Research and Clinical Utility of Thermography

Ex Vivo Thermography Studies

The concept that plaque temperature is a marker of local inflammation was originally proposed by Casscells et al. in 1996 (Figure 1) (Casscells, et al., 1996). This was the first study demonstrating that heat is generated from inflamed atheromatous plaques in humans. In this study, carotid artery samples obtained by endarterectomy were probed with a thermistor (24-gauge needle tip; accuracy 0.1 °C; time contrast 0.15s). Plaques showed several regions in which the surface temperatures varied reproducibly by 0.2–0.3°C. Points with substantially different temperatures could not be distinguished from one another by the naked eye and were sometimes very close to one another (< 1mm apart). Temperature correlated positively with cell density (r = 0.68; p = 0.0001) and inversely with the distance of the cell clusters (mostly macrophages) from the luminal surface (r = –0.38; p= 0.000 (Figure 2) (Casscells, et al., 1996). The thermal heterogeneity observed could also be confirmed using an infrared camera in vivo. In order to assess the possible contribution of infection to generation of heat, the genus-specific monoclonal antibody CF-2 against Chlamydia pneumonia was used (Madjid, Naghavi, Malik, Litovsky, Willerson, & Casscells, 2002). However, no significant association between temperature heterogeneity and C Pneumonia was found. After incubation of hot plaques with indomethacin, a gradual decrease in plaque heat production over 5 hours was observed, suggesting an inflammatory origin of heat production in atherosclerotic plaques.

Figure 1.

Marked temperature heterogeneity was observed (in degrees Celsius) over the surface of endarterectomy samples from carotid plaques.