By John W. Hallett Jr. MD FACS, Joseph L. Mills MD FACS, Jonathan Earnshaw DM FRCS, Jim A. Reekers MD PhD, Thom Rooke MD
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Additional info for Comprehensive Vascular and Endovascular Surgery: Expert Consult - Online and Print, 2nd Edition
This is most clearly demonstrated by the typical atherosclerotic plaque, often the result of longterm intimal injury. In advanced lesions, the lipid core of the plaque is rich in inflammatory cells (often apoptotic), cholesterol crystals, and TF (generated by activated macrophages within the plaque). 48 Contributing to this is the increased platelet deposition that occurs at the apex of stenoses, the points of maximal shear forces. Thrombosis in the venous circulation differs significantly. Although direct endothelial injury, blood stasis, and changes in its composition leading to hypercoagulable states are known risk factors in venous thrombosis, the inciting event involves the formation of thrombus from local procoagulant events, such as small endothelial disruptions Thrombosis and inflammation P-selectin Extrinsic pathway activation Platelet Release of tissue-factor-rich microparticles Platelet-leukocyte interactions Platelet activation P-selectin expression Thrombosis P-/E-selectin receptor Injury Stasis Hypercoagulability Leukocyteleukocyte interactions Leukocyte activation Leukocyte Endothelial activation P-/E-selectin expression Endothelial-leukocyte interactions P-/E-selectin Endothelial cell Figure 3-6.
Thrombosis is known to directly elicit an inflammatory response. 21 22 SECTION I Background However, only recently have the molecular and cellular events occurring at the thrombus–vessel wall interface been elucidated. A host of cytokines, including tumor necrosis factor (TNF) and the interleukins IL-6, IL-8, and IL-10, have been identified not only as amplifiers of inflammation but also as promoters of thrombosis. COAGULATION MECHANISMS Hemostasis is typically initiated by damage to the vessel wall and disruption of the endothelium, although it may originate in the absence of vessel wall damage.
103 The diagnosis of VWD can often be suggested from a clinical and family history of prolonged or increased episodes of bleeding. Suspicion of VWD can be confirmed with simple laboratory tests evaluating aPTT, VWF levels, VWF activity, and factor VIII activity. 104 Factor VIII activity is decreased in VWD due to its shortened half-life and indirectly prolongs aPTT. VWF levels are evaluated using plasma VWF antigen and an ELISA. VWF activity is evaluated by testing the ability of VWF to cause platelet aggregation in the presence of ristocetin.
Comprehensive Vascular and Endovascular Surgery: Expert Consult - Online and Print, 2nd Edition by John W. Hallett Jr. MD FACS, Joseph L. Mills MD FACS, Jonathan Earnshaw DM FRCS, Jim A. Reekers MD PhD, Thom Rooke MD