Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
J Cardiol. 2011 Sep;58(2):151-7. doi: 10.1016/j.jjcc.2011.04.005. Epub 2011 Jun 14.
Inflammation is a critical contributing factor to the development and progression of atherosclerosis. Pentraxin 3 (PTX3) is produced abundantly in atherosclerotic lesions while C-reactive protein (CRP) is mainly produced in the liver. In this study, we investigated whether plasma levels of PTX3 might be a sensitive marker both for the severity of coronary artery disease and vulnerable plaques. Next, we determined whether assays for inflammatory molecules can be used to monitor the therapeutic effects of telmisartan on stabilization of vulnerable atherosclerotic plaques.
We measured PTX3 concentrations in the peripheral and coronary sinus plasma of 40 patients with angina pectoris (AP) and 20 control subjects. Next, in 28 patients with AP, we determined the correlation between levels of inflammatory molecules and the computed tomography (CT) density of plaques as a quantitative index of plaque vulnerability. There was no significant difference in peripheral plasma PTX3 concentrations between patients with AP and control subjects, while coronary sinus plasma PTX3 concentrations were significantly higher in AP patients than control subjects. The concentrations of PTX3 in coronary sinus and peripheral plasma correlated with Gensini scores as an index of severity of coronary atherosclerosis. Interestingly, there was a significantly negative correlation between plasma PTX3 concentrations and CT density (r=-0.67, p<0.01). On the other hand, CT density did not correlate with the peripheral plasma concentrations of monocyte chemoattractant protein-1 (MCP-1) or high-sensitivity CRP (hsCRP). Furthermore, telmisartan treatment for 6 months decreased plasma concentrations of PTX3 but not those of MCP-1 or hsCRP in 12 patients with essential hypertension. Multivariate regression analysis revealed that changes in PTX3 levels were independent of blood pressure changes.
PTX3 is likely more specific than hsCRP as an indicator of coronary plaque vulnerability that could lead to plaque rupture.
炎症是动脉粥样硬化发生和发展的关键因素。 正五聚蛋白 3（PTX3）在动脉粥样硬化病变中大量产生，而 C 反应蛋白（CRP）主要在肝脏中产生。 在这项研究中，我们研究了血浆 PTX3 水平是否可以作为冠状动脉疾病严重程度和易损斑块的敏感标志物。 接下来，我们确定了用于炎症分子的测定是否可用于监测替米沙坦对易损动脉粥样硬化斑块稳定作用的治疗效果。
我们测量了 40 名心绞痛（AP）患者和 20 名对照者的外周和冠状窦血浆中的 PTX3 浓度。 接下来，在 28 名 AP 患者中，我们确定了炎症分子水平与斑块 CT 密度之间的相关性，作为斑块易损性的定量指标。 AP 患者与对照组之间外周血浆 PTX3 浓度没有差异，而 AP 患者冠状窦血浆 PTX3 浓度明显高于对照组。 冠状窦和外周血浆中的 PTX3 浓度与 Gensini 评分呈正相关，Gensini 评分是冠状动脉粥样硬化严重程度的指标。 有趣的是，血浆 PTX3 浓度与 CT 密度呈显著负相关（r=-0.67，p<0.01）。 另一方面，CT 密度与单核细胞趋化蛋白-1（MCP-1）或高敏 C 反应蛋白（hsCRP）的外周血浆浓度无关。 此外，替米沙坦治疗 6 个月可降低 12 例原发性高血压患者的血浆 PTX3 浓度，但不能降低 MCP-1 或 hsCRP 浓度。 多元回归分析显示，PTX3 水平的变化与血压变化无关。
PTX3 比 hsCRP 更能特异性地作为导致斑块破裂的冠状动脉斑块易损性的标志物。
