APOE4 May Raise Brain Bleed Risk in Apixaban Users With AF
Carriers of the apolipoprotein E epsilon 4 (APOE ε4) allele had a threefold higher risk for intracranial hemorrhage (ICH) when taking apixaban for atrial fibrillation (AF) compared with noncarriers, a new study suggested.
METHODOLOGY:
The study included data for more than 2000 participants (mean age, 71 years; 55% men; 84% with European ancestry) from the All of Us Research Program, collected between 2017 and 2022. The median follow-up duration was 2.9 years.
Individuals older than 50 years who were taking apixaban for AF were included in the study, which excluded those with prior ischemic stroke or ICH.
After APOE ε4 status was determined, carriers (n = 483) were defined as those having one or two alleles and noncarriers (n = 1555) as those without alleles.
The primary outcome was incident ICH after initiating apixaban therapy, including any nontraumatic intraparenchymal, subdural, or subarachnoid hemorrhage. Secondary outcomes included incidences of intraparenchymal hemorrhage, ischemic stroke, and a composite of ischemic stroke and ICH. Also used was a HAS-BLED score, which includes factors such as age, hypertension, stroke, and history of or predisposition for bleeding, to predict risk for major bleeding.
TAKEAWAY:
About 26 participants developed ICH during the study, with cumulative ICH incidence significantly higher among APOE ε4 carriers than noncarriers (3.1% vs 1%; P = .007).
Carrying the APOE ε4 allele was associated with a threefold increase in risk for ICH (hazard ratio [HR], 3.1; P = .004) and intraparenchymal hemorrhage (HR, 3.7; P = .002) compared with not carrying the allele.
There were no significant differences between carriers and noncarriers in the other two secondary outcomes.
APOE information improved the predictive power of the HAS-BLED score, with C statistics of 0.74 and 0.68 for models with and without APOE information, respectively (P = .03).
IN PRACTICE:
The findings 'underscore the importance of genetics in personalizing pharmacological therapy, aiding clinicians in identifying high-risk patients and tailoring anticoagulant strategies,' the investigators wrote.
'Further research is needed to evaluate whether cerebral amyloid angiopathy mediates the observed association and whether APOE ε4 information improves clinical decision-making about anticoagulation therapy' in patients with AF, they added.
SOURCE:
This study was led by Santiago Clocchiatti-Tuozzo, MD, Yale School of Medicine, New Haven, Connecticut. It was published online on June 23 in JAMA Neurology
LIMITATIONS:
This study could not distinguish between lobar and deep hemorrhages because of its reliance on electronic health record data, limiting the ability to determine the relative contributions of hypertension and cerebral amyloid angiopathy to each hemorrhage type. The predominant European ancestry of participants may have limited the generalizability of the findings. Additionally, external validation of the prediction analyses was not possible because of the lack of other genetic studies in the US evaluating patients with AF treated with apixaban.
DISCLOSURES:
This study was funded by the National Institutes of Health and the American Heart Association. Several investigators reported having financial ties with various organizations and companies. Full details are provided in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
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