Why the study?
Do GPIIb-IIIa antagonists compared to a combination of aspirin, dipyridamole, and AR-C69931 affect platelet-leukocyte interactions in vitro?
Do GPIIb-IIIa antagonists compared to a combination of aspirin, dipyridamole, and AR-C69931 affect platelet-leukocyte interactions in vitro?
In vitro, GPIIb-IIIa antagonists paradoxically increase platelet-monocyte interactions and tissue factor expression compared to a triple antiplatelet combination, potentially explaining adverse outcomes seen with oral GPIIb-IIIa inhibitors.
In vitro data suggest a mechanism for oral GPIIb-IIIa inhibitor risks; leaves open clinical validation.
The effects of the GPIIb-IIIa antagonists abciximab and MK-852 on platelet-leukocyte interactions in vitro were studied and the results compared with those obtained with a combination of aspirin, dipyridamole and AR-C69931 (Asp/Dip/AR-C). Platelet-monocyte (P/M) and platelet-neutrophil (P/N) conjugate formation increased when blood was stirred or a platelet agonist was added. Leukocyte activation also occurred as judged by expression of surface tissue factor antigen and CD11b. Abciximab and MK-852 potentiated P/M, especially when collagen was used. They also increased the amount of tissue factor on the monocytes, but not CD11b. The Asp/Dip/AR-C did not enhance P/M or tissue factor exposure. Augmented tissue factor expression on monocytes in the presence of a GPIIb-IIIa antagonist may be relevant to the increased mortality associated with trials of such antagonists when given orally in patients with vascular disease. The Asp/Dip/AR-C was superior to abciximab and MK-852 in inhibiting platelet and leukocyte function.
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Zhao et al. (2003) studied this question.
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