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Research

Cardiovascular Disease and Stroke


Researchers at Ohio State University Medical Center examined the use of an investigative intravenous antiplatelet drug, cangrelor, and found it to be an effective bridge between long-lasting oral antiplatelet medications and cardiac surgery. The drug’s platelet inhibition rapidly loses effect within a few hours, so it can be discontinued just prior to surgery. Results of the study are available in the January 18, 2012 edition of the Journal of the American Medical Association. In the study, 210 patients at 34 international medical centers including Ohio State were randomized to stop oral antiplatelet therapy and receive either intravenous cangrelor or placebo for up to five days prior to coronary artery bypass surgery. Treatment stopped approximately three hours before incision. Researchers found patients treated with cangrelor maintained a low risk of clotting complications from platelet deactivation without a significant excess in bleeding or bleeding complications, compared to those on placebo.

Stroke is the fourth leading cause of death in the U.S. and the leading cause of long-term disability. Department of Surgery faculty are uncovering new means and mechanisms to protect brain tissue from stroke injury. One such approach employs dietary supplementation with a lesser characterized vitamin E analog not found in Western diet called alpha-tocotrienol (TCT). Investigators in Surgery have identified both neuro- and vascular-protective properties of this unique natural form of vitamin E that significantly protect brain tissue against stroke induced injury. This multi-modal approach to protection is strengthened by a safety profile of a natural vitamin that enables combining treatment with standard of care therapies for stroke survivors. A second line of investigation by Department of Surgery researchers has uncovered mechanisms to turn otherwise neurotoxic molecules released in the brain during stroke into a source of energy that sustains neuron cell survival. Here, investigators identified an enzyme called Glutamate Oxaloacetate Transaminase (GOT) that lowers cell death-inducing levels of glutamate in the brain during stroke by converting it into a source of cellular energy. Studies are now underway to identify novel small molecules that increase expression and activity of GOT for better protection against stroke injury.