Ancrod converts
fibrinogen into soluble
fibrin products, resulting in a decrease in plasma
fibrinogen and blood viscosity, and also induces the release of endogenous
tissue-type plasminogen activator from the vessel wall. These activities suggest that treating patients with acute
ischaemic stroke with
ancrod might result in improved cerebral blood flow and patient outcome. Two large randomised placebo-controlled studies have evaluated treatment with
ancrod in patients with acute
ischaemic stroke. In the first, patients were treated within 6 hours of symptom onset: this was not successful in quickly lowering
fibrinogen levels to the target range (0.7 to 1.0 g/L) and the results were inconclusive. However, a post hoc analysis suggested that treatment with
ancrod was effective in patients whose
fibrinogen level was reduced to less than 1.3 g/L within 6 hours of starting treatment. A second larger study is still in progress, but preliminary results in patients treated within 3 hours of onset of
ischaemic stroke are available and indicate that the target
fibrinogen level of less than 1 g/L within 6 hours of instituting treatment is being achieved in most patients.