The thin-cap fibroatheroma: a type of vulnerable plaque: The major precursor lesion to acute coronary syndromes
By F. Kolodgie, A. Burke, A. Farb, H. Gold, Junying Yuan, J. Narula, A. Finn, Renu Virmani. Current Opinion in Cardiology, 2001
700 citations recorded by the source corpus.
Subfields: Cancer Research, Cardiology and Cardiovascular Medicine, Surgery
View Paper: https://www.semanticscholar.org/paper/14c58d9164aabbc6befc5feec4b023a908de92f1
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Citations in the corpus
- Pathology of the vulnerable plaque. (2007, background): “Over 50% of the TCFAs occur n the proximal portions of the major coronary arteries, left nterior, left circumflex and the right, and another one-third in he mid portion of these arteries, and the rest are distributed in istal segments (5).”
- Mechanisms of plaque formation and rupture. (2014, background): “cap (Figure 5).(86,93) Although the macrophage density in ruptured caps is usually high,(93) whole-plaque macrophage den-”
- Atherosclerotic Plaque Progression and Vulnerability to Rupture: Angiogenesis as a Source of Intraplaque Hemorrhage (2005, background): “Focal collections of T-cell– and macrophage-derived angiogenic factors contribute to: (1) the arborization of vasa vasorum around the necrotic core; (2) the formation of immature vessels; and (3) loss of basement membrane around functional capillaries.”
- From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. (2003, background): “These plaques have a cap thickness of <100 mm and a lipid core accounting for >40% of the plaque’s total volume [8].”
- From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II. (2003, background): “These plaques have a cap thickness of <100 mm and a lipid core accounting for >40% of the plaque’s total volume [8].”
- Update on acute coronary syndromes: the pathologists' view. (2013, background): “In TCFA, the necrotic core occupies 23% of plaque area.(66) The amount of inflammation varies, but culprit lesions in ACS are usually more inflamed than those in stable angina,(79,80) and the thin and disrupted fibrous caps are usually heavily inflamed (macrophage density 26%).”