1-8 The largest of these found the risk of cardiovascular disease (CVD) is more than twofold greater in high- versus low-hematocrit groups. Close modal Clinical correlations between RBC abnormalities and thrombosisĮpidemiologic studies have detected associations between elevated hematocrit and arterial thrombosis. In disease states, abnormal RBCs and RBC-derived microvesicles may also adhere to the endothelium or extracellular matrix, activate platelets and other cells, and enhance local thrombin generation during thrombosis. Once incorporated into venous thrombi, RBCs increase thrombus size and reduce thrombus permeability and susceptibility to lysis. RBCs can also directly or indirectly adhere to the vessel wall and may contribute to thrombin generation within thrombi. In veins, RBC aggregation into stacked rouleaux structures increases blood viscosity. (B) Venous thrombi form slowly in stasis or low flow (frequently in venous valve pockets) and are RBC and fibrin rich. Although RBCs increase blood viscosity, this effect is lessened in arteries by high shear-induced shape change. During arterial thrombosis, RBCs promote platelet margination, increase platelet-thrombus interactions, and enhance platelet adhesion and activation. (A) Arterial thrombi arise in vessels with high shear rates, which promotes the rapid formation of platelet-rich thrombi. Potential contributions of normal and abnormal RBCs to arterial and venous thrombosis/thromboembolism.
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