title: Evidence for altered inflammatory and repair responses in symptomatic carotid plaques from elderly patients.
abstract: OBJECTIVE
  Most acute cardiovascular events are caused by rupture of an atherosclerotic plaque. The incidence of cardiovascular events increases with age and inflammation is generally considered to be the main cause of increased plaque vulnerability. However, the relationship between age and plaque inflammation has not yet been fully clarified. The aim of our study was to determine if age-dependent plaque vulnerability is associated with increased plaque inflammation.
  
  
  METHODS
  We collected 200 endarterectomy specimens, 103 of which were from patients 70 years or older. One-hundred and five patients had a recent cerebrovascular event, whereas the rest were asymptomatic despite significant carotid stenosis. Smooth muscle cell, lipid and macrophage content were analyzed by histology. Cytokines, growth factors and extracellular matrix proteins were analyzed in whole plaque homogenates by immunoassays and biochemical methods.
  
  
  RESULTS
  Plaques from elderly patients contained less IFN-γ, TNF-α, fractalkine, sCD40L, and elastin. Lipid and macrophage content was higher in plaques from symptomatic compared to asymptomatic patients in the elderly group, but not in younger patients. The elastin and collagen content was lower in plaques from symptomatic patients in both age groups. Plaques associated with symptoms also contained more TNF-α, IL-1β, IL-6, sCD40L, MIP-1β, MCP-1, RANTES and VEGF, regardless of age.
  
  
  CONCLUSIONS
  Our data imply that increased plaque vulnerability in the symptomatic elderly patients is associated with increased lipid accumulation and impaired tissue repair, rather than with increased plaque inflammation, compared to younger individuals.
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden. Electronic address: helena.grufman@med.lu.se.
authors.forename: Helena
authors.initials: H
authors.lastname: Grufman
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden; Department of Cardiology, Skåne University Hospital, Malmö, Sweden.
authors.forename: Alexandru
authors.initials: A
authors.lastname: Schiopu
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden; Department of Cardiology, Skåne University Hospital, Malmö, Sweden.
authors.forename: Andreas
authors.initials: A
authors.lastname: Edsfeldt
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden.
authors.forename: Harry
authors.initials: H
authors.lastname: Björkbacka
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden.
authors.forename: Mihaela
authors.initials: M
authors.lastname: Nitulescu
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden; Department of Cardiology, Skåne University Hospital, Malmö, Sweden.
authors.forename: Marie
authors.initials: M
authors.lastname: Nilsson
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden; Department of Cardiology, Skåne University Hospital, Malmö, Sweden.
authors.forename: Ana
authors.initials: A
authors.lastname: Persson
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden.
authors.forename: Jan
authors.initials: J
authors.lastname: Nilsson
authors.affiliation: Experimental Cardiovascular Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden; Department of Cardiology, Skåne University Hospital, Malmö, Sweden.
authors.forename: Isabel
authors.initials: I
authors.lastname: Gonçalves
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging; D002339:Carotid Arteries / Q000503:physiopathology*; D016893:Carotid Stenosis / Q000473:pathology*; D003094:Collagen / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004549:Elastin / Q000378:metabolism; D016894:Endarterectomy, Carotid; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007249:Inflammation / Q000473:pathology*; D008055:Lipids / Q000097:blood; D008264:Macrophages / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000503:physiopathology* / Q000628:therapy
chemical_list: D016207:Cytokines; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D003094:Collagen; D004549:Elastin
keywords: Aging; Atherosclerosis; Carotid stenosis; Cytokine; Inflammation