A Drug That Could Prevent Heart Attacks Without the Risk of Bleeding May Soon Be a Reality

University of Illinois researchers have developed a drug that could prevent heart attacks in vulnerable people without the risk of bleeding.

Heart Monitor

Heart Monitor

Platelet aggregation inhibitors are drugs that inhibit platelet function, particularly platelet activation and aggregation during hemostasis, the set of mechanisms that stop bleeding.

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The main side effect of these drugs is that they produce a drug-induced thrombopathy in platelets, which is usually irreversible. “Unfortunately, current antiplatelet drugs prevent blood clotting, which causes heart attacks and strokes, but they also interfere with the ability of platelets to stop bleeding when a blood vessel ruptures,” says Professor Xiaoping Du of the University of Illinois at Chicago, author of a new study published in Science Translational Medicine. In some cases, severe bleeding can be fatal.

A treatment that acts on the clotting mechanism

The professor of pharmacology and regenerative medicine and his research team have developed a drug that “prevents blood clots, but does not make people susceptible to bleeding, something that other drugs could not do,” he says in a publication.

In a previous study, Xiaoping Du and colleagues identified an important signaling mechanism in the blood clotting process that was not necessary to cause platelets to stick to a wound or prevent bleeding. Based on this discovery, the researchers derived a peptide capable of controlling the signaling mechanism and designed a nanoparticle that successfully carries the peptide in platelets.

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The drug, which is based on peptide-derived nanoparticles – the highly charged M3mP6 HLPN peptide nanoparticles – were then tested in rats as a possible treatment for heart attacks.

Reduced risk of inflammation and bleeding

Administered by injection in rats, the drug reduced heart damage, decreased clotting, and reduced inflammation. Researchers also found better heart function and a higher chance of survival.

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These results are particularly encouraging because they limit reperfusion injury. If the heart tissue is damaged, “reopening of the artery may cause inflammation, leading to leaks and clots in small blood vessels and further damage to the heart,” which may lead to the patient’s death. “We had hoped that this new drug, which does not leak into blood vessels, would help limit reperfusion damage and reduce the risk of heart failure and death, and our hypothesis proved correct. We have seen very promising results from our study,” says Xiaoping Du. This time, new studies in humans will be conducted to confirm the effectiveness of the treatment.


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