Background: In patients with acute coronary syndromes (ACS) increased systemic and local inflammatory activation in culprit lesions is observed. It is unknown, however, whether systemic inflammation is correlated with non-culprit lesion inflammatory activation. Moreover, the effect of statins on non-culprit lesion inflammation has not been extensively investigated. The aim of the present study was to investigate in non-culprit lesions 1) the correlation between plaque temperature measurements with the levels of C-reactive protein (CRP) and 2) whether statin administration is associated with reduced heat production.
Methods: We included 71 patients with ACS or stable angina (SA) undergoing percutaneous coronary intervention in culprit lesions, having an intermediate non-culprit lesion. Forty patients were treated with statin and 31 patients were not treated. Systemic inflammatory status was assessed by CRP, and local inflammatory activation by measuring the temperature difference of non-culprit lesion (deltaT), assigned as the difference between the maximal temperature of the atherosclerotic plaque from the proximal vessel wall temperature.
Results: Mean deltaT was 0.08+/-0.07 degrees C. Patients with ACS had higher deltaT compared to patients with SA (ACS: 0.10+/-0.07 degrees C vs SA: 0.05+/-0.06, p<0.01). deltaT was less in patients treated with statin in both groups (ACS: 0.07+/-0.04 degrees C vs 0.13+/-0.08 degrees C p=0.009; SA: 0.04+/-0.05 degrees C vs 0.09+/-0.07 degrees C, p=0.04). CRP was higher in patients with ACS compared to SA (1.18+/-1.12 vs 0.47+/-0.37 mg/dL, p=0.001). There was a positive correlation of deltaT and CRP values (R=0.46, p<0.001).
Conclusions: Local inflammatory activation in non-culprit lesions is correlated with systemic inflammation. Moreover, statins have a beneficial effect on non-culprit lesion heat production.