0.014) and more necrotic core volume (31.7±23.1㎣ vs. 21.6±16.1㎣, p=0.006) than patients with stable angina. However, the percent volume of each tissue characterizations did not have any differences between two groups. Multiple linear regression analysis showed that hs-CRP level (beta=0.045, 95% CI 0.002-0.088, p=0.040) and smoking (beta=0.306, 95% CI 0.010-0.603, p=0.043) related with ACS.
Conclusions Hs-CRP level and smoking are important predictors for ACS in patients who had TCFA at culprit lesion. However, the amount of necrotic core volume and dense calcium volume did not related with development of ACS.
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