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Cited by 2,717

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The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes

Epstein, Franklin H., Fuster, Valentin, Badimon, Lina, Badimon, Juan J., Chesebro, James H.·1992·New England Journal of Medicine

Abstract

IN the 19th century there were two major hypotheses to explain the pathogenesis of atherosclerosis: the "incrustation" hypothesis and the "lipid" hypothesis. The incrustation hypothesis of von Rokitansky,1 proposed in 1852 and modified by Duguid,2 suggested that intimal thickening resulted from fibrin deposition, with subsequent organization by fibroblasts and secondary lipid accumulation. The lipid hypothesis, proposed by Virchow3 in 1856, suggested that lipid in the arterial wall represented a transduction of blood lipid, which subsequently formed complexes with acid mucopolysaccharides; lipid accumulated in arterial walls because mechanisms of lipid deposition predominated over those of removal. The two hypotheses are now . . .

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Metadata

Authors
Epstein, F. H., Fuster, V., Badimon, L., Badimon, J. J., & Chesebro, J. H.
Venue
New England Journal of Medicine
Published
1992-01-23
Volume
326
Issue
4
Pages
242-250
ISSN
  • 0028-4793 (ISSN-L)
  • 1533-4406
OpenAlex
W3194355700
Cited by
2,717
References
0
FWCI
36.87
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes. https://app.cochat.ai/papers/10.1056/nejm199201233260406
The paper
Epstein, F. H., Fuster, V., Badimon, L., Badimon, J. J., & Chesebro, J. H. (1992). The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes. New England Journal of Medicine. https://doi.org/10.1056/nejm199201233260406

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.