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Retention and Activation of Blood-Borne Proteases in the Arterial Wall

Implications for Atherothrombosis

Inserm Unit 698, Cardiovascular Hematology, Bio-Engineering and Remodeling, CHU Xavier Bichat, Paris, France.

View larger version (112K): [in this window] [in a new window] [Download PPT slide]   Figure 1 Histologic aspect of the mural thrombus in abdominal aortic aneurysm. (A) Section through the thrombus showing the red luminal layer corresponding to a newly formed clot, associating patchy areas of red blood cells and fibrin. The intermediate layer represents a structured fibrin gel in which cellular components can no longer be recognized. The abluminal layer is composed of a loose network of degraded fibrin (hematoxylin/eosin, x10). (B) Presence of polymorphonuclear leucocytes in the luminal layer; these cells predominate in the fibrin-rich areas (hematoxylin/eosin, x60). (C) Glycoprotein IIb/IIIa immunostaining showing the predominance of platelet aggregation at the luminal pole of the thrombus in fibrin-rich areas (x10). (D) Anti-CD66b antibody stains degranulating neutrophils that accumulate in the luminal layer (x20). Inset shows neutrophils at different stages of degranulation (x100). (E) Immunostaining with anti-CD68 antibody demonstrates the paucity of monocyte/macrophages in the luminal layer of the thrombus (x20). (Inset) A macrophage that appears contracted and apoptotic (x100). (F) Matrix metalloproteinase-9 immunostaining of gelatinase granules of neutrophils present at the luminal pole of the thrombus (x100). (G) Neutrophil elastase immunostaining at the luminal pole of the thrombus colocalizes with polymorphonulear leukocytes (x100).

View larger version (91K): [in this window] [in a new window] [Download PPT slide]   Figure 2 Histologic aspect of culprit lesions in carotid atheroma. (A) Macroscopic aspect of a carotid culprit lesion showing the hemorrhagic nature of the core. (B) Magnetic resonance imaging of a carotid plaque hemorrhage. Intraplaque hemorrhages are characterized by a focal post-contrast enhancement in T1 spin echocardiography, giving a hyperintensity signal. (C) Masson’s trichrome staining of a culprit carotid lesion, showing the presence of: 1) neocapillaries within the lesion; and 2) intraplaque hemorrhage in the core. This example highlights the heterogeneity of culprit lesions, involving pathologies at different stages: fibrosis and hemorrhages. (D) Alizarin red staining of a culprit carotid lesion revealing the presence of calcification within the core and at the interface between the core and the media.

View larger version (37K): [in this window] [in a new window] [Download PPT slide]   Figure 3 Representative diagram of the biological components conveyed by the intraplaque hemorrhage to the core and their roles in plaque progression. Fe = iron; MPO = myeloperoxidase; PMN = polymorphonuclear leukocyte; RBC = red blood cell.