Expression of 92 KDA Gelatinase in Human Atherosclerotic Lesions Following Recent Plaque Rupture

  • David L. Brown
  • Margaret S. Hibbs
  • Marianne Kearney
  • Eric J. Topol
  • Jeffrey M. Isner
Part of the GWUMC Department of Biochemistry Annual Spring Symposia book series (GWUN)


Coronary atherosclerosis frequently culminates with the development of the acute coronary ischemic syndromes, unstable angina, acute myocardial infarction and sudden cardiac death. These disparate syndromes occur along a clinical continuum linked by a common pathophysiologic event, intracoronary thrombosis (1, 2, 3, 4). Thrombosis is initiated by rupture of atherosclerotic plaque and exposure of highly thrombogenic plaque constituents to coronary blood flow. The extent of the resulting thrombus and its location in the coronary circulation contribute to the different resultant clinical syndromes. Although, the proximate cause of plaque rupture is not known, pathological studies performed on patients dying suddenly of acute coronary thrombosis have documented a consistent relationship between sites of plaque rupture and the presence of intense macrophage infiltration (3, 4).

Key Words

Atherosclerosis Metalloproteinase Unstable angina Plaque Rupture Coronary Artery Disease 


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Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • David L. Brown
    • 1
  • Margaret S. Hibbs
    • 2
  • Marianne Kearney
    • 3
  • Eric J. Topol
    • 4
  • Jeffrey M. Isner
    • 3
  1. 1.Division of Cardiovascular MedicineUniversity of California,San Diego Medical CenterSan DiegoUSA
  2. 2.Division of RheumatologyVeterans Affairs Medical Center NewingtonUSA
  3. 3.Division of Cardiovascular MedicineSt. Elizabeth’s HospitalBostonUSA
  4. 4.Department of CardiologyCleveland Clinic FoundationClevelandUSA

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