Dimitriadis Kyriakos, Adamopoulou Eleni, Pyrpyris Nikolaos, Dri Eirini, Vaina Sofia, Beneki Eirini, Tsioufis Panagiotis, Kasiakogias Alexandros, Antonopoulos Alexios, Aznaouridis Konstantinos, Aggeli Konstantina, Tsioufis Konstantinos
First Department of Cardiology, School of Medicine, National and Kapodistrian University of Athens, Hippokration General Hospital, Vas Sofias 114, Athens, 115 27, Greece.
Department of Cardiology, Lausanne University Hospital and University of Lausanne, Lausanne, 1005, Switzerland.
J Thromb Thrombolysis. 2025 Jul 18. doi: 10.1007/s11239-025-03152-9.
Coronary atherosclerotic plaques can lead to acute coronary syndrome (ACS) occurrence through three main mechanisms: plaque rupture, plaque erosion and calcified nodule. Many destabilized plaques, however, do not cause cardiovascular events. Instead, thrombus formation is confined, lumen patency is preserved and the arterial wall is restored in a process termed as plaque healing. Early studies regarding coronary plaque healing used arterial specimens to determine its prevalence and histological characteristics. Advances in imaging modalities later enabled the implementation of in vivo studies, which have used optical coherence tomography (OCT) to identify the repaired plaques. They are visualized as lesions with a heterogeneous signal-rich layered or multilayered pattern and a distinct optical density from underlying plaque components. On one hand, plaque healing acts as a protective mechanism against myocardial infarction and unstable angina. On the other hand, the presence of layered plaques indicates previous plaque destabilization and therefore increased cardiovascular risk. Clinicians ought to bear these in mind in order to better apply patient risk stratification and adjust medical interventions. The aim of this review is to discuss the physiology of coronary plaque healing, determine its prevalence and clinical significance, as well as propose possible pathophysiological mechanisms behind impaired plaque healing along with therapeutic options.
冠状动脉粥样硬化斑块可通过三种主要机制导致急性冠状动脉综合征（ACS）的发生：斑块破裂、斑块侵蚀和钙化结节。然而，许多不稳定斑块并不会引发心血管事件。相反，血栓形成受到限制，管腔保持通畅，动脉壁在一个被称为斑块愈合的过程中得以恢复。早期关于冠状动脉斑块愈合的研究使用动脉标本确定其发生率和组织学特征。后来成像技术的进步使得体内研究得以开展，这些研究使用光学相干断层扫描（OCT）来识别修复后的斑块。它们表现为具有异质性富信号分层或多层模式且与下层斑块成分有明显光学密度差异的病变。一方面，斑块愈合是一种预防心肌梗死和不稳定型心绞痛的保护机制。另一方面，分层斑块的存在表明先前斑块不稳定，因此心血管风险增加。临床医生应牢记这些，以便更好地进行患者风险分层并调整医疗干预措施。本综述的目的是讨论冠状动脉斑块愈合的生理学，确定其发生率和临床意义，以及提出斑块愈合受损背后可能的病理生理机制和治疗选择。
