[Specific treatment of the acute cerebral infarct. Present and future].
BACKGROUND
Specific pharmacological strategies in the treatment of the acute phase of a cerebral infarct are directed towards potentiating reperfusion (antithrombotic or thrombolytic drugs) and neuroprotection as early on as possible.


METHODS
The antithrombotic agents are anticoagulants, hypofibrinogemiant agents (Ancrod) and antiaggregants. The IST was done with anticoagulants, using heparin subcutaneously which causes increased bleeding without any obvious benefit. Others have used heparinoids (TOAST) or low molecular weight heparins (FISS or FISS bis) with no benefit either but with excessive bleeding with the former. Regarding Ancrod, a recent North American study (STAT) with administration of it within three hours showed significant benefit three months later. Another European study is still underway (ESTAT). With regard to antiaggregants, IST and CAST were done using Aspirin, showing a drop in early recurrences and increase in recoveries, so that aspirin has been recommended for use during the first 48 hours. There are studies using abciximab (Reopro), a blocker of the IIb-IIIa glycoprotein receptors, in which phase II data have shown that it is safe and tends to improve the outcome. A study on phase III is currently ongoing. The thrombolytic drugs have been evaluated in various trials. The PROACT study evaluated intraarterial pro-UK and showed significant recanalization of middle cerebral artery occlusions, but with a larger number of hemorrhages and no reduction in mortality and besides, in PROACT II the outcome of treated patients was better. The NINDS trial using intravenous rt-PA (0.9 mg/kg in < 3 hours) showed an improved functional state 3 months later. In the ECASS doses of 1.1 mg/kg of rt-PA in < 6 hours were used and improvement was seen after three months which was countered by an increase in cerebral hemorrhage and mortality. The ECASS II, with similar dosage to NINDS and an identical window to ECASS, showed a favorable tendency in the evolution of the treated group, with no increase in symptomatic intracranial hemorrhages. Neuroprotectors have shown to be effective in experimental models of ischaemia but at the moment there is no definite evidence of their benefit in the numerous trials carried out on humans, although some subgroups of patients seem to benefit from some of them. Studies therefore are still being done. In future their use in combination with thrombolysis may be considered.
Servicio de Neurología, Unidad de Ictus, Hospital Universitario La Paz, Universidad Autónoma de Madrid, Madrid, España.
J J
JJ
Muñoz-Torrero
F J
FJ
Mora
E
E
Díez-Tejedor
D000208:Acute Disease; D000925:Anticoagulants / Q000627:therapeutic use*; D002544:Cerebral Infarction / Q000188:drug therapy*; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*
D000925:Anticoagulants; D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors