After stopping daily aspirin, some older adults had a higher rate of heart attacks and strokes in the following years, but this may be because those who took aspirin were already at higher risk, or because stopping aspirin temporarily increased clotting risk—not because aspirin caused lasting harm.
Evidence from Studies
No evidence studies found yet.
What Would Prove This
Per GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this claim, ordered from strongest to weakest.
A meta-analysis of all post-trial follow-up data from aspirin RCTs would determine whether discontinuation consistently increases MACE risk across populations and whether this effect is modified by duration of prior use.
A systematic review and meta-analysis pooling individual-level post-trial data from all completed RCTs of aspirin for primary prevention in older adults, comparing MACE incidence in those randomized to aspirin versus placebo after drug cessation, with standardized definitions of discontinuation timing, duration of prior use, and adjustment for baseline risk factors.
A new RCT could test whether continuing aspirin beyond 5 years reduces post-discontinuation MACE risk compared to abrupt cessation.
A double-blind RCT of 5,000 adults aged 70+ who completed 5 years of daily aspirin, randomized to continue aspirin for 2 more years versus switch to placebo, with primary outcome being MACE during the 2-year post-randomization period, and secondary outcomes including hemorrhage and all-cause mortality.
A cohort study could assess whether MACE risk after aspirin cessation varies by duration of prior use, age at discontinuation, or presence of subclinical atherosclerosis.
A prospective cohort of 12,000 older adults who discontinued aspirin after 3–7 years of use, stratified by duration of prior use and baseline coronary calcium score, with annual cardiovascular assessments and MACE adjudication over 5 years, adjusting for statin initiation and blood pressure control.
A case-control study could identify whether individuals who experience MACE after aspirin cessation differ in platelet recovery kinetics or inflammatory markers compared to those who do not.
A nested case-control study within a cohort of aspirin discontinuers, comparing 800 individuals with post-discontinuation MACE to 2,400 matched controls, measuring platelet reactivity, thromboxane levels, and hs-CRP at discontinuation and 6 months later, using stored blood samples.
A cross-sectional survey could estimate the proportion of older adults who discontinue aspirin and report subsequent cardiovascular events, but cannot establish timing or causality.
A national survey of 8,000 adults aged 70+ who previously took aspirin for primary prevention, asking about duration of prior use, time since discontinuation, and occurrence of heart attack or stroke since stopping, with self-reported events confirmed by medical records.