Remodeling of the coronary artery after vascular injury.
Vascular injury, such as angioplasty, induces a complex healing process that is analogous to generalized wound healing. Following initial injury, platelet thrombi and an acute inflammatory response occur, followed by cellular inhibition by monocytes/macrophages, proliferation of vascular smooth muscle cells, and extracellular matrix deposition. The injury repair concludes with organization of the matrix and reendothelialization. Recent studies suggest that restenosis or renarrowing after vascular injury is due to two components: a cellular proliferative process leading to intimal hyperplasia and remodeling of the vessel with a change in vessel geometry. Animal and clinical studies have shown that at least 60% of restenosis can be explained by unfavorable remodeling with vessel constriction rather than intimal hyperplasia. Although a number of factors appear to be associated with remodeling, alterations in extracellular matrix metabolism may be most important.
Faxon
D P
DP
University of Southern California School of Medicine, Los Angeles 90033, USA.
Coats
W
W
Currier
J
J
D000800:Angioplasty, Balloon / Q000009:adverse effects*; D000818:Animals; D001161:Arteriosclerosis / Q000473:pathology / Q000503:physiopathology; D003251:Constriction, Pathologic; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D006965:Hyperplasia; D008666:Metalloendopeptidases / Q000037:antagonists & inhibitors / Q000378:metabolism; D012008:Recurrence; D012039:Regional Blood Flow; D014945:Wound Healing / Q000502:physiology*
D008666:Metalloendopeptidases