title: Intimal neovascularisation is a prominent feature of atherosclerotic plaques in diabetic patients with critical limb ischaemia.
abstract: BACKGROUND
  Neovascularisation of atherosclerotic plaques correlates with increased plaque instability and subsequent risk of vascular complications. Diabetics have widespread atherosclerotic involvement of the arterial tree and a more aggressive form of the disease culminating in increased plaque instability. This results in a greater incidence of ischaemic sequelae than in non-diabetics. Previous studies have examined neovascularisation as a marker of plaque instability in both the carotid and coronary territories and revealed a greater degree in both symptomatic and diabetic patients. This is the first study to examine intimal neovascularisation in lower limb peripheral arterial disease.
  
  
  METHODS
  Arterial specimens were taken from 20 patients, ten of whom were type 2 diabetics, undergoing major lower limb amputation for unreconstructable critical ischaemia. Sections were stained with H&E for morphological assessment and inflammatory cell characterisation. Additional sections underwent immunohistochemical staining for CD31 and von-Willebrand Factor (vWF) and the number of intimal vessels per four 40x magnification fields assessed.
  
  
  RESULTS
  There was a more prominent inflammatory infiltrate in diabetic subjects compared to non-diabetic controls. Diabetic patients had a greater degree of intimal neovascularisation compared to controls with a median of 11.5 and 2.0 vessels per field respectively (P<0.05). Sub-group analysis revealed that diabetic patients medicating with HMG-CoA Reductase inhibitors (Statins) had a greater degree of neovascularisation compared to those not taking this class of medication.
  
  
  CONCLUSIONS
  Diabetic patients with critical limb ischaemia requiring amputation demonstrate a greater degree of plaque intimal neovascularisation and inflammatory infiltrate compared to their non-diabetic counterparts. This may explain the greater plaque instability and subsequent cardiovascular complications seen in these patients.
authors.affiliation: Department of Vascular Surgery, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK.
authors.forename: A
authors.initials: A
authors.lastname: Carter
authors.forename: M O
authors.initials: MO
authors.lastname: Murphy
authors.forename: N J
authors.initials: NJ
authors.lastname: Turner
authors.forename: A T
authors.initials: AT
authors.lastname: Halka
authors.forename: J
authors.initials: J
authors.lastname: Ghosh
authors.forename: F
authors.initials: F
authors.lastname: Serracino-Inglott
authors.forename: M G
authors.initials: MG
authors.lastname: Walker
authors.forename: F
authors.initials: F
authors.lastname: Syed
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D050197:Atherosclerosis / Q000188:drug therapy / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000188:drug therapy / Q000503:physiopathology*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D007150:Immunohistochemistry; D007511:Ischemia / Q000503:physiopathology*; D007866:Leg / Q000098:blood supply*; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D017539:Tunica Intima / Q000473:pathology*
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D019408:Platelet Endothelial Cell Adhesion Molecule-1