doi: 10.1161/hc4301.097195
(Circulation. 2001;104:2228.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
Perivascular Inflammation After Balloon Angioplasty of Porcine Coronary Arteries
From the Winship Cancer Institute (E.O., T.C., H.D.L., J.N.W.), the Department of Surgery (J.V.-J.), and the Department of Medicine (N.A.S.), Emory University, Atlanta, Ga; and the Department of Medicine (R.B.G.), University of Washington, Seattle. Dr Okamoto is currently affiliated with the Second Department of Internal Medicine, Gunma University, Gunma, Japan, and Dr De Leon is currently affiliated with the Atlanta Cardiovascular Research Institute, Norcross, Ga.
Correspondence to Josiah N. Wilcox, PhD, Emory University, Division of Hematology/Oncology, 1639 Pierce Dr, Room 1115 WMRB, Atlanta, GA 30322. E-mail medjnw{at}emory.edu
Background— Inflammation has been suggested to play a role in vascular lesion formation after angioplasty. Whereas previous studies have focused on inflammatory reactions in the intima and media, less attention has been paid to adventitial and perivascular responses and their potential role in vascular remodeling.
Methods and Results— Balloon overstretch injury of porcine coronary arteries was performed with standard clinical angioplasty catheters. Vessels were examined from 0.5 hour to 14 days after injury by immunohistochemistry and in situ hybridization (ISH) for neutrophil and macrophage markers, cell adhesion molecules (P-selectin, E-selectin, and vascular cell adhesion molecule-1), and neutrophil-specific CXC chemokines (alveolar macrophage–derived neutrophil chemotactic factor [AMCF]-I/interleukin-8 and AMCF-II). Neutrophils accumulated in the adventitia surrounding the injury site from 2 hours to 3 days, followed by macrophages from 1 to 7 days after angioplasty. Inflammation was associated temporally with the expression of mRNAs encoding cell adhesion molecules and chemokines. The main inflammatory and proliferative foci were not limited to the adventitia but rather extended many millimeters away from the injured vessel throughout the surrounding adipose and myocardial tissues.
Conclusions— Inflammatory responses after angioplasty of porcine coronary arteries occurred throughout the entire perivascular tissue. We hypothesize that perivascular inflammatory cells play a role in the recruitment and/or proliferation of adventitial myofibroblasts, possibly through the release of reactive oxygen species and/or cytokines, and thus contribute to vascular remodeling associated with postangioplasty restenosis.
Key Words: angioplasty • inflammation • cell adhesion molecules • remodeling • restenosis
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