Despite improvements in diagnostic methods and the introduction of new imaging methods, neither plaque rupture nor plaque erosion can be predicted in clinical practice. Inflammation at the site of plaque rupture or erosion is an important determinant of plaque instability [1]. Activated macrophages either weaken the overlying fibrous cap of plaques, thereby leading to plaque rupture, or promote thrombosis and vasoconstriction in nonruptured but inflamed plaques. It has been suggested that measurement of temperature released by activated inflammatory cells of atherosclerotic plaques may detect plaque instability. Previous ex vivo studies have shown that there is thermal heterogeneity in human carotid atherosclerotic plaques [2].

After the development of other cardiac and vascular catheters [3, 4], we developed a catheter-based technique to measure the temperature of human arteries in vivo. The 3-French thermography catheter incorporates a thermistor at its distal end (temperature accuracy, 0.05°C; time constant, 300 msec; spatial resolution, 0.5 mm). The distal part of the catheter has a special configuration to ensure contact of the thermistor with the vessel wall. This technique has undergone extensive in vitro and experimental testing, and preliminary clinical results have been previously reported [5]. To date, this technique has been used to measure the temperature of the luminal surface in 70 patients (30 with normal coronary arteries, 20 with stable angina, and 20 with unstable angina). Temperature was constant within the arteries of the controls, whereas most atherosclerotic plaques showed higher surface temperature than the healthy segments of the coronary artery (background temperature). Temperature differences between atherosclerotic plaque (or another area of healthy vessel wall for the control group) and healthy coronary artery segments differed among the groups, increasing progressively from stable angina to unstable angina (mean ±SD, 0.010 ± 0.021°C in the control group, 0.148 ± 0.112°C in the stable angina group, and 0.778 ± 0.364°C in the unstable angina group) (Figure 1).

View larger version (11K): [in this window] [in a new window]   Figure 1. Differences in temperature between atherosclerotic plaque (or another area of healthy vessel wall for controls) and healthy coronary artery segments in controls, patients with stable angina, and patients with unstable angina.

Thermal heterogeneity within human atherosclerotic coronary arteries was shown in vivo by using a special thermography catheter. This heterogeneity is greater in unstable angina, suggesting that it may be related to the pathogenesis of acute ischemic syndromes. Thus, local temperature measurement may prove useful for identification of unstable plaques. The concept of local thermography may also be applied by other specialties to detect inflamed or malignant cells during gastrointestinal endoscopy, laparoscopy, arthroscopy, ophthalmoscopy, or transcranial imaging.