Kong Chee Hoe, Lin Xiao Yun, Woo Chin Cheng, Wong Hung Chew, Lee Chuen Neng, Richards A Mark, Sorokin Vitaly A
Department of Cardiac, Thoracic and Vascular Surgery, National University Heart Centre, Singapore.
Interact Cardiovasc Thorac Surg. 2013 Jan;16(1):11-5. doi: 10.1093/icvts/ivs421. Epub 2012 Oct 9.
Extracellular matrix (ECM) remodelling of the vessel wall is hypothesized to be an important step in atherosclerosis. Changes of the ECM are associated with the gradual progression of an atherosclerotic lesion from a lipid streak to complicated unstable plaque, leading to a complete vessel occlusion and eventually myocardial infarction (MI). Understanding of this process is critical in the treatment and prevention of ischaemic heart disease (IHD).
We investigated the histopathological characteristics of aortic wall ECM in IHD patients. Collagen I, collagen III and elastin were assessed immunohistochemically in patients with acute MI and those with stable angina, using aortic punch tissues obtained from coronary artery bypass graft surgery. Fluorescence tissue images were analysed using the tissue microarray technique.
The results showed that collagen III expression was found to be significantly lower in the acute MI group (P < 0.001). As a result of this change, the patients with MI also revealed a significant reduction in the collagen III/collagen I ratio. The elastin/collagen III ratio was significantly higher in the MI group (P < 0.001).
Our study provided evidence of a decrease in collagen III content in patients with MI, which could possibly explain the mechanism of plaque vulnerability and weakening of the plaque cap. A reduction in collagen III content, particularly away from the atherosclerotic lesions, might be explained by the systemic vascular changes in patients with MI, and inflammation and immune responses could be potential causes of these systemic transformations. The biochemical mechanisms and factors regulating collagen III production might be potential markers to predict possible cardiovascular events.
血管壁的细胞外基质(ECM)重塑被认为是动脉粥样硬化的一个重要步骤。ECM的变化与动脉粥样硬化病变从脂质条纹逐渐发展为复杂不稳定斑块相关,导致血管完全闭塞并最终引发心肌梗死(MI)。了解这一过程对于缺血性心脏病(IHD)的治疗和预防至关重要。
我们研究了IHD患者主动脉壁ECM的组织病理学特征。使用从冠状动脉搭桥手术中获取的主动脉穿刺组织,通过免疫组织化学方法评估急性心肌梗死患者和稳定型心绞痛患者的I型胶原、III型胶原和弹性蛋白。使用组织微阵列技术分析荧光组织图像。
结果显示,急性心肌梗死组的III型胶原表达显著降低(P < 0.001)。由于这种变化,心肌梗死患者的III型胶原/I型胶原比值也显著降低。MI组的弹性蛋白/III型胶原比值显著更高(P < 0.001)。
我们的研究提供了证据,表明心肌梗死患者的III型胶原含量降低,这可能解释了斑块易损性和斑块帽变薄的机制。III型胶原含量的降低,特别是在远离动脉粥样硬化病变的部位,可能是由于心肌梗死患者的全身血管变化所致,炎症和免疫反应可能是这些全身变化的潜在原因。调节III型胶原产生的生化机制和因素可能是预测可能的心血管事件的潜在标志物。