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Molecular and cellular basis of restenosis after percutaneous coronary intervention: the intertwining roles of platelets, leukocytes, and the coagulation–fibrinolysis system
Author(s) -
Lee Michael S,
David Eric M,
Makkar Raj R,
Wilentz James R
Publication year - 2004
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1598
Subject(s) - restenosis , medicine , platelet , fibrinolysis , coagulation , percutaneous coronary intervention , conventional pci , cardiology , angioplasty , platelet activation , myocardial infarction , stent
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. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.