Healed Plaque Ruptures and Sudden Coronary Death: Evidence That Subclinical Rupture Has a Role in Plaque Progression
By A. Burke, F. Kolodgie, A. Farb, D. Weber, G. Malcom, J. Smialek, Renu Virmani. Circulation, 2001
962 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Radiology, Nuclear Medicine and Imaging, Surgery
View Paper: https://www.semanticscholar.org/paper/c1a9c317070710f8518abbe0a5ae23322b76328d
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Citations in the corpus
- Mechanisms of plaque formation and rupture. (2014, background): “present, and the number of healed ruptures correlates with the severity of stenosis.(105) Other plaques may have a multilayered”
- The Vascular Endothelium and Human Diseases (2013, background): “Furthermore, thrombus reorganization following subacute rupture has been proposed as a mechanism for lesion progression (37-39).”
- From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II. (2003, methodology): “Thrombotic complications that arise from rupture or fissure (small rupture) of a vulnerable plaque may be clinically silent, yet contribute to the natural history of plaque progression and ultimately luminal stenosis [31, 32].”
- Update on acute coronary syndromes: the pathologists' view. (2013, background): “Furthermore, clinically silent plaque rupture is not a rare phenomenon,(48,49) and plaque rupture with mural thrombosis appears to be a common cause of episodic but asymptomatic progression to severe stenosis.(50,51) These pathoanatomical findings explain classical clinical observations,”
- Arterial thrombosis—insidious, unpredictable and deadly (2011, background): “These thrombi, which are often asymptomatic, have an important role in promoting the rapid progression of the underlying atherosclerotic lesion”
- From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. (2003, background): “Therefore, an active fibrinolytic system may be able to prevent luminal thrombosis in some cases of plaque disruption [119, 120].”