Detection of increased temperature of the culprit lesion after recent myocardial infarction: the favorable effect of statins.
BACKGROUND
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.


METHODS
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 (DeltaT) was designated as the temperature of the culprit atherosclerotic plaque minus the temperature of the proximal healthy vessel wall.


RESULTS
Under treatment with statins were 19 patients with recent MI and 14 with CSA. In patients with recent MI DeltaT was 0.19 +/- 0.18 degrees C, while in patients with CSA was 0.10 +/- 0.08 degrees C (P = .03). Patients treated with statins had lower DeltaT compared to untreated patients (0.10 +/- 0.11 versus 0.20 +/- 0.18 degrees C, P = .01). Treated patients with recent MI had similar DeltaT compared to CSA patients treated with statins (0.13 +/- 0.13 versus 0.07 +/- .06 degrees C, P = .14), while untreated patients with recent MI had substantially increased DeltaT compared to untreated patients with CSA (0.28 +/- 0.22 versus 0.14 +/- 0.10 degrees C, P = .04). DeltaT 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.


CONCLUSIONS
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.
Toutouzas
Konstantinos
K
Department of Cardiology, Athens Medical School, Athens, Greece. ktoutouz@otenet.gr
Vaina
Sophia
S
Tsiamis
Eleftherios
E
Vavuranakis
Manolis
M
Mitropoulos
John
J
Bosinakou
Eirini
E
Toutouzas
Pavlos
P
Stefanadis
Christodoulos
C
D000368:Aged; D000787:Angina Pectoris / Q000503:physiopathology; D001831:Body Temperature / Q000187:drug effects*; D002097:C-Reactive Protein / Q000378:metabolism; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D007249:Inflammation / Q000188:drug therapy; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D015850:Interleukin-6; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein