Background and purpose: The purpose of this study was first, to investigate which factor in the fibrinolytic cascade is responsible for the recently observed increase of fibrinolytic activity in patients with aneurysmal subarachnoid hemorrhage (SAH), and second, the cause of this increase.
Methods: Fibrinolytic activity and the main regulators of endogenous fibrinolytic activity, tissue plasminogen activator, and plasminogen activator inhibitor 1 (PAI-1) were measured in patients treated with and without nimodipine.
Results: In patients with aneurysmal SAH, fibrinolytic activity significantly increases from 2.7 IU/mL on admission to 4.2 IU/mL in week 3 (P<0.01, paired-sample t test), caused by a 1.6-fold decrease in plasma levels of PAI-1. The results also show that increased fibrinolytic activity is seen only in patients treated with nimodipine and that plasminogen activity and PAI-1 returned to baseline levels after treatment with nimodipine had been discontinued.
Conclusions: The mechanism of increased fibrinolytic activity in patients with aneurysmal SAH is a decrease in the level of PAI-1, which is most likely caused by treatment with nimodipine.