An experimental drug has been found to reduce damage to heart muscles during a heart attack and the risk of bleeding during follow-up treatments, according to a study by the Washington University School of Medicine in St. Louis.
"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, associate professor of medicine and of cell biology and physiology, in a statement. "This also may be a better way to treat strokes caused by or associated with a blood clot."
The researchers said that existing heart attack treatments often cause heart tissue damage. When the blood clot that causes the attack is removed from an artery, molecules from dead and dying cells combine with blood rushing back through the artery. One of these molecules, adenosine triphosphate (ATP), causes inflammation and another, adenosine diphosphate (ADP), triggers more clotting.
The researchers said that the experimental drug APT102 converts ATP and ADP into a benign molecule, adenosine monophosphate. Another enzyme transforms this molecule into adenosine, which is beneficial for the heart. Abendschein said that adenosine opens the blood vessels and increases blood flow among others.
For the study, the researchers tested the drug on 21 dogs. After the clots that caused the heart attacks were removed, eight of the animals were subjected to the normal post heart-attack drug clopidogrel; seven were given low doses of APT102 and six were given high doses of APT102.
The researchers found that the treatment with APT102 significantly lowered heart muscle damage and eliminated the re-occurrence of 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."
Abendschein said that this is a significant finding because majority of patients diagnosed with heart muscle damage suffer from heart failure. While other anticlotting agents have to be digested and converted into their active form in the liver, APT102 can be administered directly into a vein, where it works immediately.
