An older drug may offer a new way to stop heart-attack clots

A hospital medicine commonly used for acetaminophen poisoning has stopped artery-blocking clots in laboratory and animal experiments, pointing to a possible new strategy for lowering the risk of heart attacks and strokes. Instead of targeting platelets directly, the approach focuses on a clot-forming protein.

Researchers at the Georgia Institute of Technology explored whether N-acetylcysteine could be repurposed to disrupt the earliest steps of clot formation in narrowed arteries. The drug is already used in hospitals for a different purpose.

According to the study, published in Arteriosclerosis, Thrombosis, and Vascular Biology, the team tested human blood in a laboratory flow system and also carried out experiments in mice. The work did not show that the medicine prevents heart attacks in people.

Platelets are tiny blood components that help seal damaged vessels, which is vital when bleeding occurs. But when a platelet-rich clot forms inside an artery, it can cut off oxygen supply to the heart or brain.

The researchers concentrated on von Willebrand factor, a large protein that helps platelets latch on where clotting is needed. Under certain flow conditions, it unfolds and captures platelets.

In a severely narrowed artery, that process can contribute to a growing blockage. Blocking the interaction early could provide an alternative to drugs that mainly work by dampening platelet activity.

Many current anti-clotting medicines raise the risk of bleeding because they interfere with normal protective clotting. The investigators wanted to see whether a more precise method could reduce harmful arterial clots without causing that broader effect.

N-acetylcysteine can break chemical bonds involved in the structure of von Willebrand factor. In the lab setup, the researchers measured platelet buildup and the time it took for flowing blood to become blocked.

The drug reduced clot formation under the conditions tested, and the effect increased with dose. The team then examined clotting, clot stability and bleeding in mice to find out whether the benefit extended beyond the laboratory device.

The mouse studies also showed protection six hours after treatment, even after the drug had cleared from the bloodstream. That finding suggests its effects on the clotting protein may last longer than its presence in circulation.

These results apply to a specific pathway and to particular experimental conditions. They do not prove that all clots can be prevented, or that the medicine can safely replace existing treatments.

Approval for one medical use does not automatically mean a drug is safe or effective for another. Clinical trials would be needed to determine whether this approach can prevent important health events without unacceptable side effects.

The findings also should not be taken to mean that an over-the-counter supplement can protect someone from an imminent heart attack. The treatment tested in the study and the setting in which it was used are important.

The broader idea is that changing how a protein behaves may interrupt clot formation before an artery becomes fully blocked. Whether that can become a practical prevention strategy will depend on evidence from people, not just the drug's familiar name.

If you are interested in this topic, please read articles about Common artificial sweeteners linked to higher risk of heart disease, and Omega-3 fatty acids and heart health: What you need to know.

For more information, please see articles about Mediterranean diet could protect artery health, reduce heart disease risk, and Green Mediterranean diet may improve heart and metabolic health.

Source: Georgia Institute of Technology.