title: Metabolic syndrome and collateral vessel formation in patients with documented occluded coronary arteries: association with hyperglycaemia, insulin-resistance, adiponectin and plasminogen activator inhibitor-1.
abstract: OBJECTIVE
  The metabolic syndrome (MS) is associated with an increased cardiovascular risk. Patients with the MS have endothelial dysfunction, decreased circulating adiponectin, and a high expression of angiogenic inhibitors such as plasminogen activator inhibitor-1 (PAI-1). We hypothesized that such patients, in the event of a coronary occlusion, might exhibit a less developed collateral circulation.
  
  
  RESULTS
  Three hundred and eighty-seven consecutive patients with at least one coronary occlusion of a major coronary vessel at diagnostic angiography were prospectively enrolled. Collateral development was graded with validated angiographic methods. The MS was defined according to the ATP-III definition. Fasting glucose, adiponectin, insulin concentrations, and PAI-1 were measured at the time of angiography. MS was associated with less developed collateral vessels (P = 0.005). In multivariable analysis adjusting for potential confounding factors including the duration of coronary occlusion (P = 0.0001), fasting glycaemia (P = 0.0007), low adiponectin concentration (P = 0.01), insulin-resistance (HOMA-IR; P = 0.01), high circulating PAI-1 concentration (P = 0.01), and hypertension (P = 0.008) were independently associated with poor coronary collateral vessel development.
  
  
  CONCLUSIONS
  This study shows that in patients with coronary occlusion, collateral circulation is impaired in patients with the MS. This association is partly related to fasting glycaemia and to key parameters linked to insulin resistance.
authors.affiliation: Departments of Cardiology, Centre Hospitalier Régional Universitaire, Lille, France.
authors.forename: Frédéric
authors.initials: F
authors.lastname: Mouquet
authors.forename: François
authors.initials: F
authors.lastname: Cuilleret
authors.forename: Sophie
authors.initials: S
authors.lastname: Susen
authors.forename: Karine
authors.initials: K
authors.lastname: Sautière
authors.forename: Philippe
authors.initials: P
authors.lastname: Marboeuf
authors.forename: Pierre Vladimir
authors.initials: PV
authors.lastname: Ennezat
authors.forename: Eugène
authors.initials: E
authors.lastname: McFadden
authors.forename: Pascal
authors.initials: P
authors.lastname: Pigny
authors.forename: Florence
authors.initials: F
authors.lastname: Richard
authors.forename: Bernadette
authors.initials: B
authors.lastname: Hennache
authors.forename: Marie Christine
authors.initials: MC
authors.lastname: Vantyghem
authors.forename: Michel
authors.initials: M
authors.lastname: Bertrand
authors.forename: Jean
authors.initials: J
authors.lastname: Dallongeville
authors.forename: Brigitte
authors.initials: B
authors.lastname: Jude
authors.forename: Eric
authors.initials: E
authors.lastname: Van Belle
mesh_terms: D052242:Adiponectin / Q000378:metabolism; D000368:Aged; D003097:Collateral Circulation / Q000502:physiology*; D017023:Coronary Angiography; D054059:Coronary Occlusion / Q000150:complications* / Q000378:metabolism; D003925:Diabetic Angiopathies / Q000150:complications* / Q000378:metabolism; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D011446:Prospective Studies; D013234:Stem Cells / Q000378:metabolism
chemical_list: D052242:Adiponectin; D017395:Plasminogen Activator Inhibitor 1