Objective:In an international collaborative multicenter pooled analysis, we compared mortality, functional outcome, intracerebral hemorrhage (ICH) volume, and hematoma expansion (HE) between non–vitamin K antagonist oral anticoagulation–related ICH (NOAC-ICH) and vitamin K antagonist–associated ICH (VKA-ICH).Methods:We compared all-cause mortality within 90 days for NOAC-ICH and VKA-ICH using a Cox proportional hazards model adjusted for age; sex; baseline Glasgow Coma Scale score, ICH location, and log volume; intraventricular hemorrhage volume; and intracranial surgery. We addressed heterogeneity using a shared frailty term. Good functional outcome was defined as discharge modified Rankin Scale score ≤2 and investigated in multivariable logistic regression. ICH volume was measured by ABC/2 or a semiautomated planimetric method. HE was defined as an ICH volume increase >33% or >6 mL from baseline within 72 hours.Results:We included 500 patients (97 NOAC-ICH and 403 VKA-ICH). Median baseline ICH volume was 14.4 mL (interquartile range [IQR] 3.6–38.4) for NOAC-ICH vs 10.6 mL (IQR 4.0–27.9) for VKA-ICH (p = 0.78). We did not find any difference between NOAC-ICH and VKA-ICH for all-cause mortality within 90 days (33% for NOAC-ICH vs 31% for VKA-ICH [p = 0.64]; adjusted Cox hazard ratio (for NOAC-ICH vs VKA-ICH) 0.93 [95% confidence interval (CI) 0.52–1.64] [p = 0.79]), the rate of HE (NOAC-ICH n = 29/48 [40%] vs VKA-ICH n = 93/140 [34%] [p = 0.45]), or functional outcome at hospital discharge (NOAC-ICH vs VKA-ICH odds ratio 0.47; 95% CI 0.18–1.19 [p = 0.11]).Conclusions:In our international collaborative multicenter pooled analysis, baseline ICH volume, hematoma expansion, 90-day mortality, and functional outcome were similar following NOAC-ICH and VKA-ICH.

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Background and Purpose: The genetic relationships between stroke risk, stroke severity, and early neurological changes are complex and not completely understood. Genetic studies have identified 32 all stroke risk loci. Polygenic Risk Scores (PRS) can be used to compare the genetic architecture of related traits. In this study, we compare the genetic architecture of stroke risk, stroke severity, and early neurological changes with that of two stroke risk factors: Type 2 Diabetes Mellitus (T2DM) and Hypertension (HTN). Methods: We assessed the degree of overlap in the genetic architecture of stroke risk, T2DM, HTN, and two acute stroke phenotypes based on the NIH Stroke Scale (NIHSS), which ranges from 0 for no stroke symptoms to 21-42 for a severe stroke: baseline (within 6h after onset) and change in NIHSS (ΔNIHSS=NIHSS at baseline minus NIHSS at 24h). This was done by: 1) SNP by SNP comparison, 2) weighted PRS with sentinel variants and 3) whole genome PRS using multiple p-values thresholds. Results: We found evidence of genetic architecture overlap between stroke risk and T2DM (p=2.53×10 −169), HTN (p=3.93×10 −04) and baseline NIHSS (p=0.03). However, there was no evidence of overlap between ΔNIHSS and stroke risk, T2DM or HTN.

Objectives Quality of life (QoL) after intracerebral hemorrhage (ICH) is poorly known. This study investigated factors affecting QoL and depression after spontaneous ICH. Materials and Methods This prospective study included patients admitted to Helsinki University Hospital between May 2014 and December 2016. Health‐related QoL (HRQoL) at 3 months after ICH was measured using the European Quality of Life Scale (EQ‐5D‐5L), and the 15D scale. Logistic regression analyses were used to test factors affecting HRQoL. EQ‐5D‐5L anxiety/depression dimension was used to analyze factors associated with anxiety/depression. Results Of 277 patients, 220 were alive, and sent QoL questionnaire. The questionnaire was returned by 124 patients. Nonreturners had more severe strokes with admission National Institutes of Health Stroke Scale (NIHSS) 7.8 (IQR 3.0–14.8) versus 5.0 (IQR 2.3–11.0); p = 0.018, and worse outcome assessed as modified Rankin Scale 3–5 at 3 months 59.4% versus 44.4% ( p = 0.030). Predictors for lower HRQoL by both scales were higher NIHSS with OR 1.28 (95% CI 1.13–1.46) for EQ‐5D‐5L, and OR 1.28 (1.15–1.44) for 15D, older age (OR 1.10 [1.03–1.16], and OR 1.09 [1.03–1.15]), and chronic heart failure (OR 18.12 [1.73–189.27], and OR 12.84 [1.31–126.32]), respectively. Feeling sad/depressed for more than 2 weeks during the year prior to ICH was predictor for lower EQ‐5D‐5L (OR 10.64 [2.39–47.28]), and history of ICH for lower 15D utility indexes (OR 11.85 [1.01–138.90]). Prior feelings of sadness/depression were associated with depression/anxiety at 3 months after ICH with OR 3.62 (1.14–11.45). Conclusions In this cohort of ICH patients with milder deficits, HRQoL was affected by stroke severity, comorbidities and age. Feelings of depression before ICH had stronger influence on reporting depression/anxiety after ICH than stroke severity‐related and outcome parameters. Thus, simple questions on patient's premorbid feelings of sadness/depression could be used to identify patients at risk of depression after ICH for focusing follow‐up and treatment.