This article was originally posted in the
Few people give much consideration to the type of Aspirin they are taking. Unless you bothered to read the fine print on your pill bottle, you probably wouldn’t know if you are taking coated or uncoated Aspirin. In theory, coated Aspirin is supposed to protect your stomach. But the theory could in theory slow its absorption and hinder its effectiveness. But a recent study suggests this may not really matter at all.
Aspirin has been around for over a century, but its use in cardiovascular disease only dates back to 1988 with the publication of the . It has since become ubiquitous and is produced and manufactured under many different names. Aspirin was the original name trademarked by Bayer in 1897. Its official chemical name is acetylsalicylic acid or ASA.
It has also been tested and given at different multiple doses. When used for pain control or to treat a fever, Aspirin has to be given at high doses (one or two regular-strength Aspirins every four to six hours). While Aspirin is effective as an anti-inflammatory, few people can tolerate the stomach upset when given at these high doses, hence the general preference for pain medications like acetaminophen or ibuprofen.
But at lower doses, it can inhibit the platelets that form clots in the blood and has become the cornerstone of treating heart attacks and strokes. For a while, 325mg of Aspirin was a common dose, but results of studies like the trial have shown that 81mg (or a “baby” Aspirin) is just as effective. Interestingly, reducing the dose of Aspirin to 81mg didn’t dramatically decrease the risk of bleeding.
Medical consensus has largely settled on 81mg as the standard cardiological dose for ASA, but debate continues on whether coated Aspirin offers any advantage. In the 1980s, studies showed that coated Aspirin caused in the inner lining of the stomach. However, it hasn’t consistently shown to decrease the risk of and some early studies on its effectiveness relative to uncoated Aspirin.
The recent has shed some additional light on the subject. While the original study was about comparing low-dose versus high-dose Aspirin, about 70 per cent of the people enrolled in the trial also provided data about whether they were taking coated versus uncoated aspirin. By reanalyzing the data, researchers could see whether the enteric coating, at either dose, had any effect in terms of reducing cardiovascular end points (like heart attack, stroke or death) or bleeding end points (hospitalization requiring a transfusion or a bleed in the brain).
In short, the coated Aspirin offered little advantage or disadvantage. The cardiovascular end points were largely the same. Despite theoretical and biochemical concerns that the coating might slow and delay its absorption in the intestines, coated Aspirin seems to have the same anti-platelet blood thinning properties of uncoated Aspirin.
The bleeding end points were similarly negative. Although there was some suggestion in the raw numbers that there were more bleeds with the uncoated Aspirin, given the margin of error with the estimates, the differences were likely the play of chance.
Aspirin, in any formulation or dose, does increase the risk of bleeding. If it didn’t, it would be meaningless as a cardiac treatment. But the factors that drive bleeding risk more than anything are its co-administration with anti-inflammatories or other blood thinners. The age and individual risk factors of patients also play a major role.
The story of Aspirin highlights an important point in medicine. Beyond the theoretical risks and benefits of enteric-coated Aspirin, it does not appear as if it makes much of a difference one way or the other. Basic biology and laboratory results inform clinical practice but they are not a substitute for hard clinical end points. The adage of treat the patient, not the number, still holds true.