title: Massive fibrin formation with consecutive impairment of fibrinolysis in patients with out-of-hospital cardiac arrest.
abstract: Hypoxia and ischaemia influence blood coagulation and fibrinolysis. This study has been made to determine whether human cardiopulmonary arrest causes fibrin formation and reduction of fibrinolysis. Serial levels of fibrinopeptide A (FPA), fibrinopeptide B beta 15-42 (FPB beta 15-42), D-dimer, tissue plasminogen activator antigen concentration (t-PA antigen), t-PA activity, plasminogen activator inhibitor-1 antigen concentration (PAI-1 antigen), and PAI-1 activity were determined in 63 patients with out-of-hospital cardiopulmonary arrest. In the resuscitated patients, the markedly elevated FPA (194.8 +/- 54.2 ng/ml) at the beginning of cardiopulmonary resuscitation (CPR) significantly decreased to 32.4 +/- 9.1 ng/ml at 24 h after admission (p < 0.01), however, this was still about 20 times that of the normal controls. FPB beta 15-42 and D-dimer increased from the start of CPR to 60 min (189.3 +/- 97.4 ng/ml; p < 0.01 and 7726 +/- 3556 ng/ml; p < 0.001, respectively), and then decreased at 24 h after arrival at the Emergency Department (40.4 +/- 11.1 ng/ml and 5434 +/- 1049 ng/ml, respectively). At 30 min after arrival, FPA and FPB beta 15-42 significantly differed between the resuscitated patients and the patients who died (p < 0.001 and P < 0.05, respectively). Although t-PA antigen and t-PA activity was elevated at the time of arrival, 24 h thereafter, no-t-PA activity was detected. At 24 h after admission, PAI-1 antigen and PAI-1 activity were significantly increased (472.2 +/- 145.5 ng/ml; p < 0.001 and 103.6 +/- 36.1 IU/ml; p < 0.001, respectively). In conclusion, during and after CPR in patients with out-of-hospital cardiac arrest, massive fibrin generation with consecutive impairment of fibrinolysis were observed. These fibrin-mediated events may have some role in the derangement of vital organ function after cardiac arrest.
authors.affiliation: Department of Emergency and Critical Care Medicine, Sapporo City General Hospital, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Gando
authors.forename: T
authors.initials: T
authors.lastname: Kameue
authors.forename: S
authors.initials: S
authors.lastname: Nanzaki
authors.forename: Y
authors.initials: Y
authors.lastname: Nakanishi
mesh_terms: D000368:Aged; D015415:Biomarkers; D001779:Blood Coagulation Factors / Q000032:analysis; D002545:Brain Ischemia / Q000097:blood / Q000209:etiology; D016887:Cardiopulmonary Resuscitation; D005260:Female; D005337:Fibrin / Q000096:biosynthesis*; D005342:Fibrinolysis; D006323:Heart Arrest / Q000097:blood* / Q000150:complications / Q000628:therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000097:blood / Q000209:etiology; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D015427:Reperfusion Injury / Q000097:blood / Q000209:etiology; D010959:Tissue Plasminogen Activator / Q000032:analysis
chemical_list: D015415:Biomarkers; D001779:Blood Coagulation Factors; D017395:Plasminogen Activator Inhibitor 1; D005337:Fibrin; D010959:Tissue Plasminogen Activator