title: Impact of adventitial neovascularisation on atherosclerotic plaque composition and vascular remodelling in a porcine model of coronary atherosclerosis.
abstract: There is little in vivo data in regards to the impact of adventitial neovascularisation on vascular remodelling and plaque composition. Using a porcine model of coronary atherosclerosis, we aimed to determine the impact of adventitial neovascularisation on plaque composition and vascular remodelling evaluated by IVUS.
  
  
  
  Coronary atherosclerosis was induced by adventitial delivery of lipids and a high cholesterol diet. At termination all vessels were analysed using IVUS to determine the degree of remodelling of each individual segment containing atherosclerotic lesions. Then, each segment was correlated with its correspondent histological frame for plaque composition and neovessel density. A total of 57 atherosclerotic lesions at different stages of development were analysed. The total neovessel count (TNC) correlated to the degree of plaque burden (15.6+/-7.2 TNC in <40% stenosis versus 35.7+/-14.0 TNC in >60% stenosis, p<0.01) and to the amount of intra-plaque collagen (32.4+/-14.1%, lower TNC tertile versus 47.5+/-8.9% upper TNC tertile, p< 0.01). The amount of intra-plaque SMC content inversely correlated with the TNC (49.7+/-18.9% versus 36.4+/-14.4%, lower versus upper tertiles, p<0.05). Plaques with the highest TNC showed higher remodelling indexes by IVUS (0.89+/-0.32 in lower TNC tertile versus 1.36+/-0.73 in upper TNC tertile, p<0.05) and higher macrophage cell content (161.42+/-157.6 in lower TNC tertile versus 340.6+/-127.2 in upper TNC tertile, p<0.05) compared to non-remodelled segments.
  
  
  
  Adventitial neovascularisation is more prominent in positively remodelled segments and appears to be associated to SMC loss, increase collagen deposition and localised macrophage infiltration.
authors.affiliation: Skirball Center for Cardiovascular Research, New York, NY, USA.
authors.forename: Carlos L
authors.initials: CL
authors.lastname: Alviar
authors.forename: Armando
authors.initials: A
authors.lastname: Tellez
authors.forename: David
authors.initials: D
authors.lastname: Wallace-Bradley
authors.forename: Gabriel
authors.initials: G
authors.lastname: Lopez-Berestein
authors.forename: Angela
authors.initials: A
authors.lastname: Sanguino
authors.forename: Daryl G
authors.initials: DG
authors.lastname: Schulz
authors.forename: Angela
authors.initials: A
authors.lastname: Builes
authors.forename: Christie M
authors.initials: CM
authors.lastname: Ballantyne
authors.forename: Chao-Yuh
authors.initials: CY
authors.lastname: Yang
authors.forename: Greg L
authors.initials: GL
authors.lastname: Kaluza
authors.forename: Juan F
authors.initials: JF
authors.lastname: Granada
mesh_terms: D000818:Animals; D003094:Collagen / Q000378:metabolism; D003238:Connective Tissue / Q000098:blood supply*; D023921:Coronary Stenosis / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D004195:Disease Models, Animal; D018450:Disease Progression; D007150:Immunohistochemistry; D008264:Macrophages / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D012720:Severity of Illness Index; D013552:Swine; D018084:Ultrasonography, Interventional
chemical_list: D003094:Collagen