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Abstract
Objective: To analyze the potential impact of aspirin therapy for long-term secondary prevention after stroke of undetermined etiology in resource-limited settings without access to neuroimaging to distinguish ischemic stroke from intracerebral hemorrhage (ICH).
Methods: We conducted a decision analysis using a Markov state transition model. Sensitivity analyses were performed across the worldwide reported range of the proportion of strokes due to ICH and the 95% confidence intervals (CIs) of aspirin-associated relative risks in patients with ICH.
Results: For patients with stroke of undetermined etiology, long-term aspirin was the preferred treatment strategy across the worldwide reported range of the proportion of strokes due to ICH. At 34% of strokes due to ICH (the highest proportion reported in a large epidemiologic study), the benefit of aspirin remained beyond the upper bounds of the 95% CIs of aspirin-associated post-ICH relative risks most concerning to clinicians (ICH recurrence risk and mortality risk if ICH recurs on aspirin). Based on the estimated 11,590,204 strokes in low- and middle-income countries in 2010, our model predicts that aspirin therapy for secondary stroke prevention in all patients with stroke in these countries could lead to an estimated yearly decrease of 84,492 recurrent strokes and 4,056 stroke-related mortalities.
Conclusions: The concern that the risks of aspirin in patients with stroke of unknown etiology could outweigh the benefits is not supported by our model, which predicts that aspirin for secondary prevention in patients with stroke of undetermined etiology in resource-limited settings could lead to decreased stroke-related mortality and stroke recurrence.
GLOSSARY
- CI=
- confidence interval;
- DALY=
- disability-adjusted life-year;
- ICH=
- intracerebral hemorrhage;
- IS=
- ischemic stroke;
- LMIC=
- low- and middle-income countries;
- mRS=
- modified Rankin Scale;
- QALY=
- quality-adjusted life-year;
- RR=
- relative risk;
- SAH=
- subarachnoid hemorrhage;
- tPA=
- tissue plasminogen activator
Footnotes
↵* These authors contributed equally to the work.
Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.
- Received March 17, 2014.
- Accepted in final form June 16, 2014.
- © 2014 American Academy of Neurology
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