About 60 million Americans take an aspirin a day to reduce the risk of strokes and heart attacks. But for 10 to 30% of those who follow this recommendation, this preventive therapy turns out not to offer any protection.
An NIH-funded team, based at Duke University Medical Center, has discovered a set of blood markers that predict who will benefit from aspirin therapy and who will not
Aspirin reduces the risk of stroke and heart attack by changing the properties of platelets, which are sticky, gelatinous disc-shaped fragments of cells that help repair damaged blood vessels. The correct balance of platelets is important for good health. Too little platelet activity increases the risk of bleeding; too much boosts the risk of blood clots that can cause strokes and heart attacks. Low doses of aspirin make the platelets less sticky and thus less likely to form clots. This has been a mainstay of reducing heart attacks
The scientists discovered an “aspirin response signature”—an activity profile of 60 genes—that revealed whose platelets didn’t respond to aspirin (that is, their platelets were still sticky). Interestingly, many of the genes that turned up in the signature were expressed in platelets, rather than in other blood cells. The diagnostic signature predicting aspirin resistance was also associated with deaths from stroke or heart attack.
People who don’t respond to aspirin may need a different dose of the drug or perhaps a different antiplatelet drug entirely—there are quite a few options out there. It’s another example of how studying gene activity can lead to personalized medicine.