Summary
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
Bβ15-42 (FPBβ15-42), 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. FPBβ15-42 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 FPBβ15-42 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.
