title: Fibrinolytic response to venous occlusion is decreased in patients after Kawasaki disease.
abstract: Impaired fibrinolysis is considered a sensitive marker of endothelial dysfunction. Persistent endothelial dysfunction occurs in some patients following Kawasaki disease. The aim of the present study was to assess whether impaired fibrinolysis is present in long-term survivors of Kawasaki disease. The study included 42 children with a documented history of Kawasaki disease presenting with or without coronary lesions, and 26 healthy controls. Blood samples were collected from patients and controls prior to and following venous occlusion stress testing. Significantly decreased fibrinolytic response to venous occlusion was detected in patients compared with controls due to decreased tissue plasminogen activator. In addition, patients had significantly increased plasma concentrations of plasminogen and fibrinogen, which were related to similar increases of alpha2 -macroglobulin. Decreased fibrinolytic response was found in patients with coronary aneurysms but also in those without coronary lesions. In summary, a decreased fibrinolytic response to venous occlusion may reflect persistent endothelial damage following acute Kawasaki disease, potentially predisposing these patients to accelerated atherosclerosis and cardiovascular disease in early adult life.
authors.affiliation: Hamilton Civic Hospitals Research Centre, Hamilton, Ontario, Canada. manuela.albisetti@kispi.unizih.ch
authors.forename: Manuela
authors.initials: M
authors.lastname: Albisetti
authors.forename: Anthony K C
authors.initials: AK
authors.lastname: Chan
authors.forename: Brian W
authors.initials: BW
authors.lastname: McCrindle
authors.forename: Derek
authors.initials: D
authors.lastname: Wong
authors.forename: Patricia
authors.initials: P
authors.lastname: Vegh
authors.forename: Margaret
authors.initials: M
authors.lastname: Adams
authors.forename: Maria
authors.initials: M
authors.lastname: Dinyari
authors.forename: Paul
authors.initials: P
authors.lastname: Monagle
authors.forename: Maureen
authors.initials: M
authors.lastname: Andrew
mesh_terms: D000293:Adolescent; D000328:Adult; D001777:Blood Coagulation / Q000502:physiology; D002648:Child; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology*; D016491:Peripheral Vascular Diseases / Q000097:blood / Q000503:physiopathology*; D010949:Plasma / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010959:Tissue Plasminogen Activator / Q000097:blood; D019396:Tissue Polypeptide Antigen / Q000097:blood; D014680:Veins / Q000473:pathology; D020246:Venous Thrombosis; D000511:alpha-Macroglobulins / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; D019396:Tissue Polypeptide Antigen; D000511:alpha-Macroglobulins; C036309:fibrin fragment D; D014841:von Willebrand Factor; D010959:Tissue Plasminogen Activator