A. Geppert et al., Plasminogen activator inhibitor type 1 and outcome after successful cardiopulmonary resuscitation, CRIT CARE M, 29(9), 2001, pp. 1670-1677
Objective: Patients after successful cardiopulmonary resuscitation have bee
n shown to exhibit elevated plasma concentrations of plasminogen activator
inhibitor (PAI) type 1, the main circulating antifibrinolytic protein. It h
as been suggested that elevations in PAI-1 contribute to cerebral no-reflow
after successful cardiopulmonary resuscitation. We analyzed whether PAI-1
concentrations might predict cerebral outcome after cardiopulmonary resusci
tation.
Design: Prospective, controlled study.
Setting: Intensive care unit at a university hospital.
Patients: Thirty-five patients after successful cardiopulmonary resuscitati
on and 35 control patients who were not critically III.
Interventions. Blood sampling for determination of plasma concentrations of
active and total PAI-1 antigen.
Measurements and Main Results: Plasma concentrations of total and active PA
I-1 antigen on the second day after successful cardiopulmonary resuscitatio
n were significantly higher in patients after cardiopulmonary resuscitation
than in controls (p < .0001) and were unrelated to duration of cardiopulmo
nary resuscitation. Both active and total PAI-1 antigen were higher in pati
ents who developed acute renal failure after cardiopulmonary resuscitation.
Patients with an unfavorable cerebral outcome after cardiopulmonary resusc
itation had higher total PAI-1 antigen concentrations compared with patient
s with good outcome after cardiopulmonary resuscitation (p = .026). We iden
tified 180 ng/mL as the best cutoff value for total PAI-1 antigen with resp
ect to cerebral outcome (chi-square 11.8, p = .001). In a logistic regressi
on analysis, only systemic inflammatory response syndrome (p = .028), acute
renal failure after cardiopulmonary resuscitation (p = .017), and cardiopu
lmonary resuscitation duration > 15 mins (p = .042) were significantly and
independently associated with cerebral outcome after cardiopulmonary resusc
itation. Total PAI-1 antigen reached only borderline significance (p = .058
) but nevertheless slightly improved the correct prediction of cerebral out
come after cardiopulmonary resuscitation.
Conclusions. Acute renal failure after cardiopulmonary resuscitation, syste
mic inflammatory response syndrome, and cardiopulmonary resuscitation durat
ion are better predictors of cerebral outcome after cardiopulmonary resusci
tation than PAI-1 antigen, but determination of total PAI-1 antigen neverth
eless might improve the early prediction of cerebral outcome after cardiopu
lmonary resuscitation. Whether elevated PAI-1 concentrations, possibly via
prothrombogenic/antifibrinolytic effects, contribute causally to cerebral n
o-reflow and acute renal failure after cardiopulmonary resuscitation remain
s to be clarified.