Changes in Vascular Geometry in Atherosclerotic Plaque Rupture and Its Relationship to Thrombosis in Acute Vascular Events

  • Lina Badimon
  • Juan Jose Badimon
Part of the NATO ASI Series book series (NSSA, volume 235)


Angiography in patients with unstable angina or myocardial infarction with subtotal coronary occlusion often reveals eccentric stenoses with irregular borders suggesting ruptured atherosclerotic plaques and thrombosis, as documented by angioscopy and at autopsy. We have studied these processes “ex vivo” in a perfusion chamber, “in vivo” in porcine and canine models, and in vitro in humans. Our results suggest that specific local risk factors at the time of plaque disruption influence the degree of thrombogenicity, and therefore the different clinical syndromes. These risk factors can be subdivided into two groups: local vessel wall related factors and systemic factors of local action(1). There is clinical and experimental evidence to suggest that three systemic factors at the time of plaque rupture may enhance thrombogenicity: a) the levels of epinephrine (i.e., in stress and smoking), b) the level of serum cholesterol, and c) impaired fibrinolysis resulting from high serum lipoprotein (a). Among the local factors, besides the degree of vascular damage, there are rheological factors that significantly contribute to the outcome of thrombosis. We have experimentally demonstrated that the more severe the stenotic lesion after plaque rupture the higher the local shear rate with an enhanced platelet deposition and thrombus formation; and, that platelet deposition and thrombosis are particularly favored if the rupture includes the apex of the stenotic plaque because of its high shear rate. Plaque rupture produces a rough surface with variable geometry that stimulates platelet activation and occlusive thrombus which is enhanced depending on the degree of damage. The presence of a residual thrombus, after spontaneous or pharmacological reperfusion, induces geometrical changes with a further narrowing of the patent cross-sectional area open to flowing blood; additionally, the surface of the residual thrombus is very thrombogenic due to fibrin bound thrombin in the original fragmented thrombus.


Shear Rate High Shear Rate Perfusion Chamber High Grade Stenosis Platelet Deposition 
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Copyright information

© Springer Science+Business Media New York 1992

Authors and Affiliations

  • Lina Badimon
    • 1
    • 2
  • Juan Jose Badimon
    • 1
    • 2
  1. 1.Unidad de Investigación Cardiovascular, Centro de Investigación y DesarrolloConsejo Superior de Investigaciones CientíficasBarcelonaSpain
  2. 2.Cardiovascular Biology Research, Cardiac UnitMassachusetts General Hospital, Harvard Medical SchoolBostonUSA

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