Marshall Catriona J, Nallaratnam Mark, Mocatta Tessa, Smyth David, Richards Mark, Elliott John M, Blake James, Winterbourn Christine C, Kettle Anthony J, McClean Dougal R
Cardiology Department, Christchurch Hospital, Christchurch, New Zealand.
Am J Cardiol. 2010 Aug 1;106(3):316-22. doi: 10.1016/j.amjcard.2010.03.028.
Myeloperoxidase (MPO) is associated with risk in acute coronary syndromes. However, the precise role it plays in ST-elevation myocardial infarction (STEMI) remains unclear. In this study we tested the hypothesis that levels of MPO in plasma after a myocardial infarction are affected by its ability to bind to the endothelium and there is local release of the enzyme at the culprit lesion. We measured plasma MPO in systemic circulation and throughout the coronary circulation in patients with STEMI undergoing primary percutaneous coronary intervention (PCI). MPO levels at the femoral artery were higher (p <0.001) in patients with STEMI (n = 67, median 45 ng/ml, interquartile range 34 to 83) compared to control patients (n = 12, 25 ng/ml, 19 to 30) with chronic stable angina undergoing elective PCI. After administration of the anticoagulant bivalirudin in 13 patients with STEMI, plasma MPO was increased only at the culprit coronary artery lesion before PCI (178 ng/ml, 91 to 245) versus all other sites (femoral artery 86 ng/ml, 54 to 139, p = 0.019). Administration of heparin caused a marked increase of plasma MPO. Even so, it was still possible to detect an increase of plasma MPO at culprit lesion in patients with STEMI (n = 54, 171 ng/ml, 122 to 230) versus controls (n = 12, 136 ng/ml, 109 to 151, p <0.05) after heparin and before PCI. MPO levels were higher at the culprit lesion in patients with STEMI who presented early and in those with restricted flow (p <0.05). In conclusion, our results demonstrate that, in addition to a systemic increase of MPO in patients presenting early with STEMI, levels of this leukocyte enzyme are increased at the culprit coronary lesion before PCI.
髓过氧化物酶（MPO）与急性冠状动脉综合征的风险相关。然而，它在ST段抬高型心肌梗死（STEMI）中的确切作用仍不清楚。在本研究中，我们检验了以下假设：心肌梗死后血浆中MPO的水平受其与内皮细胞结合能力的影响，并且在罪犯病变处存在该酶的局部释放。我们测量了接受直接经皮冠状动脉介入治疗（PCI）的STEMI患者体循环和整个冠状动脉循环中的血浆MPO。与接受择期PCI的慢性稳定型心绞痛对照患者（n = 12，25 ng/ml，四分位间距19至30）相比，STEMI患者（n = 67，中位数45 ng/ml，四分位间距34至83）股动脉处的MPO水平更高（p <0.001）。在13例STEMI患者中给予抗凝剂比伐卢定后，PCI前仅罪犯冠状动脉病变处的血浆MPO升高（178 ng/ml，91至245），而其他所有部位（股动脉86 ng/ml，54至139，p = 0.019）。给予肝素导致血浆MPO显著升高。即便如此，在肝素治疗后且PCI前，仍可检测到STEMI患者（n = 54，171 ng/ml，122至230）罪犯病变处的血浆MPO升高，而对照患者（n = 12，136 ng/ml，109至151，p <0.05）则无此现象。早期就诊的STEMI患者以及血流受限患者的罪犯病变处MPO水平更高（p <0.05）。总之，我们的结果表明，除了早期出现STEMI的患者MPO出现全身性升高外，在PCI前罪犯冠状动脉病变处这种白细胞酶的水平也会升高。
