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Researchers Find New Experimental Heart Attack Drug Promising

Update Date: Aug 13, 2014 11:01 AM EDT

An experimental drug tested in animals significantly reduces damage to heart muscle from a heart attack and minimizes the risk of bleeding during follow-up treatments, according to a new study. 

"This medication, known as APT102, has the potential to change the paradigm for how heart attack patients initially are treated," said senior author Dana Abendschein, PhD, associate professor of medicine and of cell biology and physiology at Washington University, in the press release. "This also may be a better way to treat strokes caused by or associated with a blood clot."

Heart attack treatments currently available often cause tissue damage. Once the blood clot causing a heart attack is removed from an artery, molecules from dead and dying cells mix with blood rushing back through the artery. Among these molecules, adenosine triphosphate (ATP), is inflammatory; another, adenosine diphosphate (ADP), causes just clotting. 

"ATP and ADP have different roles, but they both lead to more heart damage as they flood through the reopened artery after a heart attack," said Abendschein.

The experimental drug in question is a genetically engineered version of the human protein apyrase that transforms ATP and ADP into a benign molecule. Another enzyme that this drug contains changes the molecule into adenosine, which is beneficial for the heart. 

"Adenosine opens the blood vessels, increases blood flow and also has a protective effect on the lining of the vessels," said Abendschein. "It takes the bad products away and produces a good byproduct that's protective."

The scientists treated 21 dogs for the study. n

"That's a huge benefit because the majority of patients who have a lot of heart muscle damage go on to have heart failure," Abendschein said.

The study addd that by breaking down the clotting factor ADP, treatment with APT102 also eliminates the return of the clots. 

"Virtually every agent that's being used in patients now to prevent clot formation blocks the blood clotting agents known as platelets, and that creates a risk of bleeding," Abendschein said. "This is not true of APT102."

The study is available online in Science Translational Medicine.

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