Blood coagulation and fibrinolysis in acute ischaemic and haemorrhagic (intracerebral and subarachnoid haemorrhage) stroke: does decreased plasmin inhibitor indicate increased fibrinolysis in subarachnoid haemorrhage compared to other types of stroke?

Abstract

Ischaemic and haemorrhagic stroke may cause haemostatic abnormalities, apart from concomitant brain damage. In this study, some blood coagulation and fibrinolysis parameters were investigated in 30 patients with ischaemic stroke (atherothrombotic) and 30 with haemorrhagic (20 with intracerebral and 10 with subarachnoid haemorrhage) stroke. The following parameters were determined within the first 24h after stroke: prothrombin time (PT%). activated partial thromboplastin time (aPTT). fibrinogen, activity of FVII, antithrombin. plasmin inhibitor (PI) and fibrin D-dimer. Significant decreases in PT%, FVII activity and antithrombin as well as an increase in fibrinogen and D-dimer were noticed in ischaemic stroke and in both groups of patients with haemorrhagic stroke. PI levels were significantly lower in subarachnoid haemorrhage patients compared with those in controls and those in both the intracerebral haemorrhage and the ischaemic stroke patients. With the exception of this difference, there were no other differences between ischaemic stroke and the two types of haemorrhagic stroke. This could indicate that haemostatic abnormalities are a consequence of brain damage rather than primary haemostatic activation during thrombosis and/or bleeding in the acute phase of stroke. A decrease in the plasmin inhibitor could suggest excessive fibrinolysis in subarachnoid haemorrhage.