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Drug Cuts Muscle Damage After Heart Attack

Safety trial shows novel compound blocks enzyme triggering cell and tissue death

THURSDAY, Feb. 14 (HealthDay News) -- A drug designed to lessen muscle damage from a heart attack has passed initial safety tests in humans.

The drug, known as KAI-9803, blocks the activity of an enzyme called delta protein kinase C that triggers cell and tissue death in the aftermath of percutaneous coronary intervention (PCI). PCI is a set of procedures including balloon angioplasty and stent placement that clear and prop open clogged coronary blood vessels that lead to a heart attack.

Although the trial was not designed to demonstrate the efficacy of KAI-9803, researchers said early data suggest it appears to be a promising compound. Results of the study, done at the Duke Clinical Research Institute, are available online and are expected to be published in the Feb. 19 issue of Circulation.

Earlier studies in animals showed that KAI-9803 lessened damage to the heart muscle and quickly restored its pumping function.

"We may not be able to intervene in the first stage of a heart attack, but we think there may be ways to limit damage caused by reperfusion injury," lead investigator Dr. Matthew Roe, a cardiologist at Duke, said in a prepared statement.

The heart suffers damage at two major points in a heart attack, Roe said: first, when a blockage in a coronary artery prevents blood and oxygen from getting to the heart, and then again when the patient undergoes PCI and normal blood flow is restored through reperfusion.

Researchers randomized 154 patients who had suffered heart attacks and were eligible for PCI into either one of four dosing levels of KAI-9803 or a placebo. Patients underwent PCI with physicians injecting the drug directly into their coronary blood vessels during the procedure.

"We designed the trial to find out if KAI-9803 is safe for humans, and we accomplished that goal; we did not see any serious side effects," Roe said. "We also found, however, many promising signs of beneficial drug activity such as lessened damage to the heart muscle and improvement in electrical conductivity in the heart that corresponded to restoration of blood flow to the heart muscle. As a result, we feel this drug has the potential to be helpful in reducing the impact of a heart attack in humans."

More information

To learn more about heart attack warning signs and prevention, visit the National Heart, Lung, and Blood Institute.

-- Kevin McKeever

SOURCE: Duke University Medical Center & Health System, news release, February 2008

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