N-acetyl cysteine (NAC) shows promise for heart attack prevention

Heart attacks and strokes are a leading cause of death in developed countries - accounting for ~20% of all deaths in the U.S. Frequently, heart attacks and strokes are caused by blood clots (blood platelets that form when they are not needed, causing a narrowing/blockage of blood vessels) formed through arterial thrombosis. Current antiplatelet agents (e.g., aspirin) are effective but can increase major bleeding risk. As such, there is a growing need to prevent arterial thrombosis different from antiplatelet agents.

A recent study published in Arteriosclerosis, Thrombosis, and Vascular Biology investigated the potential of NAC as an agent to prevent arterial thrombosis. Utilizing both [cell-based] human blood models and mouse (in vitro) models, the research demonstrated that NAC significantly delayed and even prevented thrombus formation dose-dependently without increasing bleeding risks.

Findings:
*NAC treatment extended clot formation times by up to 3.7 times compared to controls in the human blood [cell] model.
*NAC entirely inhibited platelet aggregation and occlusive clot formation at higher doses than the above point in the cell model.
*A 400 mg/kg (via injection in rodents) dose of NAC in mice effectively prevented arterial occlusion post-injury.
*Lower doses (200 mg/kg - via injection in rodents) of NAC reduced clot stability, suggesting working as both an acute and preventative clotting therapy.

The study showed that NAC interferes with von Willebrand factor (a large protein crucial for blood clotting) activity. NAC acts against VWF rather than platelets to prevent clot formation. Thus, providing a safer alternative to traditional antiplatelet drugs that carry higher bleeding risks.

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