tPA: Still the underused clot-buster in stroke management

Most people experiencing heart attack symptoms would immediately call 911 in order to be taken to the hospital for urgent care. Yet patients suffering a stroke or "brain attack" often do not seek immediate help, researchers say. This is of particular concern because the clot-busting drug tissue plasminogen activator (tPA, alteplase) has been shown to be most effective at limiting stroke damage the earlier it is administered - within 3 to 4.5 hours of symptom onset.

Need for education

"This delay points to a need for more awareness and education about early stroke symptoms among patients and emergency personnel," said John Galbraith Simmons, co-author of tPA for Stroke: The Story of a Controversial Drug.

Furthermore, neurologists typically have not been trained to make decisions in emergency settings about such matters as stroke care, but more often treat conditions that develop slowly, such as Parkinson's disease.

How can pharmacists help improve stroke care? According to Simmons, pharmacists can play a crucial role in educating patients about stroke risk factors and primary stroke prevention, such as smoking cessation and blood pressure control.

Hospital pharmacists can actively work with a multidisciplinary team to develop treatment protocols and start appropriate therapy for select patients in a safe and timely manner.

Emerging data

Independent of its clot-busting properties, a modified form of tPA exerts neuroprotective effects on brain cells when they are deprived of oxygen and glucose, a recent study reported in The Journal of Neuroscience. The investigators studied the effects of modified tPA in mice by blocking a vessel supplying blood to the brain for one hour, simulating a stroke. A decrease in the volume of ischemic lesion was seen following treatment with the mutated form of tPA.

A main implication of the study findings, the authors suggested, is that those ischemic stroke patients who currently remain untreated due to contraindications to protease-active tPA as a thrombolytic may still benefit from administration of inactive tPA as a neuroprotector. These preliminary findings, however, still need further validation in a pilot clinical trial.