Atherosclerosis is the main pathophysiological process underlying coronary artery disease (CAD). Acute complications of atherosclerosis, such as myocardial infarction, are caused by the rupture of vulnerable atherosclerotic plaques, which are characterized by thin, highly inflamed, and collagen-poor fibrous caps. Several lines of evidence mechanistically link the heme peroxidase myeloperoxidase (MPO), inflammation as well as acute and chronic manifestations of atherosclerosis. MPO and MPO-derived oxidants have been shown to contribute to the formation of foam cells, endothelial dysfunction and apoptosis, the activation of latent matrix metalloproteinases, and the expression of tissue factor that can promote the development of vulnerable plaque. As such, detection, quantification and imaging of MPO mass and activity have become useful in cardiac risk stratification, both for disease assessment and in the identification of patients at risk of plaque rupture. This review summarizes the current knowledge about the role of MPO in CAD with a focus on its possible roles in plaque rupture and recent advances to quantify and image MPO in plasma and atherosclerotic plaques.

动脉粥样硬化是冠状动脉疾病（CAD）的主要病理生理过程。动脉粥样硬化的急性并发症，例如心肌梗塞，是由脆弱的动脉粥样硬化斑块破裂引起的，这些斑块的特征是薄，高度发炎且胶原蛋白稀疏的纤维帽。机械地将血红素过氧化物酶髓过氧化物酶（MPO），炎症以及动脉粥样硬化的急性和慢性表现联系在一起。已显示MPO和MPO衍生的氧化剂有助于泡沫细胞的形成，内皮功能障碍和细胞凋亡，潜在基质金属蛋白酶的活化以及组织因子的表达，这些因子可促进易损斑块的发展。因此，检测，对MPO的质量和活性进行定量和成像对心脏病风险分层，疾病评估和斑块破裂风险患者的识别都非常有用。这篇综述总结了有关MPO在CAD中的作用的当前知识，重点是它在斑块破裂中的可能作用以及量化和成像血浆和动脉粥样斑块中MPO的最新进展。