C-reactive protein is a marker for a complex culprit lesion anatomy in unstable angina

Background: The putative theory is that the clinical syndrome of unstable angina is caused by rupture of the athero-sclerotic plaque with superimposed thrombus formation. It is characterized by angiographically complex coronary lesions in the majority of patients. Hypothesis: This study aimed at assessing the correlation between C-reactive protein (CRP) and the complexity of culprit coronary lesions in unstable angina. Methods: We identified culprit lesion complexity in 96 patients with unstable angina and normal creatine kinase (CK) and CK-MB mass. Serum concentrations of CRP (N < 5.0 mg/l) and cardiac troponin T (cTnT;N < 0.1 ng/ml) were measured on admission. Results: There was a trend toward a higher grade of anatomical complexity of the culprit lesion in patients with elevated CRP (p = 0.007) and cTnT levels (p = 0.027). Patients who had intermediate- or high-grade lesion severity had a higher level of CRP (8.5 +/- 5.7 mg/l) and cTnT (0.118 +/- 0.205 ng/ml) on admission than those who had normal or low-grade lesions (5.7 +/- 4.0 mg/l, 0.017 +/- 0.021 ng/ml, respectively); Mann-Whitney U, p = 0.002 and p < 0.001, respectively. Furthermore,the likelihood of having intermediate- or high-grade complexity of the culprit lesion was higher when CRP levels were elevated in all patients (p = 0.007, odds ratio [OR] = 4.286; 95% confidence interval [CI] 1.492-12.310) and in those with normal cTnT levels (p = 0.025, OR = 3.876; 95% CI 1.185-12.678). Also, higher CRP levels strongly correlated with the need for revascularization interventions (p < 0.0005). Conclusion. Elevated CRP level on admission is a marker for anatomic complexity of culprit lesions and need for revascularization interventions in unstable angina.