Heat Production of Atherosclerotic Plaques and Inflammation Assessed by the Acute Phase Proteins in Acute Coronary Syndromes

Abstract

C. Stefanadis, L. Diamantopoulos, J. Dernellis, E. Economou, E. Tsiamis, K. Toutouzas, C. Vlachopoulos and P. Toutouzas. Heat Production of Atherosclerotic Plaques and Inflammation Assessed by the Acute Phase Proteins in Acute Coronary Syndromes. Journal of Molecular and Cellular Cardiology (2000) 32, 43–52. Several studies have shown that inflammation plays an important role in the pathogenesis of coronary heart disease (CHD). Serum amyloid A (SAA) and C-reactive protein (CRP) reactants of the acute phase of inflammation, have been shown to be increased in patients with CHD. Recently ex vivo studies demonstrated that some types of atherosclerotic plaques show substantially warmer regions. A catheter-based technique has been developed to measure the temperature of human arteries in vivo. Therefore, the aim of the present study was to measure the luminal surface temperature in patients with CHD and to correlate it with the acute phase proteins in order to discriminate the role of inflammation in heat production in acute coronary syndromes. Sixty patients were studied with CHD (20 with stable angina, 20 with unstable angina and 20 with acute myocardial infarction) and 20 sex- and age-matched controls without coronary artery disease, by measuring plasma levels of SAA, CRP, plasma lipids and intracoronary arterial luminal wall temperature. Intracoronary temperature was measured with a thermography catheter developed in our Institution: a thermistor probe with a temperature accuracy of 0.05°C, was attached at the distal end of a long 3F polyurethane shaft. It was found that the median temperature differences at the site of the lesion from the core temperature was increased in patients with unstable angina (1.025°C) and acute myocardial infarction (2.150°C) compared with stable angina (0.300°C), P<0.001 for each comparison. Furthermore, stable angina has increased temperature differences compared with controls (0.200°C, P<0.001). There were very good correlations between CRP and SAA with the temperature (r=0.796, P=0.01 and r=0.848, P=0.01, respectively). Local heat at the site of lesion is increased in patients with acute coronary syndromes and may arise from an aggressive inflammatory response occurring in these situations. The sensitive measurement of plaque temperature as a prognostic marker may be useful in the management of coronary heart disease.