Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy.
Circulation. 2010 Dec 14;122(24):2505-13. doi: 10.1161/CIRCULATIONAHA.110.955302. Epub 2010 Nov 29.
Systemic levels of myeloperoxidase predict prognosis in patients with acute coronary syndromes and are considered a marker of plaque vulnerability. It is not known whether myeloperoxidase is associated with different coronary morphologies (ie, rupture or erosion of the culprit lesion) in patients with acute coronary syndrome.
Twenty-five consecutive patients (aged 67±11 years; 15 men [60%]; 13 [52%] with non-ST-segment elevation acute coronary syndrome and 12 [48%] with acute ST-segment elevation myocardial infarction) were enrolled. Optical coherence tomography classified the culprit lesion as ruptured in 18 (72%) or eroded in 7 patients (28%) and detected intraluminal thrombus in 89% of ruptured plaques and 100% of eroded plaques. Baseline systemic levels of serum myeloperoxidase were significantly higher in patients with an eroded plaque than in those with a ruptured plaque (median, 2500 ng/mL; 25th to 75th percentile, 1415 to 2920 versus median, 707 ng/mL; 25th to 75th percentile, 312 to 943; P=0.001), whereas C-reactive protein levels did not differ significantly (median, 11.3 mg/L; 25th to 75th percentile, 1.3 to 28.5 versus median, 3.9 mg/L; 25th to 75th percentile, 1.3 to 17.8; P=0.76, respectively). In addition, the density of myeloperoxidase-positive cells within thrombi overlying plaques in postmortem coronary specimens retrieved from sudden coronary death victims was significantly higher in lesions with erosion (n=11) than ruptures (n=11) (median, 1584; 25th to 75th percentile, 1,088 to 2,135 cells/mm(2) versus median, 579; 25th to 75th percentile, 442 to 760 cells/mm(2); P=0.0012).
Systemic myeloperoxidase levels are significantly elevated in patients with acute coronary syndrome presenting with eroded culprit plaque compared with patients presenting with ruptured culprit plaque. Consistently, in postmortem coronary specimens, luminal thrombi superimposed on eroded plaques contain a higher density of myeloperoxidase-positive cells than thrombi superimposed on ruptured plaques. This study supports the concept that elevations in selective inflammatory biomarkers reflect specific acute complications of coronary atherosclerosis.
髓过氧化物酶的全身水平可预测急性冠脉综合征患者的预后，被认为是斑块易损性的标志物。目前尚不清楚髓过氧化物酶是否与急性冠脉综合征患者不同的冠脉形态（即罪犯病变的破裂或侵蚀）有关。
连续纳入 25 例患者（年龄 67±11 岁；15 例男性[60%]；13 例非 ST 段抬高型急性冠脉综合征患者[52%]和 12 例急性 ST 段抬高型心肌梗死患者[48%]）。光学相干断层成像术将罪犯病变分类为破裂 18 例（72%）或侵蚀 7 例（28%），并检测到破裂斑块 89%和侵蚀斑块 100%的管腔内血栓。与破裂斑块相比，侵蚀斑块患者的血清髓过氧化物酶的基础全身性水平明显升高（中位数为 2500ng/ml；25%至 75%为 1415 至 2920 与中位数 707ng/ml；25%至 75%为 312 至 943；P=0.001），而 C 反应蛋白水平差异无统计学意义（中位数为 11.3mg/L；25%至 75%为 1.3 至 28.5 与中位数 3.9mg/L；25%至 75%为 1.3 至 17.8；P=0.76）。此外，从冠状动脉猝死患者的死后冠状动脉标本中，在斑块上覆盖的血栓中，髓过氧化物酶阳性细胞的密度在侵蚀病变（n=11）中明显高于破裂病变（n=11）（中位数，1584；25%至 75%为 1088 至 2135 细胞/mm2 与中位数 579；25%至 75%为 442 至 760 细胞/mm2；P=0.0012）。
与破裂的罪犯斑块相比，急性冠脉综合征患者中出现侵蚀性罪犯斑块的患者其全身髓过氧化物酶水平明显升高。一致地，在死后冠状动脉标本中，在侵蚀性斑块上叠加的管腔内血栓含有比在破裂斑块上叠加的血栓更高密度的髓过氧化物酶阳性细胞。这项研究支持这样的概念，即选择性炎症生物标志物的升高反映了冠状动脉粥样硬化的特定急性并发症。
