Thrombophilia in ischemic stroke subtypes: implications for treatment.
Abstract
The current understanding of thrombogenesis is modeled on Virchow's triad: stasis, hypercoagulability, and vessel wall injury. There is a dynamic (always changing) nonlinear interaction between the vascular wall, blood components, and flow, which at times defined "pathologic" leads to thrombosis or hemorrhage, at other times called "healthy" to normal hemostasis. The triad named after Virchow was not designated as such in Virchow's work. Instead, Virchow showed that thrombosis itself leads to endothelial damage, hypercoagulability, and stasis. Thus, cause and effect regarding the elements of Virchow's triad and thrombosis become indistinguishable if linearity is considered mandatory. Considering a nonlinear relation solves this problem. In the real patient, each element is present to a degree. At every moment in time, the direction of coagulation (toward hemostasis, thrombosis, or hemorrhage) and the dynamic of interaction of the elements of the triad change. The complexity and nonlinearity of the thrombotic context is evident. These facts suggest a new venue for diagnostic classification of stroke (ischemic and hemorrhagic) by causation and have implications for its prevention and treatment. Clinical and laboratory evidence ca...Continue Reading
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