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The association of elevated hematocrit and fibrinogen levels with increased stroke risk has led to continued interest in hemorheologic factors and their role in the development of vascular disease and acute stroke. Viscosity increases logarithmically at the lowest shear rates and this effect is magnified at higher hematocrit levels. Fibrinogen may play a causal role in ischemic stroke through several mechanisms. The most prominent of these is its essential role in thrombosis, both as the substrate for fibrin clot formation and as a facilitator of platelet aggregation. The risk of stroke in sickle cell disease (SCD) varies according to genotype and is highest in patients with homozygous SS. Plasma hyperviscosity syndromes are treated by plasmapheresis (plasma exchange) to remove the paraproteins and thereby reduce hyperviscosity and hypervolemia. Newer techniques of cell centrifugation, plasma separation, and filtration may also be useful.
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