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斑块侵蚀与急性冠状动脉综合征:表型、分子特征及未来方向。

Plaque erosion and acute coronary syndromes: phenotype, molecular characteristics and future directions.

机构信息

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.

Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA, USA.

出版信息

Nat Rev Cardiol. 2021 Oct;18(10):724-734. doi: 10.1038/s41569-021-00542-3. Epub 2021 May 5.

DOI:10.1038/s41569-021-00542-3
PMID:33953381
Abstract

Although acute coronary syndromes (ACS) remain one of the leading causes of death, the clinical presentation has changed over the past three decades with a decline in the incidence of ST-segment elevation myocardial infarction (STEMI) and an increase in non-STEMI. This epidemiological shift is at least partially explained by changes in plaque biology as a result of the widespread use of statins. Historically, atherosclerotic plaque rupture of the fibrous cap was thought to be the main culprit in ACS. However, plaque erosion with an intact fibrous cap is now responsible for about one third of ACS and up to two thirds of non-STEMI. Two major research approaches have enabled a better understanding of plaque erosion. First, advanced intravascular imaging has provided opportunities for an 'optical biopsy' and extensive phenotyping of coronary plaques in living patients. Second, basic science experiments have shed light on the unique molecular characteristics of plaque erosion. At present, patients with ACS are still uniformly treated with coronary stents irrespective of the underlying pathobiology. However, pilot studies indicate that patients with plaque erosion might be treated conservatively without coronary stenting. In this Review, we discuss the patient phenotype and the molecular characteristics in atherosclerotic plaque erosion and provide our vision for a potential major shift in the management of patients with plaque erosion.

摘要

尽管急性冠状动脉综合征(ACS)仍然是主要死亡原因之一,但在过去的三十年中,其临床表现发生了变化,ST 段抬高型心肌梗死(STEMI)的发生率下降,而非 ST 段抬高型心肌梗死(NSTEMI)的发生率上升。这种流行病学转变至少部分归因于他汀类药物的广泛应用导致斑块生物学的变化。从历史上看,纤维帽下的粥样斑块破裂被认为是 ACS 的主要罪魁祸首。然而,现在有大约三分之一的 ACS 和多达三分之二的非 ST 段抬高型心肌梗死是由纤维帽完整的斑块侵蚀引起的。两种主要的研究方法使我们能够更好地了解斑块侵蚀。首先,先进的血管内成像为活体患者的冠状动脉斑块提供了“光学活检”和广泛表型分析的机会。其次,基础科学实验揭示了斑块侵蚀的独特分子特征。目前,ACS 患者仍然统一接受冠状动脉支架治疗,而不论其潜在的病理生物学如何。然而,初步研究表明,斑块侵蚀患者可能可以通过保守治疗而无需进行冠状动脉支架治疗。在这篇综述中,我们讨论了动脉粥样硬化斑块侵蚀的患者表型和分子特征,并对斑块侵蚀患者管理的潜在重大转变提出了我们的看法。

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