Clinical cardiology · 2001
C-reactive protein is a marker for a complex culprit lesion anatomy in unstable angina.
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Moukarbel G V, Arnaout M S, Alam S E
Аннотация
BACKGROUND: The putative theory is that the clinical syndrome of unstable angina is caused by rupture of the atherosclerotic 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.
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.