Stroke ASAP

Rates and Determinants of 5-Year Outcomes After Atrial Fibrillation-Related Stroke: A Population Study [Original Contribution]Background and Purpose—Demographic trends in atrial fibrillation (AF) incidence may yield a substantial rise in the societal burden of AF-related stroke (AF-stroke). Accurate population-wide outcome data are essential to inform health service planning to improve AF-stroke prevention, and provision of rehabilitation, nursing home, and community supports for AF-stroke survivors.Methods—We investigated rates and determinants of 5-year fatality, stroke recurrence, functional outcomes, and prescribing of secondary prevention medications in AF-stroke in the North Dublin Population Stroke Study. Ascertainment included hot and cold pursuit using multiple overlapping sources. Survival analysis was performed using lifetables and Kaplan–Meier survival curves, and Cox proportional hazard modeling was performed to identify predictors of death and recurrent stroke.Results—Five hundred sixty-eight patients with new stroke were identified, including 177 (31.2%) AF-stroke. At 5 years, 39.2% (confidence interval, 31.5–46.8) of ischemic AF-stroke patients were alive. Congestive heart failure, hypertension, age <65, 65–74 years, and ≥75 years, diabetes mellitus, prior stroke, transient ischemic attack or thromboembolism, vascular disease and female sex (CHA2DS2-VASc) score (hazard ratio [HR], 1.34; P<0.001), CHADS2 score (HR 1.42, P=0.004), National Institute of Health Stroke Scale (HR, 1.09; P<0.0001), and subtherapeutic international normalized ratio (<2.0) at stroke onset (HR, 3.29;P=0.003) were independently associated with 5-year fatality, whereas warfarin (HR, 0.40; P=0.001) and statin use after index stroke (HR, 0.52; P=0.005) were associated with improved survival. The 5-year recurrence rate after ischemic AF-stroke was 21.5% (confidence interval, 14.5–31.3). Trends toward greater risk of recurrence were observed for persistent AF (HR, 3.09; P=0.07) and CHA2DS2-VASc score (HR, 1.34; P=0.07). Nursing home care was needed for 25.9% of patients.Conclusion—AF-stroke is associated with considerable long-term morbidity, fatality, stroke recurrence, and nursing home requirement. Adequately resourced national AF strategies to improve AF detection and prevention are needed.

Endovascular Treatment for Acute Ischemic Stroke in the Setting of Anticoagulation [Brief Report]Background and Purpose—Oral anticoagulation (OAC) plays a major role in atrial fibrillation stroke prevention but represents a contraindication to intravenous tissue-type plasminogen activator. Intra-arterial therapy remains a potential reperfusion strategy in these patients; however, supporting data are scarce.Methods—Retrospective analysis of prospectively collected consecutive intra-arterial therapies from October 2010 to March 2015 comparing OAC (vitamin-K antagonists and novel oral anticoagulants) versus normal hemostasis versus intravenous tissue-type plasminogen activator patients. Primary safety end point is parenchymal hematoma. Secondary safety end point is 90-day mortality. Efficacy end points are successful reperfusion (modified Thrombolysis in Cerebral Infarction, 2b-3) and good outcome (90-day modified Rankin Scale score of 0–2). Logistic regression for predictors of parenchymal hematoma was performed.Results—A total of 604 patients were qualified for the study. Baseline and outcomes variables were overall similar for vitamin-K antagonists (n=29) and novel oral anticoagulants (n=17) patients. When compared with normal hemostasis (n=265) and intravenous tissue-type plasminogen activator (n=297), OAC (n=46) patients were older and had more comorbidities. There were no statistically significant differences in the rates of parenchymal hematoma (8% versus 5%; P=0.42), 90-day modified Rankin Scale score of 0 to 2 (30% versus 40%; P=0.26), and 90-day mortality (32% versus 26%; P=0.46) among OAC and normal hemostasis patients. Similarly, there were no significant differences between OAC and intravenous tissue-type plasminogen activator patients in terms of parenchymal hematoma (8% versus 4%; P=0.16), 90-day modified Rankin Scale score of 0 to 2 (30% versus 43%; P=0.13), and 90-day mortality (32% versus 22%; P=0.18). The use of OAC was not associated with the occurrence of parenchymal hematoma on multivariate logistic regression analysis.Conclusions—Intra-arterial therapy seems to be safe in patients taking OACs; however, our study showed a nonsignificant increase in hemorrhage and mortality with a nonsignificant decrease in good outcomes in comparison with non-OAC patients. Although these nominal differences may have been related to older age and more comorbidities in the OAC group, larger studies are needed to confirm our findings given our limited sample size.

Montreal Cognitive Assessment: One Cutoff Never Fits All [Brief Report]Background and Purpose—The objective of this study is to examine the discrepancy between single versus age and education corrected cutoff scores in classifying performance on the Montreal Cognitive Assessment (MoCA) in patients with stroke or transient ischemic attack.Methods—MoCA norms were collected from 794 functionally independent and stroke- and dementia-free persons aged ≥65 years. magnetic resonance imaging was used to exclude healthy controls with significant brain pathology and medial temporal lobe atrophy. Cutoff scores at 16th, 7th, and 2nd percentiles by age and education were derived for the MoCA and MoCA 5-minute Protocol. MoCA performance in 919 patients with stroke or transient ischemic attack was classified using the single and norm-derived cutoff scores.Results—The norms for the Hong Kong version of the MoCA total and domain scores and the total score of the MoCA 5-minute protocol are described. Only 65.1% and 25.7% healthy controls and 45.2% and 19.0% patients scored above the conventional cutoff scores of 21/22 and 25/26 on the MoCA. Using classification with norm-derived cutoff scores as reference, locally derived cutoff score of 21/22 yielded a classification discrepancy of ≤42.4%. Discrepancy increased with higher age and lower education level, with the majority being false positives by single cutoffs. With the 25/26 cutoff of the original MoCA, discrepancy further increased to ≤74.3%.Conclusions—Conventional single cutoff scores are associated with substantially high rates of misclassification especially in older and less-educated patients with stroke. These results caution against the use of one-size-fits-all cutoffs on the MoCA.

Prophylactic Antiepileptic Drug Use and Outcome in the Ethnic/Racial Variations of Intracerebral Hemorrhage Study [Brief Report]Background and Purpose—The role of antiepileptic drug (AED) prophylaxis after intracerebral hemorrhage (ICH) remains unclear. This analysis describes prevalence of prophylactic AED use, as directed by treating clinicians, in a prospective ICH cohort and tests the hypothesis that it is associated with poor outcome.Methods—Analysis included 744 patients with ICH enrolled in the Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study before November 2012. Baseline clinical characteristics and AED use were recorded in standardized fashion. ICH location and volume were recorded from baseline neuroimaging. We analyzed differences in patient characteristics by AED prophylaxis, and we used logistic regression to test whether AED prophylaxis was associated with poor outcome. The primary outcome was 3-month modified Rankin Scale score, with 4 to 6 considered poor outcome.Results—AEDs were used for prophylaxis in 289 (39%) of the 744 subjects; of these, levetiracetam was used in 89%. Patients with lobar ICH, craniotomy, or larger hematomas were more likely to receive prophlyaxis. Although prophylactic AED use was associated with poor outcome in an unadjusted model (odds ratio, 1.40; 95% confidence interval, 1.04–1.88; P=0.03), this association was no longer significant after adjusting for clinical and demographic characteristics (odds ratio, 1.11; 95% confidence interval, 0.74–1.65; P=0.62).Conclusions—We found no evidence that AED use (predominantly levetiracetam) is independently associated with poor outcome. A prospective study is required to assess for a more modest effect of AED use on outcome after ICH.

Knowledge of Thrombolytic Therapy Amongst Hospital Staff: Preliminary Results and Treatment Implications [Brief Report]Background and Purpose—In-hospital stroke is associated with slower access to thrombolysis than community-occurring stroke. It has been suggested that lack of knowledge regarding appropriate stroke response among hospital staff may contribute to delays in referral, assessment, and treatment of in-hospital stroke.Method—A survey was conducted among hospital ward staff members using the Stroke Awareness Questionnaire, which was adapted for use among hospital staff to assess their knowledge of stroke symptoms, acute treatments, and hospital protocols for treatment of stroke.Results—Ninety-six staff members were interviewed, 81% of whom were clinical staff (medical, nursing, allied health professionals). Ninety-two percent of staff could name ≥3 stroke symptoms. Only 49% of staff were aware of thrombolysis treatment, and only 48% could identify the time window for thrombolysis administration, with staff from stroke-related specialties likely to name thrombolysis as an acute treatment for stroke (71%; odds ratio =3.36, 95% confidence interval 1.17–9.61) and identify the correct treatment window (71%; odds ratio =3.55, 95% confidence interval 1.24–10.16). Only 52% of staff on general wards were aware of an in-hospital stroke protocol.Conclusions—Hospital staff had adequate knowledge of stroke signs and symptoms; however, there was low awareness of thrombolysis therapy and its correct treatment time window among hospital staff. Targeted educational programmes among hospital staff regarding stroke are required to optimize acute stroke care.

Summary of Evidence on Early Carotid Intervention for Recently Symptomatic Stenosis Based on Meta-Analysis of Current Risks [Original Contribution]Background and Purpose—This study aimed to assess the evidence on the periprocedural (<30 days) risks of carotid intervention in relation to timing of procedure in patients with recently symptomatic carotid stenosis.Methods—A systematic literature review of studies published in the past 8 years reporting periprocedural stroke/death after carotid endarterectomy (CEA) and carotid stenting (CAS) related to the time between qualifying neurological symptoms and intervention was performed. Pooled estimates of periprocedural risk for patients treated within 0 to 48 hours, 0 to 7 days, and 0 to 15 days were derived with proportional meta-analyses and reported separately for patients with stroke and transient ischemic attack as index events.Results—Of 47 studies included, 35 were on CEA, 7 on CAS, and 5 included both procedures. The pooled risk of periprocedural stroke was 3.4% (95% confidence interval [CI], 2.6–4.3) after CEA and 4.8% (95% CI, 2.5–7.8) after CAS performed <15 days; stroke/death rates were 3.8% and 6.9% after CEA and CAS, respectively. Pooled periprocedural stroke risk was 3.3% (95% CI, 2.1–4.6) after CEA and 4.8% (95% CI, 2.5–7.8) after CAS when performed within 0 to 7 days. In hyperacute surgery (<48 hours), periprocedural stroke risk after CEA was 5.3% (95% CI, 2.8–8.4) but with relevant risk differences among patients treated after transient ischemic attack (2.7%; 95% CI, 0.5–6.9) or stroke (8.0%; 95% CI, 4.6–12.2) as index.Conclusions—CEA within 15 days from stroke/transient ischemic attack can be performed with periprocedural stroke risk <3.5%. CAS within the same period may carry a stroke risk of 4.8%. Similar periprocedural risks occur after CEA and CAS performed earlier, within 0 to 7 days. Carotid revascularization can be safely performed within the first week (0–7 days) after symptom onset.

Stroke Disparities: Large Global Problem That Must Be Addressed [Topical Review]

Response to Letter Regarding Article, "Proteinuria, but Not eGFR, Predicts Stroke Risk in Chronic Kidney Disease: Chronic Renal Insufficiency Cohort Study" [Letter to the Editor]

Letter by Hu et al Regarding Article, "Monocyte Count and 30-Day Case Fatality in Intracerebral Hemorrhage" [Letter to the Editor]

Response to Letter Regarding "Monocyte Count and 30-Day Case Fatality in Intracerebral Hemorrhage" [Letter to the Editor]

Clinical Implications [Clinical Implications]

Angiotensin-II, the Brain, and Hypertension: An Update [Recent Advances in Hypertension]

High B-Type Natriuretic Peptide Hypertensives at Target Blood Pressure: Potential Role of {beta}-Blockers to Reduce Their Elevated Risk [Brief Review]

Organic Nitrates in Heart Failure Revisited: Pentaerythritol Tetranitrate Induces Heme Oxygenase 1 to Protect the Myocardium [Editorial Commentaries]

Another Piece to the Puzzle: Linking the Cardiac Nervous System to Atrial Fibrillation in Pulmonary Arterial Hypertension [Editorial Commentaries]

Maternal Obesity During Pregnancy Associates With Premature Mortality and Major Cardiovascular Events in Later Life [Epidemiology/Population]One in 5 pregnant women is obese but the impact on later health is unknown. We aimed to determine whether maternal obesity during pregnancy associates with increased premature mortality and later life major cardiovascular events. Maternity records of women who gave birth to their first child between 1950 and 1976 (n=18 873) from the Aberdeen Maternity and Neonatal databank were linked to the National Register of Deaths, Scotland and Scottish Morbidity Record. The effect of maternal obesity at first antenatal visit on death and hospital admissions for cardiovascular events was tested using time-to-event analysis with Cox proportional hazard regression to compare outcomes of mothers in underweight, overweight, or obese body mass index (BMI) categories compared with normal BMI. Median follow-up was at 73 years. All-cause mortality was increased in women who were obese during pregnancy (BMI>30 kg/m2) versus normal BMI after adjustment for socioeconomic status, smoking, gestation at BMI measurement, preeclampsia, and low birth weight (hazard ratio, 1.35; 95% confidence interval, 1.02–1.77). In adjusted models, overweight and obese mothers had increased risk of hospital admission for a cardiovascular event (1.16; 1.06–1.27 and 1.26; 1.01–1.57) compared with normal BMI mothers. Adjustment for parity largely unchanged the hazard ratios (mortality: 1.43, 1.09–1.88; cardiovascular events overweight: 1.17, 1.07–1.29; and obese: 1.30, 1.04–1.62). In conclusion, maternal obesity is associated with increased risk of premature death and cardiovascular disease. Pregnancy and early postpartum could represent an opportunity for interventions to identify obesity and reduce its adverse consequences.

Left Ventricular Wall Stress-Mass-Heart Rate Product and Cardiovascular Events in Treated Hypertensive Patients: LIFE Study [Clinical Trial]In the Losartan Intervention for End Point Reduction in Hypertension (LIFE) study, 4.8 years’ losartan- versus atenolol-based antihypertensive treatment reduced left ventricular hypertrophy and cardiovascular end points, including cardiovascular death and stroke. However, there was no difference in myocardial infarction (MI), possibly related to greater reduction in myocardial oxygen demand by atenolol-based treatment. Myocardial oxygen demand was assessed indirectly by the left ventricular massxwall stressxheart rate (triple product) in 905 LIFE participants. The triple product was included as time-varying covariate in Cox models assessing predictors of the LIFE primary composite end point (cardiovascular death, MI, or stroke), its individual components, and all-cause mortality. At baseline, the triple product in both treatment groups was, compared with normal adults, elevated in 70% of patients. During randomized treatment, the triple product was reduced more by atenolol, with prevalences of elevated triple product of 39% versus 51% on losartan (both P≤0.001). In Cox regression analyses adjusting for age, smoking, diabetes mellitus, and prior stroke, MI, and heart failure, 1 SD lower triple product was associated with 23% (95% confidence interval 13%–32%) fewer composite end points, 31% (18%–41%) less cardiovascular mortality, 30% (15%–41%) lower MI, and 22% (11%–33%) lower all-cause mortality (allP≤0.001), without association with stroke (P=0.34). Although losartan-based therapy reduced ventricular mass more, greater heart rate reduction with atenolol resulted in larger reduction of the triple product. Lower triple product during antihypertensive treatment was strongly, independently associated with lower rates of the LIFE primary composite end point, cardiovascular death, and MI, but not stroke.

Blood Pressure Is Not Associated With Cerebral Blood Flow in Older Persons [Aging]Many studies showing a relation between low blood pressure (BP) and adverse health outcomes in older persons suggest that low BP gives rise to reduced cerebral blood flow (CBF). However, limited evidence is available about this association. Baseline data of 203 participants in the Discontinuation of Antihypertensive Treatment in the Elderly (DANTE) trial were used (mean age, 81 years, using antihypertensive medication and with mild cognitive deficits). BP, BP changes on standing, and CBF derived from pseudo-continuous arterial spin-labeling magnetic resonance imaging were assessed in all participants. In 102 participants who were randomly assigned to 4-month continuation (n=47) or discontinuation of antihypertensive treatment (n=55), BP and CBF change were evaluated at 4-month follow-up. Systolic and diastolic BP were not associated with CBF (B=–0.21, P=0.50 and B=–1.07, P=0.07), neither were mean arterial pressure, pulse pressure, and BP changes on standing. In subgroups of participants with small vessel–related cerebral pathologies, including high white matter hyperintensity volume, microbleeds, and lacunar infarcts, or in participants with lower cognition or diabetes mellitus, no association was found between any BP parameters and CBF. Furthermore, compared to the continuation group, CBF change at 4 months was not different in the discontinuation group (B=–0.12, P=0.23). Contrary to the notion that lower BP in old age is associated with decreased CBF, our data do not show this association in older persons using antihypertensive medication and with mild cognitive deficits. Also, this association was not present in subgroups of more vulnerable persons, reflected by small vessel–related cerebral pathologies, lower cognition, or diabetes mellitus.

Galectin-3 Participates in Cardiovascular Remodeling Associated With Obesity [Heart]Remodeling, diastolic dysfunction, and arterial stiffness are some of the alterations through which obesity affects the cardiovascular system. Fibrosis and inflammation are important mechanisms underlying cardiovascular remodeling, although the precise promoters involved in these processes are still unclear. Galectin-3 (Gal-3) induces inflammation and fibrosis in the cardiovascular system. We have investigated the potential role of Gal-3 in cardiac damage in morbidly obese patients, and we have evaluated the protective effect of the Gal-3 inhibition in the occurrence of cardiovascular fibrosis and inflammation in an experimental model of obesity. Morbid obesity is associated with alterations in cardiac remodeling, mainly left ventricular hypertrophy and diastolic dysfunction. Obesity and hypertension are the main determinants of left ventricular hypertrophy. Insulin resistance, left ventricular hypertrophy, and circulating levels of C-reactive protein and Gal-3 are associated with a worsening of diastolic function in morbidly obese patients. Obesity upregulates Gal-3 production in the cardiovascular system in a normotensive animal model of diet-induced obesity by feeding for 6 weeks a high-fat diet (33.5% fat). Gal-3 inhibition with modified citrus pectin (100 mg/kg per day) reduced cardiovascular levels of Gal-3, total collagen, collagen I, transforming and connective growth factors, osteopontin, and monocyte chemoattractant protein-1 in the heart and aorta of obese animals without changes in body weight or blood pressure. In morbidly obese patients, Gal-3 levels are associated with diastolic dysfunction. In obese animals, Gal-3 blockade decreases cardiovascular fibrosis and inflammation. These data suggest that Gal-3 could be a novel therapeutic target in cardiac fibrosis and inflammation associated with obesity.

Cardiomyocyte Mineralocorticoid Receptor Activation Impairs Acute Cardiac Functional Recovery After Ischemic Insult [Heart]Loss of mineralocorticoid receptor signaling selectively in cardiomyocytes can ameliorate cardiac fibrotic and inflammatory responses caused by excess mineralocorticoids. The aim of this study was to characterize the role of cardiomyocyte mineralocorticoid receptor signaling in ischemia–reperfusion injury and recovery and to identify a role of mineralocorticoid receptor modulation of cardiac function. Wild-type and cardiomyocyte mineralocorticoid receptor knockout mice (8 weeks) were uninephrectomized and maintained on (1) high salt (0.9% NaCl, 0.4% KCl) or (2) high salt plus deoxycorticosterone pellet (0.3 mg/d, 0.9% NaCl, 0.4% KCl). After 8 weeks of treatment, hearts were isolated and subjected to 20 minutes of global ischemia plus 45 minutes of reperfusion. Mineralocorticoid excess increased peak contracture during ischemia regardless of genotype. Recovery of left ventricular developed pressure and rates of contraction and relaxation post ischemia–reperfusion were greater in knockout versus wild-type hearts. The incidence of arrhythmic activity during early reperfusion was significantly higher in wild-type than in knockout hearts. Levels of autophosphorylated Ca2+/calmodulin protein kinase II (Thr287) were elevated in hearts from wild-type versus knockout mice and associated with increased sodium hydrogen exchanger-1 expression. These findings demonstrate that cardiomyocyte-specific mineralocorticoid receptor–dependent signaling contributes to electromechanical vulnerability in acute ischemia–reperfusion via a mechanism involving Ca2+/calmodulin protein kinase II activation in association with upstream alteration in expression regulation of the sodium hydrogen exchanger-1 Nursing Interventions for Poststroke Fatigue [State-of-the-Science Nursing Review] Stroke Literature Synopses: Basic Science [Stroke Literature Synopses: Basic Science] Letter by Gross and Du Regarding Article, "Intracranial Dural Arteriovenous Fistulae: Clinical Presentation and Management Strategies" [Letters to the Editor] Response to Letter Regarding Article, "Intracranial Dural Arteriovenous Fistulae: Clinical Presentation and Management Strategies" [Letters to the Editor] Correction [Correction] Stroke: Highlights of Selected Articles [Stroke: Highlights of Selected Articles] Prevalence and Risk Factors of Acute Incidental Infarcts [Clinical Sciences]Background and Purpose—The study of silent stroke has been limited to imaging of chronic infarcts; acute incidental infarcts (AII) detected on brain magnetic resonance imaging have been less investigated. This study aims to describe prevalence and risk factors of AII in a community and a clinic-based population.Methods—Subjects were drawn from 2 ongoing studies: Epidemiology of Dementia in Singapore study, which is a subsample from a population-based study, and a clinic-based case–control study. Subjects from both studies underwent similar clinical and neuropsychological assessments and brain magnetic resonance imaging. Prevalence of AII from these studies was determined. Subsequently, risk factors of AII were examined using multivariable logistic regression models.Results—AII were seen in 7 of 623 (1.2%) subjects in Epidemiology of Dementia in Singapore (mean age, 70.9±6.8 years; 45% men) and in 12 of 389 (3.2%) subjects (mean age, 72.1±8.3 years; 46% men) in the clinic-based study. AII were present in 0.8% of subjects with no cognitive impairment, 1.9% of those with cognitive impairment not dementia, and 4.2% of subjects with dementia. Significant association of AII was found with cerebral microbleeds (≥5) in the Epidemiology of Dementia in Singapore (odds ratio, 6.76; 95% confidence interval, 1.28–35.65; P=0.02) and in the clinic-based cohort (odds ratio, 4.65; 95% confidence interval, 1.39–15.53; P=0.01). There was no association of AII with hypertension, diabetes mellitus, or hyperlipidemia.Conclusions—AII are more likely to be present in those with cognitive impairment. Although a cause–effect relationship between the presence of AII and cognitive impairment is plausible, the association may be because of under-reporting of symptoms by individuals with cognitive impairment. The association between AII and cerebral microbleeds may indicate cerebral vasculopathy, independent of traditional vascular risk factors. Trends in Stroke Incidence and 28-Day Case Fatality in a Nationwide Stroke Registry of a Multiethnic Asian Population [Clinical Sciences]Background and Purpose—This study investigated trends in stroke incidence and case fatality overall and according to sex, age, ethnicity, and stroke subtype in a multiethnic Asian population.Methods—The Singapore Stroke Registry identifies all stroke cases in all public hospitals using medical claims, hospital discharge summaries, and death registry data. Age-standardized incidence rates and 28-day case-fatality rates were calculated for individuals aged ≥15 years between 2006 and 2012. To estimate the annual percentage change of the rates, a linear regression model was fitted to the log rates, and a Wald test was performed to test for trend. P values <0.05 were considered significant.Results—A total of 40 623 cases were recorded. The total stroke incidence fell by 12.0%, and case fatality fell by 17.2% in the study. Declining trends in stroke incidence were stronger in women (female: –2.94; 95% confidence interval [CI], –3.43 to –2.44; male: –1.80; 95% CI, –2.58 to –1.02); in the older age groups (≥65 years: –3.62; 95% CI, –4.30 to –2.94; 50–64 years: –1.26; 95% CI, –1.97 to –0.55; <50 years: 3.33; 95% CI, 1.49 to 5.20), in Chinese (–2.64; 95% CI, –3.15 to –2.13), Indians (–3.78; 95% CI, –5.93 to –1.58), and others (–12.73; 95% CI, –18.93 to –6.06) compared with Malays (2.58; 95% CI, 1.17 to 4.02); and in ischemic stroke subtype (ischemic: –2.43; 95% CI, –3.13 to –1.73; hemorrhagic: –1.02; 95% CI, –2.04 to 0.01). Subgroup-specific findings for case fatality were similar.Conclusion—This is the first countrywide hospital-based registry study in a multiethnic Asian population, and it revealed marked overall reductions in stroke incidence and case fatality. However, it also identified important population groups with less favorable trends, especially younger adults and those of Malay ethnicity. Association Between Anemia and Cerebral Venous Thrombosis: Case-Control Study [Clinical Sciences]Background and Purpose—Anemia is often considered to be a risk factor for cerebral venous thrombosis (CVT), but this assumption is mostly based on case reports. We investigated the association between anemia and CVT in a controlled study.Methods—Unmatched case–control study: cases were adult patients with CVT included in a single-center, prospective database between July 2006 and December 2014. Controls were subjects from the control population of the Multiple Environmental and Genetic Assessment of Risk Factors for Venous Thrombosis (MEGA) study. Anemia was defined according to World Health Organization criteria: nonpregnant women hemoglobin <7.5 mmol/L, pregnant women <6.9 mmol/L, and men <8.1 mmol/L. We used logistic regression analysis, adjusting for age, sex, malignancy, oral contraceptive use, and pregnancy/puerperium.Results—We included 152 cases and 2916 controls. Patients with CVT were younger (mean age, 40 versus 48 years) and more often women (74% versus 53%) than controls. Anemia was more frequent in cases (27.0%) than in controls (6.5%; P<0.001). Anemia was associated with CVT, both in univariate analysis (odds ratio, 5.3; 95% confidence interval [CI], 3.6–7.9) and after adjustment for potential confounders (adjusted odds ratio, 4.4; 95% CI, 2.8–6.9). Hemoglobin as a continuous variable was inversely associated with CVT (adjusted odds ratio per 1 mmol/L change 0.53; 95% CI, 0.42–0.66). Stratification by sex showed a stronger association between anemia and CVT in men (adjusted odds ratio, 9.9; 95% CI, 4.1–23.8) than in women (3.6; 95% CI, 2.1–6.0).Conclusion—Our data suggest that anemia is a risk factor for CVT. Point-of-Care Testing of Coagulation in Patients Treated With Non-Vitamin K Antagonist Oral Anticoagulants [Clinical Sciences]Background and Purpose—Specific coagulation assays for non–vitamin K antagonist oral anticoagulants (NOAC) are relatively slow and often lack availability. Although specific point-of-care tests (POCT) are currently not available, NOAC are known to affect established coagulation POCT. This study aimed at determining the diagnostic accuracy of the CoaguChek POCT to rule out relevant concentrations of rivaroxaban, apixaban, and dabigatran in real-life patients.Methods—We consecutively enrolled 60 ischemic stroke patients newly started on NOAC treatment and obtained blood samples at 6 prespecified time points. Samples were tested using the CoaguChek POCT, laboratory-based coagulation assays (prothrombin time and activated partial thromboplastin time, anti-Xa test and Hemoclot), and liquid chromatography–tandem mass spectrometry for direct determination of NOAC concentrations.Results—Three hundred fifty-six blood samples were collected. The CoaguChek POCT strongly correlated (r=0.82 P<0.001) with rivaroxaban concentrations but did not accurately detect dabigatran or apixaban. If used to estimate the presence of low rivaroxaban concentrations, POCT was superior to predictions based on normal prothrombin time and activated partial thromboplastin time values even if sensitive reagents were used. POCT-results ≤1.0 predicted rivaroxaban concentrations <32 and <100 ng/mL with a specificity of 90% and 96%, respectively.Conclusions—If anti-Xa test is not available, we propose the use of the CoaguChek POCT to guide thrombolysis decisions after individual risk assessment in rivaroxaban-treated patients having acute ischemic stroke.Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT02371044.