Key result
In mice with vascular injury, ticagrelor administered before and 4 hours after injury significantly reduced neointima area compared to control (3705±2600 vs 39921±22749 μm2; P<0.01).
Why the study?
Does ticagrelor inhibit platelet function, thrombosis, and neointima formation in murine models of vascular injury?
Does ticagrelor inhibit platelet function, thrombosis, and neointima formation in murine models of vascular injury?
Ticagrelor effectively inhibits P2Y12-mediated platelet function and thrombosis in mice, demonstrating that sustained inhibition is required to prevent neointima formation after vascular injury.
Answers are grounded in this paper and cite their sources.
Preclinical data extend P2Y12 inhibition evidence in vascular injury; leaves open human translation and practice change.
OBJECTIVE: Our goal was to study the effects of ticagrelor on murine platelet function and thrombosis and characterize the time course of P2Y(12) inhibition required to inhibit neointima formation following vascular injury. METHODS AND RESULTS: Mice were treated with ticagrelor or vehicle. Platelet aggregation and P-selectin expression were assessed over time, and thrombus formation was assessed in laser-injured cremasteric arterioles of P2Y(12)+/+ and P2Y(12)-/- mice. Neointima formation in FeCl(3)-injured carotid artery was assessed in C57BL/6 mice treated with different regimens of ticagrelor. Ticagrelor inhibited platelet aggregation and P-selectin expression in a dose-dependent, reversible manner. Ticagrelor inhibited thrombus formation to the same extent as seen in P2Y(12)-/- mice. Neointima formation was markedly reduced in mice treated with ticagrelor before and 4 hours after injury (neointima area: control, 39 921±22 749 μm(2), versus ticagrelor, 3705±2600 μm(2); P<0.01), whereas administration of ticagrelor either before injury only or from 4 hours postinjury was ineffective. CONCLUSIONS: Ticagrelor effectively and reversibly inhibits P2Y(12)-mediated platelet function and thrombosis in mice. P2Y(12) inhibition is required both at the time of and after injury to effectively inhibit neointima formation. Additional studies are warranted to evaluate the role of P2Y(12) inhibition in preventing restenosis.
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Patil et al. (2010) studied Vascular injury and thrombosis. Ticagrelor vs. Vehicle / control was evaluated on Neointima area (p=<0.01). In mice with vascular injury, ticagrelor administered before and 4 hours after injury significantly reduced neointima area compared to control (3705±2600 vs 39921±22749 μm2; P<0.01).
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