Experimental Heart Medicine Minimizes Blood-Clot Risk

Heart disease remains the number one cause of death for both men and women in the United States. Those with certain cardiovascular issues may also be at an increased risk of stroke or heart attack.

Now, recent findings published in the journal Science Translational Medicine have found that an experimental drug could help to significantly reduce damage to the heart muscle following a heart attack, as well as minimize a need for follow-up treatments.

"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 a news release. "This also may be a better way to treat strokes caused by or associated with a blood clot."

Treatments available to deal with this health issue carry costly side-effects. For instance, once a blood clot that's responsible for the heart attack is removed from an artery, molecules from dead and dying cells can mix with blood that's rushing back to the same area, including the the inflammatory molecule adenosine triphosphate (ATP) as well as adenosine diphosphate (ADP).

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

Scientists based their findings on the treatment of 21 canines. They found that the experimental product was extremely succesful in preventing damage to the heart muscle. Furthermore, ATP102 also helped to eliminate the return of blood clots that are commonly associated with the clotting factor ADP.