Pathophysiology of native coronary, vein graft, and in-stent atherosclerosis
Abstract
Plaque rupture, usually of a precursor lesion known as a 'vulnerable plaque' or 'thin-cap fibroatheroma', is the leading cause of thrombosis. Less-frequent aetiologies of coronary thrombosis are erosion, observed with greatest incidence in women aged <50 years, and eruptive calcified nodules, which are occasionally identified in older individuals. Various treatments for patients with coronary artery disease, such as CABG surgery and interventional therapies, have led to accelerated atherosclerosis. These processes occur within months to years, compared with the decades that it generally takes for native disease to develop. Morphological identifiers of accelerated atherosclerosis include macrophage-derived foam cells, intraplaque haemorrhage, and thin fibrous cap. Foam-cell infiltration can be observed within 1 year of a saphenous vein graft implantation, with subsequent necrotic core formation and rupture ensuing after 7 years in over one-third of patients. Neoatherosclerosis occurs early and with greater prevalence in drug-eluting stents than in bare-metal stents and, although rare, complications of late stent thrombosis from rupture are associated with high mortality. Comparison of lesion progression in native atherosclerotic disease, atherosclerosis in saphenous vein grafts, and in-stent neoatherosclerosis provides insight into the pathogenesis of atheroma formation in natural and iatrogenic settings.
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Studies of plaque histology from human autopsy tissues have culminated in a scheme for classification of plaques that encapsulates the progression of atherosclerosis.
“Studies of plaque histology from human autopsy tissues have culminated in a scheme for classification of plaques that encapsulates the progression of atherosclerosis 88,89 and, based on careful observations of plaque composition from human autopsy and animal models, it is clear that VSMCs are major contributors to plaque development at all stages (summarised in FIG. 1).”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [89]
Based on careful observations of plaque composition from human autopsy and animal models, VSMCs are major contributors to plaque development at all stages.
“Studies of plaque histology from human autopsy tissues have culminated in a scheme for classification of plaques that encapsulates the progression of atherosclerosis 88,89 and, based on careful observations of plaque composition from human autopsy and animal models, it is clear that VSMCs are major contributors to plaque development at all stages (summarised in FIG. 1).”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [89]
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- Authors
- Yahagi, K., Kolodgie, F. D., Otsuka, F., Finn, A. V., Davis, H. R., Joner, M., & Virmani, R.
- Affiliations
- CVPath Institute (US)
- Emory University Hospital (US)
- Corresponding author
- Virmani, Renu
- ORCID
- Venue
- Nature Reviews Cardiology
- Published
- 2015-10-27
- Volume
- 13
- Issue
- 2
- Pages
- 79-98
- ISSN
- 1759-5002 (ISSN-L)
- 1759-5010
- OpenAlex
- W2264045234
- Cited by
- 548
- References
- 122
- Citations by year
- 2026: 29 · 2025: 41 · 2024: 70 · 2023: 56 · 2022: 62 · 2021: 59 · 2020: 70 · 2019: 50 · 2018: 49 · 2017: 36 · 2016: 24
- FWCI
- 6.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Cardiology (publishedVersion)
- PubMed (publishedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK094434)
- Topics
- Health Sciences › Medicine › Surgery › Coronary Interventions and Diagnostics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cerebrovascular and Carotid Artery Diseases
- Keywords
- coronary artery disease, vein graft atherosclerosis, in-stent neoatherosclerosis, premature atherosclerosis, atherosclerotic plaque morphology, plaque rupture, vulnerable plaque, thin-cap fibroatheroma, coronary thrombosis, plaque erosion, saphenous vein graft, drug-eluting stents, bare-metal stents, stent thrombosis, intraplaque hemorrhage, foam cells
- MeSH terms
- Coronary Artery Bypass, Coronary Artery Disease, Humans, Saphenous Vein, United States, Incidence, Prevalence, Survival Rate, Disease Progression, Coronary Restenosis, Drug-Eluting Stents, Plaque, Atherosclerotic
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