After revisiting aspirin indications earlier this month, I received a few excellent questions that prompted me to delve further into the mysteries of this remarkable antiplatelet drug.
First, T.D. Murray asked:
Hello Dr. P. Thanks for your very informative website. I have read that as little as 30 mg of aspirin per day is sufficient to slow coagulation. One of my cardiologists states that the lowest effective dosage for aspirin has not been established. Would lower dosage cause fewer side effects? Your thoughts please.
After scanning the literature I could only find one study supporting a 30-mg dosage in secondary prevention, the Dutch TIA trial, which found no difference in efficacy between 30 mg and 283 mg aspirin, and less bleeding at the lower dosage.
“In the group assigned to receive 30 mg of aspirin, the frequency of death from vascular causes, nonfatal stroke, or nonfatal myocardial infarction was 228 of 1555 (14.7 percent), as compared with 240 of 1576 (15.2 percent) in the group assigned to receive 283 mg. The age- and sex-adjusted hazard ratio for the group receiving the lower dose was 0.91 (95 percent confidence interval, 0.76 to 1.09). There were slightly fewer major bleeding complications in the 30-mg group than in the 283-mg group (40 vs. 53), and significantly fewer reports of minor bleeding (49 vs. 84). Fewer patients receiving 30 mg of aspirin reported gastrointestinal symptoms (164 vs. 179) and other adverse effects (73 vs. 90).”
There aren’t a lot of studies with that low a dosage, and I haven’t found any comparing 30 mg to what has become the standard — 81 mg.
Most of the these aspirin trials in secondary prevention took place in the 1980s and 1990s before the era of widespread statin usage, better blood pressure control, and early and effective treatment of myocardial infarction, so they may not be applicable in our current medical environment.
A 2002 review concluded:
Within a few days of beginning 75 mg aspirin daily, cyclo-oxygenase is virtually completely inhibited in platelets, producing an antithrombotic effect. The present analyses indicate that high doses of 500-1500 mg aspirin daily (which are more gastrotoxic) are no more effective than medium doses of 160-325 mg/day or low doses of 75-150 mg/day (figs 5 and 6). Results from trials of lower doses are less conclusive. Hence, the available evidence supports daily doses of aspirin in the range 75-150 mg for the long term prevention of serious vascular events in high risk patients. In clinical situations where an immediate antithrombotic effect is required (such as acute myocardial infarction, acute ischaemic stroke, unstable angina), a loading dose of about 150-300 mg, which is sufficient to produce rapid and complete inhibition of thromboxane mediated platelet aggregation, should probably be given.
Unacceptable Bleeding on Aspirin
I’ve had patients develop unacceptable bruising or bleeding issues on 81-mg aspirin, and we’ve agreed to trial lower dosages.
I describe in detail my own experience when I cut my philtrum shaving and bled seemingly forever here.
In that post I discussed various tests and devices that had been proposed to monitor platelet activity on aspirin, but none of these are utilized by anyone I know. It is entirely possible that 30-mg aspirin is the perfect dosage for T.D. Murray but an imperfect one for someone else based on individual pharmacokinetics.
Bottom line, I would say, is that 30 mg may be just as effective as doses >75 mg, but unless you have concerns about bleeding or gastric irritation on the higher dosage you are best served by staying with the dosage that has been studied extensively and found to be effective in the largest number of patients.
Clopidogrel As an Alternate
One option to consider is clopidogrel (Plavix) at 75 mg daily, which according to this recent Korean study in patients >1 year after a coronary stent, appears to have less bleeding issues than aspirin.
Clopidogrel monotherapy, compared with aspirin monotherapy during the chronic maintenance period after percutaneous coronary intervention with [drug-eluting stents] significantly reduced the risk of the composite of all-cause death, non-fatal myocardial infarction, stroke, readmission due to acute coronary syndrome, and BARC bleeding type 3 or greater.
Of course, you may be leery of studies that come from the same country that gave us “The Squid Game.”
Anthony C. Pearson, MD, is a noninvasive cardiologist and professor of medicine at St. Louis University School of Medicine. He blogs on nutrition, cardiac testing, quackery, and other things worthy of skepticism at The Skeptical Cardiologist, where a version of this post first appeared.