In recent years, new information about the morphological and functional characteristics of vulnerable atherosclerotic plaques has become available, as well as various diagnostic tools which recognize these features. In Part I of the presentation Dr. Toutouzas describes techniques used to evaluate coronary plaque composition, plaque inflammation, plaque temperature, tissue strain and shear stress of the plaque, neovascularization, and coronary sinus temperature.

In Part 2 of the presentation Dr. Toutouzas talks about non-culprit lesions, specifically the local inflammatory activity within these lesions, and the relationship with systemic inflammation. A number of studies have already shown the presence of ruptured non-culprit lesions in patients with acute coronary syndromes, and other studies have identified 'high-risk' non-culprit lesions.

In 1996, Casscells et al. published an endarterectomy study showing the presence of thermal heterogeneity in human atherosclerotic plaques. Temperature was found to correlate positively with cell density and inversely with the distance of the cell clusters from the luminal surface, and most of the cells were macrophages (1). This suggests that techniques that can localise heat may be able to identify plaques at high risk of rupture or thrombosis. Thermal heterogeneity within human atherosclerotic coronary arteries is also larger in unstable angina and acute myocardial infarction, suggesting that it may be related to the pathogenesis (2).

The present study by Dr. Toutouzas and colleagues was conducted in patients with stable angina or acute coronary syndromes. Temperature measurements of culprit and non-culprit lesions were taken, and the Temperature Difference (called delta T or DT) was calculated as the maximal temperature of the atherosclerotic plaque minus the most frequent temperature at the proximal vessel wall. DT was found to be similar in culprit and non-culprit lesions, and there was an increase in DT by type of clinical syndrome in both culprit and non-culprit lesions. Further, C-reactive protein (CRP) levels were found to be positively correlated with DT in all lesions.

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After viewing this presentation the participant will be able to discuss:

- Features of vulnerable atherosclerotic plaques and diagnostic tools used to evaluate these features
- Evidence for high-risk non-culprit lesions in patients with acute coronary syndromes
- Increased temperature in human atherosclerotic plaques as an indicator of local inflammatory activity
- The correlation of CRP levels with heat production of culprit and non-culprit lesions

1. Casscells W, Hathorn B, David M, Krabach T, Vaughn WK, McAllister HA, Bearman G, Willerson JT.
Thermal detection of cellular infiltrates in living atherosclerotic plaques: possible implications for plaque rupture and thrombosis. Lancet. 1996 May 25;347(9013):1447-51.

2. Christodoulos Stefanadis, MD; Leonidas Diamantopoulos, MD; Charalambos Vlachopoulos, MD; Eleftherios Tsiamis, MD; John Dernellis, MD; Konstantinos Toutouzas, MD; Elli Stefanadi, MS; Pavlos Toutouzas, MD Thermal Heterogeneity Within Human Atherosclerotic Coronary Arteries Detected In Vivo: A New Method of Detection by Application of a Special Thermography Catheter Circulation. 1999;99:1965-1971.

Toutouzas K, Drakopoulou M, Markou V, Karabelas I, Vaina S, Vavuranakis M, Tsiamis E, Tsioufis C, Androulakis A, Stefanadis C.
Correlation of systemic inflammation with local inflammatory activity in non-culprit lesions: beneficial effect of statins. Int J Cardiol. 2007 Jul 31;119(3):368-73.