Anticoagulant Use and Incident Intracerebral Hemorrhage: An Exploration of Hemorrhage Etiology and Location

 I don't see anything here that even minimally represents a protocol that would prevent this problem.

Anticoagulant Use and Incident Intracerebral Hemorrhage: An Exploration of Hemorrhage Etiology and Location

• Kristina A. Rankine , MD

Wilson M, Incontri D, Vu S, Marchina S, Wang JY, Andreev A, Heistand E, Carvalho F, Selim M, Lioutas VA. Association of Anticoagulant Use With Hemorrhage Location and Etiology in Incident Spontaneous Intracerebral Hemorrhage. Stroke. 2024;55:2677–2684.

Wilson et al. investigated the relationship between anticoagulant use and the location and etiology of intracerebral hemorrhage (ICH), focusing on whether hypertensive microangiopathy or cerebral amyloid angiopathy (CAA) is more likely to predispose patients to anticoagulant-associated ICH (AA-ICH). This research is crucial for clinicians managing anticoagulation therapy patients at risk for ICH.

This was a cross-sectional analysis of 1,104 patients who experienced their first spontaneous ICH, admitted to a tertiary hospital in Boston between 2008 and 2023. Using MRI and CT imaging based on the Boston Criteria 2.0 and Simplified Edinburgh Criteria, the researchers examined whether AA-ICH was associated with lobar hemorrhages and probable CAA. There were statistically significant differences between the anticoagulant and no anticoagulant use groups with regards to sex, hypertension, hyperlipidemia, atrial fibrillation, coronary artery disease, smoking, statin use, and INR that they then ran a multivariable logistical regression model for analyses excluding those they felt lacked biological plausibility for an association. There was no significant difference in the occurrence of lobar hemorrhages between patients with and without anticoagulant exposure in their adjusted and unadjusted analyses. Additionally, using Vitamin K antagonists versus DOACs showed no difference in the probability of lobar hemorrhage.

Interestingly, the study found that patients with AA-ICH were less likely to have probable CAA, which the researchers posit suggests that hypertensive microangiopathy might predispose more towards AA-ICH than CAA. This maintains the importance of rigorous blood pressure control in reducing ICH risk in anticoagulated patients and encourages more targeted management strategies focusing on hypertension in these patients.

The authors discuss how their findings differ from research by Pezzini et al. that linked anticoagulation with increased risk of lobar ICH, particularly in the context of CAA,¹ which they attributed to the inclusion of all cerebellar hemorrhages in the Pezzini study and the lower proportion of patients taking anticoagulation. Additionally, the authors discussed how their finding of a lack of association between AA-ICH and lobar hemorrhage and the reduced odds of probable CAA differs from the Edoxaban for Intracranial Hemorrhage Survivors with Atrial Fibrillation (ENRICH-AF). Interim data from ENRICH-AF found a high risk of recurrent lobar ICH in patients with lobar ICH and convexity SAH, suggesting CAA as a predisposing factor. The authors highlight the difference in the study populations with ENRICH-AF examining the risk of recurrent ICH in patients on anticoagulation with this study assessing anticoagulation use before first ICH.

Further longitudinal and prospective cohort studies will help assess the long-term risk(Assessments do nothing; DO THE RESEARCH THAT PREVENTS THIS!) of incident and recurrent ICH in anticoagulated patients, considering hypertensive microangiopathy and CAA. They should also evaluate the correlation with the location of cerebellar hemorrhages. It may also be important to examine the trajectory of patients with initial ICH of suspected hypertensive etiology and the proportion that go on to develop CAA. Additional studies could explore the effect of comprehensive management strategies, including blood pressure control, on ICH incidence or delve further into AA-ICH pathophysiology.

Wilson et al.’s study provides insights into the etiology of AA-ICH, suggesting a substantial role for hypertensive microangiopathy, and should encourage vigilant monitoring and treatment of hypertension to prevent ICH in clinical practice. Notably, considering the limitations of this cross-sectional study, further research to address these gaps should widen our understanding of anticoagulant use in relation to ICH.

References at link.