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Large collaborative research networks provide opportunities to jointly analyze multicenter electronic health record (EHR) data, which can improve the sample size, diversity of the study population, and generalizability of the results. However, there are challenges to analyzing multicenter EHR data including privacy protection, large-scale computation resource requirements, heterogeneity across sites, and correlated observations. In this paper, we propose a federated algorithm for generalized linear mixed models (Fed-GLMM), which can flexibly model multicenter longitudinal or correlated data while accounting for site-level heterogeneity. Fed-GLMM can be applied to both federated and centralized research networks to enable privacy-preserving data integration and improve computational efficiency. By communicating a limited amount of summary statistics, Fed-GLMM can achieve nearly identical results as the gold-standard method where the GLMM is directly fitted to the pooled dataset. We demonstrate the performance of Fed-GLMM in numerical experiments and an application to longitudinal EHR data from multiple healthcare facilities.

This trial assessed the value of brain imaging to guide treatment for stroke. Clinical outcomes with embolectomy were not superior to those with standard care in all patients or in the subgroup identified by brain imaging as most likely to benefit from embolectomy. Multiple randomized, controlled trials have shown the efficacy of the use of intravenous tissue plasminogen activator (t-PA), administered up to 4.5 hours after the onset of symptoms of acute ischemic stroke. 1 , 2 However, the global effect of this therapy has been limited, largely because of the narrow time window available for treatment and the risk of symptomatic intracerebral hemorrhage. Although endovascular approaches, including thrombectomy devices, have been shown to achieve greater rates of recanalization than the use of intravenous t-PA, no randomized, controlled trial has been completed comparing clinical outcomes versus standard medical care. Moreover, the potential to benefit from . . .

Digital health, virtual care, telehealth, and telemedicine are all terms often used interchangeably to refer to the practice of care delivered from a distance. Because virtual care collapses the barriers of time and distance, it is ideal for providing care that is patient-centered, lower cost, more convenient and at greater productivity. All these factors make virtual care tools indispensable elements in the COVID19 response. In this perspective, we offer implementation guidance and policy insights relevant to the use of virtual care tools to meet the challenges of the COVID19 pandemic.

AbstractObjectiveThe coronavirus disease 2019 pandemic has presented emergency departments (EDs) with many challenges to address the acute care needs of patients. Many EDs have leveraged telehealth to innovatively respond to these challenges. This review describes the landscape of telehealth initiatives in emergency care that have been described during the coronavirus disease 2019 pandemic. MethodsWe conducted a comprehensive, systematic review of the literature using PubMed, supplemented by a review of the gray literature (ie, non‐peer reviewed), with input from subject matter experts to identify telehealth initiatives in emergency care during coronavirus disease 2019. We categorized types of telehealth use based on purpose and user characteristics. ResultsWe included 27 papers from our review of the medical literature and another 8 sources from gray literature review. The vast majority of studies (32/35) were descriptive in nature, with the additional inclusion of 2 cohort studies and one randomized clinical trial. There were 5 categories of ED telehealth use during the pandemic: (1) pre‐ED evaluation and screening, (2) within ED (including as a means of limiting staff and patient exposure and facilitating consultation with specialists), (3) post‐ED discharge monitoring and treatment, (4) educating trainees and health care workers, and (5) coordinating resources and patient care. ConclusionTelehealth has been used in a variety of manners during the coronavirus disease 2019 pandemic, enabling innovation in emergency care delivery. The findings from this study can be used by institutions to consider how telehealth may address challenges in emergency care during the coronavirus disease 2019 pandemic and beyond. Because few studies included cost data and given the variability in institutional resources, how organizations implement telehealth programs will likely vary. Future work should further explore barriers and facilitators of innovation, and the impact on care delivery and patient outcomes.

\"Telehealth\" refers to the use of electronic services to support a broad range of remote services, such as patient care, education, and monitoring. Telehealth must be integrated into traditional ambulatory and hospital-based practices if it is to achieve its full potential, including addressing the six domains of care quality defined by the Institute of Medicine: safe, effective, patient-centered, timely, efficient, and equitable. Telehealth is a disruptive technology that appears to threaten traditional health care delivery but has the potential to reform and transform the industry by reducing costs and increasing quality and patient satisfaction. This article outlines seven strategies critical to successful telehealth implementation: understanding patients' and providers' expectations, untethering telehealth from traditional revenue expectations, deconstructing the traditional health care encounter, being open to discovery, being mindful of the importance of space, redesigning care to improve value in health care, and being bold and visionary. [PUBLICATION ABSTRACT]

Current treatment of ischaemic stroke with thrombolytic therapy is restricted to 3–4·5 h after symptom onset. We aimed to assess the safety and efficacy of desmoteplase, a fibrin-dependent plasminogen activator, given between 3 h and 9 h after symptom onset in patients with occlusion or high-grade stenosis in major cerebral arteries. In a prospective, double-blind, multicentre, parallel-group, randomised trial, we enrolled patients from 77 hospitals in 17 countries who had ischaemic stroke and occlusion or high-grade stenosis in major cerebral arteries. We randomly assigned patients in a 1:1 ratio, using computer-generated randomisation lists with stratification for baseline National Institutes of Health Stroke Scale and age, to treatment with desmoteplase (90 μg/kg) given 3–9 h after symptom onset or to placebo. Patients, investigators, staff, and the funder were masked to treatment assignment. The primary outcome was a favourable modified Rankin Scale score (0–2) at day 90 in all treated patients who had at least one postbaseline measurement of the modified Rankin Scale. Safety was assessed in all randomly assigned patients who received study drugs. This trial is registered with ClinicalTrials.gov, number NCT00790920. Between Feb 6, 2009, and Nov 27, 2013, we enrolled 492 patients and randomly assigned 247 to desmoteplase and 245 to placebo (236 in the desmoteplase group and 237 in the placebo group were included in the analysis of the primary endpoint). Median time from stroke onset to treatment was 6·9 h (IQR 5·7–8·0) for placebo and 7·0 h (6·0–7·9) for desmoteplase. Modified Rankin Scale score (0–2) at day 90 occurred in 121 (51%) patients given desmoteplase and 118 (50%) patients given placebo (adjusted odds ratio 1·20, 95% CI 0·79–1·81, p=0·40). 24 (10%) of 240 patients given desmoteplase died compared with 23 (10%) of 238 patients given placebo. Serious adverse events occurred in 64 (27%) of 240 patients receiving desmoteplase compared with 69 (29%) of 238 patients receiving placebo; frequency of symptomatic intracranial haemorrhage (six [3%] patients in the desmoteplase group vs five [2%] in the placebo group), symptomatic cerebral oedema (five [2%] vs four [2%]), and major haemorrhage (ten [4%] vs 15 [6%]) was much the same between treatment groups. Treatment with desmoteplase did not cause safety concerns and did not improve functional outcome when given to patients who had ischaemic stroke and major cerebral artery occlusion beyond 3 h of symptom onset. H Lundbeck A/S.

Previous studies have suggested that desmoteplase, a novel plasminogen activator, has clinical benefit when given 3–9 h after the onset of the symptoms of stroke in patients with presumptive tissue at risk that is identified by magnetic resonance perfusion imaging (PI) and diffusion-weighted imaging (DWI). In this randomised, placebo-controlled, double-blind, dose-ranging study, patients with acute ischaemic stroke and tissue at risk seen on either MRI or CT imaging were randomly assigned (1:1:1) to 90 μg/kg desmoteplase, 125 μg/kg desmoteplase, or placebo within 3–9 h after the onset of symptoms of stroke. The primary endpoint was clinical response rates at day 90, defined as a composite of improvement in National Institutes of Health stroke scale (NIHSS) score of 8 points or more or an NIHSS score of 1 point or less, a modified Rankin scale score of 0–2 points, and a Barthel index of 75–100. Secondary endpoints included change in lesion volume between baseline and day 30, rates of symptomatic intracranial haemorrhage, and mortality rates. Analysis was by intention to treat. This study is registered with ClinicalTrials.gov, NCT00111852. Between June, 2005, and March, 2007, 193 patients were randomised, and 186 patients received treatment: 57 received 90 μg/kg desmoteplase; 66 received 125 μg/kg desmoteplase; and 63 received placebo. 158 patients completed the study. The median baseline NIHSS score was 9 (IQR 6–14) points, and 30% (53 of 179) of the patients had a visible occlusion of a vessel at presentation. The core lesion and the mismatch volumes were small (median volumes were 10·6 cm 3 and 52·5 cm 3, respectively). The clinical response rates at day 90 were 47% (27 of 57) for 90 μg/kg desmoteplase, 36% (24 of 66) for 125 μg/kg desmoteplase, and 46% (29 of 63) for placebo. The median changes in lesion volume were: 90 μg/kg desmoteplase 14·0% (0·5 cm 3); 125 μg/kg desmoteplase 10·8% (0·3 cm 3); placebo −10·0% (−0·9 cm 3). The rates of symptomatic intracranial haemorrhage were 3·5% (2 of 57) for 90 μg/kg desmoteplase, 4·5% (3 of 66) for 125 μg/kg desmoteplase, and 0% for placebo. The overall mortality rate was 11% (5% [3 of 57] for 90 μg/kg desmoteplase; 21% [14 of 66] for 125 μg/kg desmoteplase; and 6% [4 of 63] for placebo). The DIAS-2 study did not show a benefit of desmoteplase given 3–9 h after the onset of stroke. The high response rate in the placebo group could be explained by the mild strokes recorded (low baseline NIHSS scores, small core lesions, and small mismatch volumes that were associated with no vessel occlusions), which possibly reduced the potential to detect any effect of desmoteplase. PAION Deutschland GmbH; Forest Laboratories.

AbstractBackgroundThere are significant racial and ethnic disparities in receipt of reperfusion interventions for acute ischemic stroke. Our objective was to determine whether there are disparities in access to stroke center care by race or ethnicity that help explain differences in reperfusion therapy and to understand whether interhospital patient transfer plays a role in improving access. MethodsUsing statewide administrating data including all emergency department and hospital discharges in California from 2010 to 2017, we identified all acute ischemic stroke patients. Primary outcomes of interest included presentation to primary or comprehensive stroke center (PSC or CSC), interhospital transfer, discharge from PSC or CSC, and discharge from CSC alone. We used hierarchical logistic regression modeling to identify the relationship between patient‐ and hospital‐level characteristics and outcomes of interest. ResultsOf 336,247 ischemic stroke patients, 55.4% were non‐Hispanic White, 19.6% Hispanic, 10.6% non‐Hispanic Asian/Pacific Islander, and 10.3% non‐Hispanic Black. There was no difference in initial presentation to stroke center hospitals between groups. However, adjusted odds of reperfusion intervention, interhospital transfer and discharge from CSC did vary by race and ethnicity. Adjusted odds of interhospital transfer were lower among Hispanic (odds ratio [OR] 0.94, 95% confidence interval [CI] 0.89 to 0.98) and non‐Hispanic Asian/Pacific Islander patients (OR 0.84, 95% CI 0.79 to 0.90) and odds of discharge from a CSC were lower for Hispanic (OR 0.91, 95% CI 0.85 to 0.97) and non‐Hispanic Black patients (OR 0.74, 95% CI 0.67 to 0.81). ConclusionsThere are racial and ethnic disparities in reperfusion intervention receipt among stroke patients in California. Stroke system of care design, hospital resources, and transfer patterns may contribute to this disparity.

Background Ischemic strokes (IS) occurring in patients taking non-vitamin K antagonist oral anticoagulants (NOACs) are becoming increasingly more frequent. We aimed to determine the clinical, echocardiographic, and neuroimaging markers associated with developing IS in patients taking NOACs for atrial fibrillation. Methods From a quaternary care center, clinical/radiologic data were collected from consecutive NOAC users with IS and age-matched controls without IS. Brain MRIs were reviewed for markers of cerebral small vessel disease. Variables with significant differences between groups were entered into a multivariable regression model to determine predictors of IS. Among IS patients, a Cox regression analysis was constructed to determine predictors of IS recurrence during follow-up. Results 112 patients with IS and 94 controls were included in the study. Variables significantly different between groups included apixaban use, dabigatran use, prior cerebrovascular events, hemoglobin A1c (HbA1c), left ventricular hypertrophy, left atrial volume index, and severe white matter hyperintensities. After multivariable adjustment, prior cerebrovascular events (aOR 23.86, 95% CI [6.02–94.48]), HbA1c levels (aOR 2.36, 95% CI [1.39–3.99]), left ventricular hypertrophy (aOR 2.73, 95% CI [1.11–6.71]) and left atrial volume index (aOR 1.05, 95% CI [1.01–1.08]) increased the risk of stroke, whereas apixaban use appeared to decrease the risk (aOR 0.38, 95% CI [0.16–0.92]). Malignancy was associated with IS recurrence (aHR 4.90, 95% CI [1.35–18.42]) after adjustment for age and chronic renal failure. Conclusions Prior cerebrovascular events, diabetes, left ventricular hypertrophy, and increased left atrial size are risk factors for developing an IS among NOAC users.

Older adults receive benzodiazepines for agitation, anxiety, and insomnia after acute ischemic stroke (AIS). No trials have been conducted to determine if benzodiazepine use affects poststroke mortality in the elderly. We examined the association between initiating benzodiazepines within 1 week after AIS and 30-day mortality. We included patients ≥65 years, admitted for new nonsevere AIS (NIH-Stroke-Severity[NIHSS]≤ 20), 2014–2020, with no recorded benzodiazepine use in the previous 3 months and no contraindication for use. We linked a stroke registry to electronic health records, used inverse-probability weighting to address confounding, and estimated the risk difference (RD). A process of cloning, weighting, and censoring was used to avoid immortal time bias. Among 2,584 patients, 389 received benzodiazepines. The crude 30-day mortality risk from treatment initiation was 212/1,000 among patients who received benzodiazepines, while the 30-day mortality was 34/1,000 among those who did not. When follow-up was aligned on day of AIS admission and immortal time was assigned to the two groups, the estimated risks were 27/1,000 and 22/1,000, respectively. Upon further adjustment for confounders, the RD was 5 (−12 to 19) deaths/1,000 patients. The observed higher 30-day mortality associated with benzodiazepine initiation within 7 days was largely due to bias. [Display omitted] •Quantifying the effect of benzodiazepines on mortality is not straightforward.•Immortal time bias threatens the validity of benzodiazepine effect estimates.•A process of cloning, weighting, and censoring is used to avoid immortal time bias.•The observed benzodiazepine-related 30-day mortality was largely due to confounding.