Pathophysiology of native coronary, vein graft, and in-stent atherosclerosis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2016-02

AUTHORS

Kazuyuki Yahagi, Frank D. Kolodgie, Fumiyuki Otsuka, Aloke V. Finn, Harry R. Davis, Michael Joner, Renu Virmani

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. More... »

PAGES

79-98

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nrcardio.2015.164

DOI

http://dx.doi.org/10.1038/nrcardio.2015.164

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008175121

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26503410


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