Takeshita S, Isshiki T, Ochiai M, Ishikawa T, Nishiyama Y, Fusano T, Toyoizumi H, Kondo K, Ono Y, Sato T
Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan.
Atherosclerosis. 1997 Dec;135(2):187-92. doi: 10.1016/s0021-9150(97)00160-3.
Local inflammation within the coronary arteries is involved in the pathogenesis of acute coronary syndrome. However, the contribution of a systemic inflammatory response to the pathogenesis of this syndrome has not been well characterized. Accordingly, we investigated systemic inflammatory responses in patients with acute coronary syndrome.
A total of 83 patients with ischemic heart disease (15 with stable exertional angina and 68 with acute coronary syndrome) were studied. The luminol-dependent chemiluminescence (CL) response of polymorphonuclear leukocytes (PMNs), which reflects their ability to generate oxygen species, was used as a marker for PMN activation. Soluble interleukin-2 receptor (sIL-2R) levels were measured to assess T-lymphocyte activation.
CL counts of whole blood from patients with acute coronary syndrome were twice those of patients with stable angina (2.38 +/- 0.22 vs 1.10 +/- 0.17 x 10(6) counts, P < 0.05). A comparison of CL counts between patients with unstable angina and those with acute myocardial infarction revealed no significant differences. T-lymphocyte activity, measured by serum sIL-2R, was significantly lower in patients with acute coronary syndrome than those with stable angina (214.3 +/- 11.5 vs. 358.3 +/- 115.7 U/ml, P < 0.05).
This investigation shows that there is a systemic increase in PMN activity and a decrease in T-lymphocyte activity in patients with acute coronary syndrome. This contrasts with the pattern of cellular activation seen at sites of local inflammation within atherosclerotic plaques, suggesting that two independent inflammatory processes (local and systemic) may be involved in the pathogenesis of this syndrome.
冠状动脉内的局部炎症参与急性冠状动脉综合征的发病机制。然而，全身炎症反应对该综合征发病机制的作用尚未得到充分阐明。因此，我们研究了急性冠状动脉综合征患者的全身炎症反应。
共研究了83例缺血性心脏病患者（15例稳定型劳力性心绞痛患者和68例急性冠状动脉综合征患者）。多形核白细胞（PMN）的鲁米诺依赖性化学发光（CL）反应反映了其产生活性氧的能力，用作PMN活化的标志物。测量可溶性白细胞介素-2受体（sIL-2R）水平以评估T淋巴细胞活化。
急性冠状动脉综合征患者全血的CL计数是稳定型心绞痛患者的两倍（2.38±0.22对1.10±0.17×10⁶计数，P<0.05）。不稳定型心绞痛患者与急性心肌梗死患者的CL计数比较无显著差异。通过血清sIL-2R测量的T淋巴细胞活性在急性冠状动脉综合征患者中显著低于稳定型心绞痛患者（214.3±11.5对358.3±115.7 U/ml，P<0.05）。
本研究表明，急性冠状动脉综合征患者存在PMN活性全身升高和T淋巴细胞活性降低。这与动脉粥样硬化斑块内局部炎症部位所见的细胞活化模式相反，提示两个独立的炎症过程（局部和全身）可能参与该综合征的发病机制。
