Among healthy adults aged 70 or older, those who previously took daily aspirin in a clinical trial had a higher rate of serious heart problems in the years after the trial ended, compared to those...
Mechanism
Synthesis from 1 study
After years of taking aspirin, stopping it can cause the body's blood-clotting cells to become overly active for a while, increasing the chance of dangerous clots forming in arteries. This happens because the drug's effect wears off, and new cells start producing clot-promoting chemicals again.
Most probable mechanism
After taking aspirin daily for years, the body's platelets become more likely to clump together and form dangerous clots once the drug is stopped, increasing the risk of heart attacks and strokes.
Aspirin permanently blocks the cyclooxygenase-1 enzyme in platelets, preventing the production of thromboxane A2, a molecule that promotes platelet activation and clotting.
When aspirin is stopped, newly formed platelets that were not exposed to aspirin enter the bloodstream and produce normal levels of thromboxane A2.
The sudden return of thromboxane A2 production, combined with a temporary imbalance in other clotting regulators, causes platelets to become hyperactive and more likely to stick together.
This heightened platelet aggregation increases the likelihood of blood clots forming inside arteries that are already narrowed by fatty deposits.
These clots can block blood flow to the heart or brain, causing heart attacks or ischemic strokes.
Evidence from Studies
Supporting (1)
Community contributions welcome
Aspirin, cardiovascular events, and major bleeding in older adults: extended follow-up of the ASPREE trial
Contradicting (0)
Community contributions welcome
Gold Standard Evidence Needed
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