Plaque erosion and acute coronary syndromes: phenotype, molecular characteristics and future directions
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 le...
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Published in: | Nature reviews cardiology Vol. 18; no. 10; pp. 724 - 734 |
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Main Authors: | , |
Format: | Journal Article |
Language: | English |
Published: |
London
Nature Publishing Group UK
01-10-2021
Nature Publishing Group |
Subjects: | |
Online Access: | Get full text |
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Summary: | 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.
Atherosclerotic plaque erosion is becoming an increasingly common characteristic of culprit lesions in acute coronary syndromes. In this Review, Fahed and Jang discuss the patient phenotype and the molecular characteristics in plaque erosion and provide their vision for a potential major shift in the management of patients with plaque erosion.
Key points
Plaque erosion rather than plaque rupture has become the predominant mechanism of non-ST-segment elevation myocardial infarction as a result of better control of cardiovascular risk factors since the introduction of statins.
Plaque erosion starts with changes in endothelial shear stress gradients that activate Toll-like receptor 2 in endothelial cells, resulting in loss of basement membrane integrity and endothelial cell desquamation, with subsequent formation of neutrophil extracellular traps and thrombosis.
Optical coherence tomography has enabled the in vivo diagnosis of plaque erosion, providing a better understanding of the characteristics and vascular biology of plaque erosion in patients with acute coronary syndromes.
Plaque erosion is characterized by preserved vascular integrity, a larger vessel lumen than in plaque rupture and the presence of a platelet-rich thrombus and, overall, is associated with a better risk profile and outcomes than plaque rupture.
Multiple clinical, angiographic and laboratory predictors of plaque erosion can help identify patients with plaque erosion, but more specific point-of-care biomarkers and non-invasive imaging techniques are needed.
Early clinical studies suggest that patients with plaque erosion might be managed without percutaneous coronary intervention, ushering in a new era of precision medicine in the management of patients with acute coronary syndromes. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-2 |
ISSN: | 1759-5002 1759-5010 |
DOI: | 10.1038/s41569-021-00542-3 |