Toutouzas Konstantinos, Vaina Sophia, Tsiamis Eleftherios, Vavuranakis Manolis, Mitropoulos John, Bosinakou Eirini, Toutouzas Pavlos, Stefanadis Christodoulos
Department of Cardiology, Athens Medical School, Athens, Greece.
Am Heart J. 2004 Nov;148(5):783-8. doi: 10.1016/j.ahj.2004.05.013.
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 (DeltaT) 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 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.
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.
动脉粥样硬化斑块中已证实热不均一性增加，急性心肌梗死（MI）时记录到的温度更高。饮食或治疗干预可减少热量产生。本研究的目的是调查MI后斑块温度升高是否会持续较长时间以及他汀类药物治疗的作用。
我们纳入了55例患者，其中29例为近期MI患者，26例为慢性稳定型心绞痛（CSA）患者。在研究人群中测量了总胆固醇、C反应蛋白（CRP）、白细胞介素-6（IL-6）和可溶性黏附分子。所有患者均接受了冠状动脉斑块温度测量。温度差（ΔT）定义为罪犯动脉粥样硬化斑块的温度减去近端健康血管壁的温度。
接受他汀类药物治疗的近期MI患者有19例，CSA患者有14例。近期MI患者的ΔT为0.19±0.18℃，而CSA患者为0.10±0.08℃（P = 0.03）。与未治疗患者相比，接受他汀类药物治疗的患者ΔT更低（0.10±0.11对0.20±0.18℃，P = 0.01）。近期MI的治疗患者与接受他汀类药物治疗的CSA患者的ΔT相似（0.13±0.13对0.07±0.06℃，P = 0.14），而近期MI的未治疗患者与CSA的未治疗患者相比，ΔT显著升高（0.28±0.22对0.14±0.10℃，P = 0.04）。ΔT与CRP（R = 0.50，P < 0.01）、IL-6（R = 0.58，P < 0.01）和细胞间黏附分子-1（R = 0.40，P = 0.03）水平呈正相关。
心肌梗死后较长时间内观察到斑块温度升高，表明斑块破裂后炎症过程持续存在。他汀类药物在MI后对斑块温度有有益作用。
