Background and Purpose-The purpose of this study was first, to investigate
which factor in the fibrinolytic cascade is responsible for the recently ob
served increase of fibrinolytic activity in patients with aneurysmal subara
chnoid hemorrhage (SAH), and second, the cause of this increase.
Methods-Fibrinolytic activity and the main regulators of endogenous fibrino
lytic activity, tissue plasminogen activator, and plasminogen activator inh
ibitor 1 (PAI-1) were measured in patients treated with and without nimodip
ine.
Results-In patients with aneurysmal SAH, fibrinolytic activity significantl
y increases from 2.7 IU/mL on admission to 4.2 IU/mL in week 3 (P <0.01, pa
ired-sample t test), caused by a 1.6-fold decrease in plasma levels of PAI-
I. The results also show that increased fibrinolytic activity is seen only
in patients treated with nimodipine and that plasminogen activity and PAI-I
returned to baseline levels after treatment with nimodipine had been disco
ntinued.
Conclusions-The mechanism of increased fibrinolytic activity in patients wi
th aneurysmal SAH is a decrease in the level of PAI-1. which is most likely
caused by treatment with nimodipine.