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Allen P. Burke

Researcher at University of Maryland, Baltimore

Publications -  358
Citations -  41025

Allen P. Burke is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Sudden death & Sudden cardiac death. The author has an hindex of 81, co-authored 339 publications receiving 38011 citations. Previous affiliations of Allen P. Burke include University of Maryland Medical Center & Fudan University.

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Lessons From Sudden Coronary Death A Comprehensive Morphological Classification Scheme for Atherosclerotic Lesions

TL;DR: This review will reconsider the current paradigm for understanding the critical, final steps in the progression of atherosclerotic lesions, and devise a simpler classification scheme that is consistent with the AHA categories but is easier to use, able to deal with a wide array of morphological variations, and not overly burdened by mechanistic implications.
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From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II.

Morteza Naghavi, +63 more
- 07 Oct 2003 - 
TL;DR: The term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future and a quantitative method for cumulative risk assessment of vulnerable patients needs to be developed.
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Pathology of the Vulnerable Plaque

TL;DR: Of the three types of coronary thrombosis, a precursor lesion for acute rupture has been postulated and the non-thrombosed lesion that most resembles the acute plaque rupture is the thin cap fibroatheroma (TCFA).
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Coronary Risk Factors and Plaque Morphology in Men with Coronary Disease Who Died Suddenly

TL;DR: Among men with coronary disease who die suddenly, abnormal serum cholesterol concentrations - particularly elevated ratios of total cholesterol to HDL cholesterol - predispose patients to rupture of vulnerable plaques, whereas cigarette smoking predisposes patients to acute thrombosis.
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Intraplaque hemorrhage and progression of coronary atheroma.

TL;DR: By contributing to the deposition of free cholesterol, macrophage infiltration, and enlargement of the necrotic core, the accumulation of erythrocyte membranes within an atherosclerotic plaque may represent a potent atherogenic stimulus that may increase the risk of plaque destabilization.