The mechanisms of plaque rupture in acute coronary syndromes : Role of Oxidative stress and vasoactive factor

斑块破裂或糜烂伴附壁血栓形成被认为是稳定性冠状动脉病变转变为临床不稳定性病变的最重要形态学变化，导致急性冠状动脉综合征。然而，急性冠状动脉综合征的发病机制尚不清楚，我们以前曾报道血管活性物质包括血管紧张素II和内皮素-1在人类冠状动脉粥样硬化的进展中发挥作用。在本研究中，我们已经证明了氧化低密度脂蛋白在糖尿病患者斑块不稳定性的发生中的重要作用（J Diabetes Complications 16：60 - 64，2002）。此外，我们已经显示了在急性冠状动脉综合征的动脉粥样硬化斑块中嗜中性粒细胞的明显存在，表明嗜中性粒细胞在介导人动脉粥样硬化斑块的不稳定中起作用（Circulation 106：2894-2900，2002）。

Plaque rupture or erosion with mural thrombus formation is considered to represent the most important morphological changes that underlie the transformation of stable coronary lesions into clinically unstable lesions, causing acute coronary syndromes. However, the mechanisms that cause acute coronary syndromes are still unclear.We have previously reported that vasoactive substances including angiotensin II and endothelin-1 play a role in the progression of human coronary atherosclerosis. We have also shown that oxidative stress is a key factor in coronary atherogenesis.In the present study, we have demonstrated an important role of oxidized low density lipoprotein in the genesis of plaque instability in patients with diabetes mellitus ( J Diabetes Complications 16 : 60 - 64, 2002 ). Moreover, we have shown the distinct presence of neutrophils in atherosclerotic plaques underlying acute coronary syndromes, suggesting that neutrophils play a role in mediating destabilization of human atherosclerotic plaques ( Circulation 106 : 2894-2900, 2002 ).