Saloheimo P et al. (2006) Regular aspirin-use preceding the onset of primary intracerebral hemorrhage is an independent predictor for death. Stroke 37: 129–133
Hematoma volume predicts outcome and mortality risk following intracerebral hemorrhage (ICH). Therapies that decrease coagulability could cause enlargement of hematomas, thereby increasing the risk of mortality in patients with ICH. Saloheimo et al. studied outcomes in ICH patients regularly taking aspirin or warfarin at presentation.
In this population-based investigation, patients with spontaneous ICH were identified by head CT scan (n = 203) or autopsy (n = 5) over a 33-month study course. Regular aspirin use before ICH was significantly linked with hematoma enlargement in the week immediately following hemorrhage (P = 0.006). The 3-month mortality rate in all patients was 33%, and independent risk factors for death were regular aspirin use or warfarin use at onset of ICH (relative risk 2.5, 95% CI 1.3–4.6, P = 0.004, and 3.2, 95% CI 1.6–6.1, P = 0.001, respectively).
The results show that patients who had regularly used aspirin or warfarin before ICH were at increased risk of death within 3 months of onset compared with nonusers. In aspirin users, this increased risk probably results from early hematoma growth; however, the authors were unable to confirm this hypothesis because only some patients underwent second CT scans. Nevertheless, the results indicate a need to block hematoma growth and to stop anticoagulation in ICH patients taking regular aspirin or warfarin. Further work is required to test whether occasional aspirin use affects outcome after ICH, and whether the benefits of interventions that increase platelet function in ICH patients taking aspirin would outweigh their risks.
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17 May 2018
This article was published with the same DOI as a previous publication. A new DOI has been assigned and registered at Crossref, and has been corrected in the article.
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Matthews, K. Aspirin use before intracerebral hemorrhage increases mortality risk. Nat Rev Neurol 2, 180 (2006). https://doi.org/10.1038/ncpcardio0467x
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DOI: https://doi.org/10.1038/ncpcardio0467x