ABSTRACT
Atherosclerosis is an inflammatory process characterized by presence of macrophages and lymphocytes.1,2 Casscells et al reported increased temperature heterogeneity in ex vivo atherosclerotic specimens of human carotid arteries.3
Stefanadis et al showed that in vivo temperature heterogeneity was markedly increased in patients presenting with an acute coronary syndrome as opposed to patients having stable angina.4 We have subsequently shown that by using a dedicated temperature catheter in an animal model of atherosclerosis, in vivo temperature heterogeneity was determined by plaque composition and more specifically by the total macrophage mass.5 Recently, temperature heterogeneity in the presence of flow appeared to be underestimated in patients with effort angina due to coronary stenosis which was related to cooling of the vessel wall by the blood flow.6
