Relation between local temperature and C-reactive protein levels in patients with coronary artery disease: effects of atorvastatin treatment

Abstract

Although previous studies have shown systemic inflammatory activation the relation with the local plaque inflammatory activation has not been extensively studied. The present study investigated the relation between local and systemic inflammatory activation in patients with coronary artery disease and the impact of atorvastatin treatment. We included 215 patients undergoing percutaneous coronary intervention; of them 140 were treated with atorvastatin. Patients with stable angina (SA) and acute coronary syndromes (ACS) were included. Systemic inflammation was assessed by serum C-reactive protein (CRP), soluble adhesion molecules levels and local plaque inflammatory activation by coronary thermography. Temperature difference (DeltaT) was assigned as the difference between the proximal vessel wall temperature from the maximal temperature at the culprit plaque. Patients with ACS (n=78) had increased DeltaT compared to patients with SA (n=137) (0.16+/-0.10 degrees C versus 0.08+/-0.07 degrees C, P<0.001). Patients treated with atorvastatin had lower DeltaT compared to untreated patients (0.10+/-0.07 degrees C versus 0.15+/-0.10 degrees C, P<0.01). DeltaT was less in the treated group compared to the untreated group in patients with SA and ACS (ACS: 0.13+/-0.08 degrees C versus 0.20+/-0.11 degrees C, P<0.01, SA: 0.08+/-0.06 degrees C versus 0.13+/-0.08 degrees C, P=0.03). Although a correlation was found between CRP levels and DeltaT (R=0.29, P<0.01), in certain groups a discrepancy between CRP levels and DeltaT was observed. In 25% of patients with low DeltaT CRP levels were >1mg/dl and in 35.5% of patients with high DeltaT CRP was <2mg/dl. The correlation between soluble adhesion molecules and DeltaT did not reach statistical significance. Although there is a correlation between widespread and local inflammatory activation in patients with coronary artery disease, a discrepancy between culprit plaque and systemic inflammatory activation is observed. Atorvastatin has a parallel effect on systemic and local inflammatory process in patients with coronary artery disease.