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<p>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.</p>

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Coronary plaque healing: a safety net or a hazard indicator?

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月18日

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  • Kyriakos Dimitriadis,
  • Eleni Adamopoulou,
  • Nikolaos Pyrpyris,
  • Eirini Dri,
  • Sofia Vaina,
  • Eirini Beneki,
  • Panagiotis Tsioufis,
  • Alexandros Kasiakogias,
  • Alexios Antonopoulos,
  • Konstantinos Aznaouridis,
  • Konstantina Aggeli,
  • Konstantinos Tsioufis

摘要

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.