Increased thermal heterogeneity has been demonstrated in atherosclerotic plaques, with the higher temperature recorded in acute myocardial infarction (MI). Dietary or treatment interventions reduce heat production. The purpose of the present study was to investigate whether increased plaque temperature is maintained for a prolonged period after MI and the role of statin administration.

We enrolled 55 patients, 29 with recent MI and 26 with chronic stable angina (CSA). Total cholesterol, C-reactive protein (CRP), interleukin-6 (IL-6) and soluble adhesion molecules were measured in the study population. All patients underwent coronary plaque temperature measurements. Temperature difference (ΔT) was designated as the temperature of the culprit atherosclerotic plaque minus the temperature of the proximal healthy vessel wall.

Under treatment with statins were 19 patients with recent MI and 14 with CSA. In patients with recent MI ΔT was 0.19 ± 0.18°C, while in patients with CSA was 0.10 ± 0.08°C (P = .03). Patients treated with statins had lower ΔT compared to untreated patients (0.10 ± 0.11 versus 0.20 ± 0.18°C, P = .01). Treated patients with recent MI had similar ΔT compared to CSA patients treated with statins (0.13 ± 0.13 versus 0.07 ± .06° C, P = .14), while untreated patients with recent MI had substantially increased ΔT compared to untreated patients with CSA (0.28 ± 0.22 versus 0.14 ± 0.10°C, P = .04). ΔT was positively correlated with CRP (R = 0.50, P < .01), IL-6 (R = 0.58, P < .01), and intercellular adhesion molecule-1 (R = 0.40, P = .03) levels.

Increased plaque temperature is observed for an extended period after myocardial infarction, indicating that the inflammatory process is sustained after plaque rupture. Statins have a beneficial effect after MI on plaque temperature.