Stefanadis C, Diamantopoulos L, Dernellis J, Economou E, Tsiamis E, Toutouzas K, Vlachopoulos C, Toutouzas P
Hippokration Hospital, Department of Cardiology, Greece.
J Mol Cell Cardiol. 2000 Jan;32(1):43-52. doi: 10.1006/jmcc.1999.1049.
Several studies have shown that inflammation plays an important role in the pathogenesis of coronary heart disease (CHD). Serum amyloid A (SAA) and C-reactive protein (CRP) reactants of the acute phase of inflammation, have been shown to be increased in patients with CHD. Recently ex vivo studies demonstrated that some types of atherosclerotic plaques show substantially warmer regions. A catheter-based technique has been developed to measure the temperature of human arteries in vivo. Therefore, the aim of the present study was to measure the luminal surface temperature in patients with CHD and to correlate it with the acute phase proteins in order to discriminate the role of inflammation in heat production in acute coronary syndromes. Sixty patients were studied with CHD (20 with stable angina, 20 with unstable angina and 20 with acute myocardial infarction) and 20 sex- and age-matched controls without coronary artery disease, by measuring plasma levels of SAA, CRP, plasma lipids and intracoronary arterial luminal wall temperature. Intracoronary temperature was measured with a thermography catheter developed in our Institution: a thermistor probe with a temperature accuracy of 0.05 degrees C, was attached at the distal end of a long 3F polyurethane shaft. It was found that the median temperature differences at the site of the lesion from the core temperature was increased in patients with unstable angina (1.025 degrees C) and acute myocardial infarction (2.150 degrees C) compared with stable angina (0.300 degrees C), P<0.001 for each comparison. Furthermore, stable angina has increased temperature differences compared with controls (0.200 degrees C, P<0.001). There were very good correlations between CRP and SAA with the temperature (r=0.796, P=0.01 and r=0.848, P=0.01, respectively). Local heat at the site of lesion is increased in patients with acute coronary syndromes and may arise from an aggressive inflammatory response occurring in these situations. The sensitive measurement of plaque temperature as a prognostic marker may be useful in the management of coronary heart disease.
多项研究表明,炎症在冠心病(CHD)的发病机制中起重要作用。血清淀粉样蛋白A(SAA)和C反应蛋白(CRP)作为炎症急性期反应物,在冠心病患者中已被证明会升高。最近的体外研究表明,某些类型的动脉粥样硬化斑块显示出明显更温暖的区域。一种基于导管的技术已被开发用于在体内测量人体动脉的温度。因此,本研究的目的是测量冠心病患者的管腔表面温度,并将其与急性期蛋白相关联,以区分炎症在急性冠状动脉综合征产热中的作用。通过测量SAA、CRP、血脂水平以及冠状动脉内动脉管腔壁温度,对60例冠心病患者(20例稳定型心绞痛、20例不稳定型心绞痛和20例急性心肌梗死)以及20例年龄和性别匹配的无冠状动脉疾病的对照者进行了研究。冠状动脉内温度采用我们机构研发的热成像导管进行测量:一个温度精度为0.05摄氏度的热敏电阻探头,附着在一根长3F聚氨酯轴的远端。结果发现,与稳定型心绞痛患者(0.300摄氏度)相比,不稳定型心绞痛患者(1.025摄氏度)和急性心肌梗死患者(2.150摄氏度)病变部位与核心温度的中位温差增加,每次比较P<0.001。此外,与对照组(0.200摄氏度,P<0.001)相比,稳定型心绞痛患者的温差也有所增加。CRP和SAA与温度之间存在非常好的相关性(分别为r=0.796,P=0.01和r=0.848,P=0.01)。急性冠状动脉综合征患者病变部位的局部热量增加,可能源于这些情况下发生的强烈炎症反应。作为预后标志物对斑块温度进行敏感测量可能有助于冠心病的管理。