Induction of platelet white blood cell (WBC) aggregate formation by platelets and WBCs in red blood cell units.

Background: Transfusion of red blood cell (RBC) preparations is independently associated with adverse clinical outcomes in patients with acute cardiovascular disease. This study was designed to define mechanisms potentially contributing.
Study Design and Methods: The presence of platelets (PLTs), activated PLTs (PLTs expressing P-selectin), PLT-monocyte aggregates (PMAs), and PLT-neutrophil aggregates (PNAs) was determined in vitro with the use of flow cytometry in whole blood from healthy volunteers, in RBCs, and in whole blood after adding aliquots of RBCs. Both prestorage leukoreduced and nonleukoreduced RBCs were analyzed. Nonleukoreduced RBCs were subfractionated with the use of centrifugation and filtration to obtain a RBC-free and a cell-free fraction. Formation of PMAs and PNAs was determined in whole blood after the addition of aliquots of these subfractions.
Results: Nonleukoreduced RBCs contained 50 +/- 18 percent of the PLTs found in whole blood from healthy volunteers, and 43 +/- 16 percent of the PLTs were activated. Leukoreduced RBCs contained few PLTs (0.2 +/- 0.1% of volunteer blood). The majority (>60%) of white blood cells (WBCs) in nonleukoreduced RBCs were associated with PLTs. The formation of PMAs and PNAs in whole blood was increased approximately fivefold after addition of nonleukoreduced-RBCs (p < 0.0001) and by less than twofold with leukoreduced RBCs (p = 0.01). Addition of the essentially cell-free fraction of nonleukoreduced RBCs did not increase the formation of PNA or PMA in whole blood significantly.
Conclusion: RBC preparations, particularly nonleukoreduced RBCs, contain activated PLTs and PLT-WBC aggregates and induce formation of PLT-WBC aggregates. This may be one mechanism contributing to adverse outcomes linked to transfusions in patients with cardiovascular disease.