Key result
Restenosis after percutaneous coronary intervention is driven by an elaborate web of cellular and molecular responses involving platelets, leukocytes, and the coagulation-fibrinolysis system.
Understanding the cellular interactions between platelets and neutrophils may guide future pharmacotherapies to prevent restenosis after PCI.
Describes restenosis pathways post-PCI; leaves open identification of actionable molecular targets.
The major limitation of percutaneous coronary intervention (PCI) is restenosis. Restenosis is considered to be an overreaction of the natural healing process after traumatic balloon dilatation. An elaborate web of cellular and molecular responses, including the interaction of platelets, leukocytes, and the coagulation-fibrinolysis system, as well as the secretion of various growth factors and pro-inflammatory cytokines, contributes to neointimal hyperplasia and the development of restenosis. Moreover, platelet and neutrophil activation after stenting appears to be different from that after balloon angioplasty alone. Pharmacotherapy targeting the cell-to-cell interaction between platelets and neutrophils may potentially offer an effective treatment strategy against restenosis after PCI.
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Lee et al. (2004) conducted a review in Restenosis after percutaneous coronary intervention. Restenosis after percutaneous coronary intervention is driven by an elaborate web of cellular and molecular responses involving platelets, leukocytes, and the coagulation-fibrinolysis system.
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