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Background and Purpose— We sought to determine the long-term risk of seizures after stroke according to age, sex, race, and stroke subtype. Methods— We performed a retrospective cohort study using administrative claims from 2 complementary patient data sets. First, we analyzed data from all emergency department visits and hospitalizations in California, Florida, and New York from 2005 to 2013. Second, we evaluated inpatient and outpatient claims from a nationally representative 5% random sample of Medicare beneficiaries. Our cohort consisted of all adults at the time of acute stroke hospitalization without a prior history of seizures. Our outcome was seizure occurring after hospital discharge for stroke. Poisson regression and demographic data were used to calculate age-, sex-, and race-standardized incidence rate ratios (IRR). Results— Among 777 276 patients in the multistate cohort, the annual incidence of seizures was 1.68% (95% confidence interval [CI], 1.67%–1.70%) after stroke versus 0.15% (95% CI, 0.15%–0.15%) among the general population (IRR, 7.3; 95% CI, 7.3–7.4). By 8 years, the cumulative rate of any emergency department visit or hospitalization for seizure was 9.27% (95% CI, 9.16%–9.38%) after stroke versus 1.21% (95% CI, 1.21%–1.22%) in the general population. Stroke was more strongly associated with a subsequent seizure among patients Conclusions— Almost 10% of patients with stroke will develop seizures within a decade. Hemorrhagic stroke, nonwhite race, and younger age seem to confer the greatest risk of developing seizures.

ObjectiveWe aimed to evaluate the association between cancer and cerebrovascular disease in a prospective cohort study with adjudicated cerebrovascular diagnoses.MethodsWe analyzed participants from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study who were 45 years and older and had Medicare coverage for 365 days before their baseline study visit. Participants with a history of cancer or cerebrovascular events were excluded. The time-dependent exposure was a new diagnosis of malignant cancer identified through Medicare claims algorithms. Participants were prospectively followed from their baseline study visit (2003–2007) through 2014 for the outcome of a neurologist-adjudicated cerebrovascular event defined as a composite of stroke (ischemic or hemorrhagic) or TIA. Cox regression was used to evaluate the association between a new cancer diagnosis and subsequent cerebrovascular events. Follow-up time was modeled in discrete time periods to fulfill the proportional hazard assumption.ResultsAmong 6,602 REGARDS participants who met eligibility criteria, 1,149 were diagnosed with cancer during follow-up. Compared to no cancer, a new cancer diagnosis was associated with subsequent cerebrovascular events in the first 30 days after diagnosis (hazard ratio 6.1, 95% confidence interval 2.7–13.7). This association persisted after adjustment for demographics, region of residence, and vascular risk factors (hazard ratio 6.6, 95% confidence interval 2.7–16.0). There was no association between cancer diagnosis and incident cerebrovascular events beyond 30 days. Cancers considered high risk for venous thromboembolism demonstrated the strongest associations with cerebrovascular event risk.ConclusionA new diagnosis of cancer is associated with a substantially increased short-term risk of cerebrovascular events.

Background and Purpose— We sought to model the effects of interhospital transfer network design on endovascular therapy eligibility and clinical outcomes of stroke because of large-vessel occlusion for the residents of a large city. Methods— We modeled 3 transfer network designs for New York City. In model A, patients were transferred from spoke hospitals to the closest hub hospitals with endovascular capabilities irrespective of hospital affiliation. In model B, which was considered the base case, patients were transferred to the closest affiliated hub hospitals. In model C, patients were transferred to the closest affiliated hospitals, and transfer times were adjusted to reflect full implementation of streamlined transfer protocols. Using Monte Carlo methods, we simulated the distributions of endovascular therapy eligibility and good functional outcomes (modified Rankin Scale score, 0–2) in these models. Results— In our models, 200 patients (interquartile range [IQR], 168–227) with a stroke amenable to endovascular therapy present to New York City spoke hospitals each year. Transferring patients to the closest hub hospital irrespective of affiliation (model A) resulted in 4 (IQR, 1–9) additional patients being eligible for endovascular therapy and an additional 1 (IQR, 0–2) patient achieving functional independence. Transferring patients only to affiliated hospitals while simulating full implementation of streamlined transfer protocols (model C) resulted in 17 (IQR, 3–41) additional patients being eligible for endovascular therapy and 3 (IQR, 1–8) additional patients achieving functional independence. Conclusions— Optimizing acute stroke transfer networks resulted in clinically small changes in population-level stroke outcomes in a dense, urban area.

Posterior reversible encephalopathy syndrome (PRES) is characterized by the acute onset of neurologic symptoms (headache, altered mental status, visual changes, seizures) with accompanying vasogenic edema on brain imaging. Risk factors for PRES include infection, uremia, malignancy, autoimmune disorders, the peripartum state and hypertension. PRES is classically described as being posterior (i.e. parieto-occipital) but radiologic variants are increasingly recognized. This pictorial review demonstrates the heterogeneity of the different radiologic presentations of PRES in reference to lesion distribution, hemorrhage, diffusion restriction, contrast enhancement, and other associated findings.

Background Mobile stroke units (MSUs) reduce time to thrombolytic therapy in acute ischemic stroke. These units are widely used, but the clinical information systems underlying MSU operations are understudied. Objective The first MSU on the East Coast of the United States was established at New York Presbyterian Hospital (NYP) in October 2016. We describe our program's 7-month pilot, focusing on the integration of our hospital's clinical information systems into our MSU to support patient care and research efforts. Methods NYP's MSU was staffed by two paramedics, one radiology technologist, and a vascular neurologist. The unit was equipped with four laptop computers and networking infrastructure enabling all staff to access the hospital intranet and clinical applications during operating hours. A telephone-based registration procedure registered patients from the field into our admit/discharge/transfer system, which interfaced with the institutional electronic health record (EHR). We developed and implemented a computerized physician order entry set in our EHR with prefilled values to permit quick ordering of medications, imaging, and laboratory testing. We also developed and implemented a structured clinician note to facilitate care documentation and clinical data extraction. Results Our MSU began operating on October 3, 2016. As of April 27, 2017, the MSU transported 49 patients, of whom 16 received tissue plasminogen activator (t-PA). Zero technical problems impacting patient care were reported around registration, order entry, or intranet access. Two onboard network failures occurred, resulting in computed tomography scanner malfunctions, although no patients became ineligible for time-sensitive treatment as a result. Thirteen (26.5%) clinical notes contained at least one incomplete time field. Conclusion The main technical challenges encountered during the integration of our hospital's clinical information systems into our MSU were onboard network failures and incomplete clinical documentation. Future studies are necessary to determine whether such integrative efforts improve MSU care quality, and which enhancements to information systems will optimize clinical care and research efforts.

Background and Purpose— We sought to evaluate the real-world rate of safety outcomes after patent foramen ovale (PFO) closure in patients with ischemic stroke or transient ischemic attack (TIA). Methods— We performed a retrospective cohort study using administrative claims data on all hospitalizations from 2005 to 2013 in New York, California, and Florida. Using International Classification of Diseases, Ninth Revision, Clinical Modification codes, we identified patients who underwent percutaneous transcatheter PFO closure within 1 year of ischemic stroke or TIA. Our outcome was an adverse event occurring during the hospitalization for PFO closure, defined as in prior studies as atrial fibrillation or flutter, cardiac tamponade, pneumothorax, hemothorax, a vascular access complication, or death. Crude rates were reported with exact confidence intervals. Results— We identified 1887 patients who underwent PFO closure after ischemic stroke or TIA. The rate of any adverse outcome during the hospitalization for PFO closure was 7.0% (95% confidence interval [CI], 5.9%–8.2%). Rates of adverse outcomes varied by age and type of preceding cerebrovascular event. In patients >60 years of age, the rate of adverse outcomes was 10.9% (95% CI, 8.6%–13.6%) versus 4.9% (95% CI, 3.8%–6.3%) in patients ≤60 years of age. The rate of adverse outcomes was 9.9% (95% CI, 7.3%–12.5%) in patients with preceding ischemic stroke versus 5.9% (95% CI, 4.7%–7.1%) after TIA. Conclusions— Approximately 1 in 14 patients who underwent percutaneous transcatheter PFO closure after ischemic stroke or TIA experienced a serious periprocedural adverse outcome or death. The risk of adverse outcomes was highest in older patients and in those with preceding ischemic stroke.

Male breast cancer is a rare and understudied disease predominantly affecting men over age 60. Risk of arterial thromboembolic events (ATE) in men increases with age. We examined ATE risk following primary breast cancer diagnosis in elderly men. Men with primary breast cancer diagnoses from 2002 to 2011 were identified using the Surveillance, Epidemiology, and End Results (SEER)-Medicare-linked database. Cases were individually matched by age, sex, race, registry, and comorbidities with controls without cancer using SEER-Medicare’s 5% noncancer sample. Medicare claims were used to identify ATE, defined as myocardial infarction or ischemic stroke. Cumulative incidence of ATE was calculated using competing risk methodology, with death considered a competing event. Cox proportional hazards analysis was used to compare rates of ATE among cases and controls. Three months following primary breast cancer diagnosis, ATE risk in the cohort of 881 men was 80% higher than matched controls (hazard ratio 1.8; 95% confidence interval 1.0–3.2). Six months post-cancer diagnosis, 5.7% of cases had experienced ATE, whereas only 3.5% of controls had (HR 1.6; 95% CI 1.0–2.6). ATE risk remained elevated 12 months post-cancer diagnosis. Among cases, risk of death was threefold higher in men who developed ATE. We provide population-based evidence that male breast cancer patients have a substantially elevated risk of ATE in the first year following a cancer diagnosis compared with matched controls. Care providers should consider this heightened risk when evaluating cardiovascular health in men with a recent breast cancer diagnosis.

Background and Purpose— The rate of spinal cord infarction (SCI) after surgical or endovascular repair of an aortic aneurysm or dissection is unclear. Methods— Using administrative claims data, we identified adult patients discharged from nonfederal acute care hospitals in California, New York, and Florida who underwent surgical or endovascular repair of an aortic aneurysm or dissection between 2005 and 2013. Patients with SCI diagnosed before the aortic repair were excluded. Our primary outcome was an SCI during the index hospitalization for aortic repair. Descriptive statistics were used to estimate crude rates of SCI. Analyses were stratified by whether the aneurysm or dissection had ruptured and by type of repair (surgical versus endovascular). Results— We identified 91 212 patients who had repair of an aortic aneurysm or dissection. SCI occurred in 235 cases (0.26%; 95% confidence interval [CI], 0.22%–0.29%). In patients with ruptured aneurysm or dissection, the rate of SCI was 0.74% (95% CI, 0.60%–0.88%) compared with 0.16% (95% CI, 0.13%–0.19%) with unruptured aneurysm. In secondary analyses, rates of SCI were similar after endovascular repair (0.91%; 95% CI, 0.62%–1.19%) compared with surgical repair (0.68%; 95% CI, 0.53%–0.83%; P =0.147) of ruptured aortic aneurysm or dissection; however, rates of SCI were higher after surgical repair (0.20%; 95% CI, 0.15%–0.25%) versus endovascular repair (0.11%; 95% CI, 0.08%–0.14%; P Conclusions— SCI occurs in ≈1 in 130 patients undergoing aortic dissection or ruptured aortic aneurysm repair and in 1 in 600 patients undergoing unruptured aortic aneurysm repair.

Objective:To compare outcomes after intracerebral hemorrhage (ICH) from cerebral arteriovenous malformation (AVM) rupture and other causes of ICH.Methods:We performed a retrospective population-based study using data from the Nationwide Inpatient Sample. We used standard diagnosis codes to identify ICH cases from 2002 to 2011. Our predictor variable was cerebral AVM. Our primary outcomes were inpatient mortality and home discharge. We used logistic regression to compare outcomes between patients with ICH with and without AVM while adjusting for demographics, comorbidities, and hospital characteristics. In a confirmatory analysis using a prospective cohort of patients hospitalized with ICH at our institution, we additionally adjusted for hematoma characteristics and the Glasgow Coma Scale score.Results:Among 619,167 ICH hospitalizations, the 4,485 patients (0.7%, 95% confidence interval [CI] 0.6–0.8) with an AVM were younger and had fewer medical comorbidities than patients without AVM. After adjustment for confounders, patients with AVM had lower odds of death (odds ratio [OR] 0.5, 95% CI 0.4–0.7) and higher odds of home discharge (OR 2.0, 95% CI 1.4–3.0) than patients without AVM. In a confirmatory analysis of 342 patients with ICH at our institution, the 34 patients (9.9%, 95% CI 7.2–13.6) with a ruptured AVM had higher odds of ambulatory independence at discharge (OR 4.4, 95% CI 1.4–13.1) compared to patients without AVM.Conclusions:Patients with ICH due to ruptured AVM have more favorable outcomes than patients with ICH from other causes.

Because some cryptogenic strokes may result from large-artery atherosclerosis that goes unrecognized as it causes50% luminal stenosis, we compared the prevalence of nonstenosing intracranial atherosclerotic plaques ipsilateral to cryptogenic cerebral infarcts versus the unaffected side using imaging biomarkers of calcium burden.In a prospective stroke registry, we identified patients with cerebral infarction limited to the territory of one internal carotid artery (ICA). We included patients with stroke of undetermined etiology and, as controls, patients with cardioembolic stroke. We used noncontrast computed tomography to measure calcification in both intracranial ICAs, including qualitative calcium scoring and quantitative scoring utilizing the Agatston-Janowitz (AJ) calcium scoring. Within subjects, the Wilcoxon signed-rank sum test for nonparametric paired data was used to compare the calcium burden in the ICA upstream of the infarction versus the ICA on the unaffected side.We obtained 440 calcium measures from 110 ICAs in 55 patients. Among 34 patients with stroke of undetermined etiology, we found greater calcium in the ICA ipsilateral to the infarction (mean Modified Woodcock Visual Scale score, 6.7 ± 4.6) compared with the contralateral side (5.4 ± 4.1) (P = .005). Among 21 patients with cardioembolic stroke, we found no difference in calcium burden ipsilateral to the infarction (6.7 ± 5.9) versus the contralateral side (7.3 ± 6.3) (P = .13). The results were similar using quantitative calcium measurements, including the AJ calcium scores.In patients with strokes of undetermined etiology, the burden of calcified intracranial large-artery plaque was associated with downstream cerebral infarction.

We agree with Dr. Sorigue and colleagues that besides cancer stage, cancer histology might also affect arterial thromboembolism risk, particularly in patients with non-Hodgkin lymphoma (NHL). To investigate this hypothesis, we performed the subgroup analyses suggested by the correspondents. Using

Background It is uncertain whether there is an association between left ventricular (LV) ejection fraction ( LVEF ) or LV wall motion abnormality and embolic stroke of undetermined source ( ESUS ). Methods and Results We performed a retrospective, cross‐sectional study of patients with acute ischemic stroke enrolled in the CAESAR (Cornell Acute Stroke Academic Registry) from 2011 to 2016. We restricted this study to patients with ESUS and, as controls, those with small‐ and large‐artery ischemic strokes. LVEF had to be above 35% to be considered ESUS . In a secondary analysis, we excluded patients with ESUS who had any evidence of ipsilateral carotid atherosclerosis. Multiple logistic regression was used to evaluate whether LVEF or LV wall motion abnormality was associated with ESUS . We performed a confirmatory study at another tertiary‐care center. We identified 885 patients with ESUS (n=503) or small‐ or large‐artery strokes (n=382). Among the entire cohort, LVEF was not associated with ESUS (odds ratio per 5% decrement in LVEF , 1.0; 95% CI, 1.0–1.1) and LV wall motion abnormality was not associated with ESUS (odds ratio, 0.9; 95% CI, 0.5–1.6). The results were identical in our confirmatory study. In our secondary analysis excluding ESUS patients with any evidence of ipsilateral carotid atherosclerosis, there was an association between LVEF and ESUS (odds ratio per 5% decrement in LVEF , 1.2; 95% CI, 1.0–1.5; P =0.04). Conclusions Among the entire cohort, no association existed between LVEF or LV wall motion abnormality and ESUS ; however, after excluding ESUS patients with any evidence of ipsilateral carotid atherosclerosis, lower LVEF appeared to be associated with ESUS .

OBJECTIVE: We sought to characterize the United States nationwide temporal trends in recanalization therapy utilization for ischemic stroke among patients with and without cancer. METHODS: We identified all acute ischemic stroke hospitalizations in the National Inpatient Sample from January 1, 1998-September 30, 2015. The primary exposure was solid or hematologic cancer. The primary outcome was use of intravenous thrombolysis. The secondary outcome was use of endovascular therapy. RESULTS: Among 9,508,804 acute ischemic stroke hospitalizations, 503,510 (5.3%) involved cancer patients. Intravenous thrombolysis use among ischemic stroke patients with cancer increased from 0.01% (95% CI, 0.00–0.02%) in 1998 to 4.91% (95% CI, 4.33–5.48%) in 2015; while intravenous thrombolysis use among ischemic stroke patients without cancer increased from 0.02% (95% CI, 0.01–0.02%) in 1998 to 7.22% (95% CI, 6.98–7.45%) in 2015. The demographic- and comorbidity-adjusted odds ratio/year of receiving intravenous thrombolysis was similar in patients with cancer (1.21; 95% CI, 1.20–1.23) versus those without (1.20; 95% CI, 1.19–1.21). Endovascular therapy use among ischemic stroke patients with cancer increased from 0.05% (95% CI, 0.02–0.07%) in 2006 to 1.90% (95% CI, 1.49–2.31%) in 2015; while endovascular therapy use among ischemic stroke patients without cancer increased from 0.09% (95% CI, 0.00–0.18%) in 2006 to 1.88% (95% CI, 1.68–2.09%) in 2015. CONCLUSIONS: Among 9.5 million acute ischemic stroke hospitalizations, patients with cancer received intravenous thrombolysis about two-thirds as often as patients without cancer. This difference persisted over time despite increased utilization in both groups. Endovascular therapy utilization was similar between cancer and non-cancer acute ischemic stroke patients.

Background and Purpose— Recent landmark trials provided overwhelming evidence for effectiveness of endovascular stroke therapy (EST). Yet, the impact of these trials on clinical practice and effectiveness of EST among lower volume centers remains poorly characterized. Here, we determine population-level patterns in EST performance in US hospitals and compare EST outcomes from higher versus lower volume centers. Methods— Using validated diagnosis codes from data on all discharges from hospitals and Emergency Rooms in Florida (2006–2016) and the National Inpatient Sample (2012–2016) we identified patients with acute ischemic stroke treated with EST. The primary end point was good discharge outcome defined as discharge to home or acute rehabilitation facility. Multivariate regressions adjusted for medical comorbidities, intravenous tPA (tissue-type plasminogen activator) usage and annual hospital stroke volume were used to evaluate the likelihood of good outcome over time and by annual hospital EST volume. Results— A total of 3890 patients (median age, 73 [61–82] years, 51% female) with EST were identified in the Florida cohort and 42 505 (median age, 69 [58–79], 50% female) in the National Inpatient Sample. In both Florida and the National Inpatient Sample, the number of hospitals performing EST increased continuously. Increasing numbers of EST procedures were performed at lower annual EST volume hospitals over the studied time period. In adjusted multivariate regression, there was a continuous increase in the likelihood of good outcomes among patients treated in hospitals with increasing annual EST procedures per year (odds ratio, 1.1; 95% CI, 1.1–1.2 in Florida and odds ratio, 1.3; 95% CI, 1.2–1.4 in National Inpatient Sample). Conclusions— Analysis of population-level datasets of patients treated with EST from 2006 to 2016 demonstrated an increase in the number of centers performing EST, resulting in a greater number of procedures performed at lower volume centers. There was a positive association between EST volume and favorable discharge outcomes in EST-performing hospitals.

Study objective Although most transient ischemic attack and minor stroke patients in US emergency departments (EDs) are admitted, experience in other countries suggests that timely outpatient evaluation of transient ischemic attack and minor stroke can be safe. We assess the feasibility and safety of a rapid outpatient stroke clinic for transient ischemic attack and minor stroke: Rapid Access Vascular Evaluation–Neurology (RAVEN). Methods Transient ischemic attack and minor stroke patients presenting to the ED with a National Institutes of Health Stroke Scale score of 5 or less and nondisabling deficit were assessed for potential discharge to RAVEN with a protocol incorporating social and medical criteria. Outpatient evaluation by a vascular neurologist, including vessel imaging, was performed within 24 hours at the RAVEN clinic. Participants were evaluated for compliance with clinic attendance and 90-day recurrent transient ischemic attack and minor stroke and hospitalization rates. Results Between December 2016 and June 2018, 162 transient ischemic attack and minor stroke patients were discharged to RAVEN. One hundred fifty-four patients (95.1%) appeared as scheduled and 101 (66%) had a final diagnosis of transient ischemic attack and minor stroke. Two patients (1.3%) required hospitalization (one for worsening symptoms and another for intracranial arterial stenosis caused by zoster) at RAVEN evaluation. Among the 101 patients with confirmed transient ischemic attack and minor stroke, 18 (19.1%) had returned to an ED or been admitted at 90 days. Five were noted to have had recurrent neurologic symptoms diagnosed as transient ischemic attack (4.9%), whereas one had a recurrent stroke (0.9%). No individuals with transient ischemic attack and minor stroke died, and none received thrombolytics or thrombectomy, during the interval period. These 90-day outcomes were similar to historical published data on transient ischemic attack and minor stroke. Conclusion Rapid outpatient management appears a feasible and safe strategy for transient ischemic attack and minor stroke patients evaluated in the ED, with recurrent stroke and transient ischemic attack rates comparable to historical published data.

Background and Purpose— It is uncertain whether heart transplantation decreases the risk of stroke. The objective of our study was to determine whether heart transplantation is associated with a decreased risk of subsequent stroke among patients with heart failure awaiting transplantation. Methods— We performed a retrospective cohort study using administrative data from New York, California, and Florida between 2005 and 2015. Individuals with heart failure awaiting heart transplantation were identified using previously validated International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis codes for heart failure in combination with code V49.83 for awaiting organ transplant status. Individuals with prior stroke were excluded. Our primary exposure variable was heart transplantation, modeled as a time-varying covariate and defined by procedure code 37.51. The primary outcome was stroke, defined as the composite of ischemic and hemorrhagic stroke. Survival statistics were used to calculate stroke incidence, and Cox proportional hazards analysis was used to determine the association between heart transplantation and stroke while adjusting for demographics, stroke risk factors, Elixhauser comorbidities, and implantation of a left ventricular assist device. Results— We identified 7848 patients with heart failure awaiting heart transplantation, of whom 1068 (13.6%) underwent heart transplantation. During a mean follow-up of 2.7 years, we identified 428 strokes. The annual incidence of stroke was 0.7% (95% CI, 0.5%–1.0%) after heart transplantation versus 2.4% (95% CI, 2.2%–2.6%) among those awaiting heart transplantation. After adjustment for potential confounders, heart transplantation was associated with a lower risk of stroke (hazard ratio, 0.4; 95% CI, 0.2–0.6). Conclusions— Heart transplantation is associated with a decreased risk of stroke among patients with heart failure awaiting transplantation.

Introduction: The computed tomography (CT) capabilities of mobile stroke units (MSUs) may facilitate prehospital triaging of patients with suspected large-vessel occlusion directly to thrombectomy-capable centers. However, little is known about the reliability of radiological interpretation of early ischemic changes on prehospital CTs. Methods: We identified all patients transported by the NewYork-Presbyterian MSU to Weill Cornell Medical Center with the diagnosis of acute ischemic stroke, transient ischemic attack, or stroke mimic between October 3, 2016 and December 31, 2017. All patients underwent noncontrast head CT on board the MSU using a CereTom® scanner. As controls, we matched these patients 1:1 by diagnosis to patients who were transported by standard ambulance and underwent noncontrast brain CT in our emergency department (ED) over the same period. Two neuroradiologists, blinded to patients’ characteristics and final diagnosis, independently calculated Alberta Stroke Program Early CT Scores (ASPECTS) on all scans. Weighted percent agreement and Cohen’s κ were used to assess inter-rater reliability, and paired t-tests were used to compare these metrics between MSU and ED scans. Results: Among 46 MSU patients and 46 ED patients, 52% had a diagnosis of acute ischemic stroke, 46% a diagnosis of stroke mimic, and 2% a diagnosis of transient ischemic attack. For ASPECTS score as a continuous outcome, the weighted inter-rater agreement was 98% for MSU scans versus 96% for ED scans (mean difference, 2%; 95% CI, -1% to 5%) and the weighted κ was 0.49 for MSU scans versus 0.54 for ED scans (mean difference, -0.05; 95% CI, -0.61 to 0.51). For ASPECTS score categorized as 0-4, 5-7, or 8-10, the weighted inter-rater agreement was 99% for MSU scans versus 97% for ED scans (mean difference, 2%; 95% CI, -2% to 7%) and the weighted κ was 0.66 for MSU scans versus 0.55 for ED scans (mean difference, 0.10; 95% CI, -0.87 to 1.08). Conclusions: In a sample of 96 patients, which limited our power to detect small differences, we found no substantial difference in the inter-rater reliability of ASPECTS scores obtained from MSU CTs versus ED CTs.

Introduction: Dissection of a cervical artery has been well described as a cause of ischemic stroke in the young. The role of dissection as a cause of stroke among older adults is less clear, but there are no obvious reasons why older patients would have less of a predisposition to dissection than younger patients. Hypothesis: We hypothesized that the incidence of dissection-related ischemic stroke would remain constant across age. Methods: We used inpatient discharge data included in the 2012-2015 releases of the National Inpatient Survey (NIS). We used previously validated ICD-9-CM codes to identify adults who were hospitalized with ischemic stroke and a concomitant diagnosis of either carotid- or vertebral-artery dissection. We compared the prevalence of concomitant dissection among stroke hospitalizations across patient subgroups defined by age. Survey weights provided by the NIS were used to calculate nationally representative estimates. Population estimates from the U.S. census were used to calculate the incidence of hospitalization with stroke and concomitant dissection per million person-years. Results: From 2012-2015, there were 17,325 hospitalizations with ischemic stroke and a concomitant dissection in the US. The prevalence of cervical-artery dissection among stroke hospitalizations was highest among those under 40 years of age and gradually decreased across increasing 10-year age intervals (Figure 1A). On the other hand, the overall incidence of hospitalization for stroke and concomitant dissection increased with increasing age (Figure 1B). Conclusions: In a nationally representative sample, we found that cervical-artery dissection accounts for a greater proportion of ischemic strokes among younger patients, but the absolute incidence of dissection-related stroke increases with age.

Introduction: Severely reduced left ventricular (LV) ejection fraction (EF) is an established risk factor for ischemic stroke. It is uncertain whether a modest reduction in LVEF (between 35%-50%) or the presence of LV wall motion abnormality may be a potential explanation for some embolic strokes of undetermined source (ESUS). Methods: We performed a retrospective cross-sectional study of patients with acute ischemic stroke enrolled in the Cornell AcutE Stroke Academic Registry (CAESAR) from 2011 through 2016. For this analysis, we restricted the study cohort to patients with ESUS and, as controls, those with small- and large-artery ischemic strokes who received an echocardiogram within 14 days of stroke. A single investigator blinded to stroke subtype recorded LVEF and the presence of LV wall motion abnormalities from reports of echocardiograms performed for routine evaluation of stroke. These variables are uniformly reported in echocardiogram reports at our institution. Multiple logistic regression models adjusted for demographics and stroke risk factors were used to evaluate whether LVEF or LV wall motion abnormality was associated with ESUS. Results: We identified 885 patients with ESUS or small- or large-artery strokes. The mean LVEF was 62.4% (+/- 7.9%). There was no difference in LVEF in patients with ESUS (62.4%; 95% CI, 61.8-63.1%) as compared to patients with small- or large-artery strokes (62.3%; 95% CI, 61.4-63.2%; P =0.8). After adjustment for demographics and stroke risk factors, LVEF was not associated with ESUS (OR per 10% incremental increase in LVEF, 0.9; 95% CI, 0.8-1.0; P = 0.4). LV wall motion abnormality was present in 5.9% of patients, and in multivariable analysis, its presence was not associated with ESUS (OR 0.9; 95% CI, 0.5-1.6; P = 0.7). Conclusions: We found that neither a modest reduction in LVEF nor the presence of LV wall motion abnormality was associated with ESUS.

Introduction: Cervicocephalic artery dissection is an important cause of stroke, particularly in the young. The initial presentation of cervicocephalic artery dissection can resemble benign neurological conditions resulting in delayed or incorrect diagnosis. We therefore sought to quantify the rate of possible cervicocephalic artery dissection misdiagnosis and to assess the impact of misdiagnosis on patient outcomes in a large heterogeneous cohort. Methods: We performed a retrospective cohort study using administrative claims data from all ED visits and nonfederal hospitalizations in New York, California, and Florida from 2005-2015. Using previously validated ICD-9-CM codes, we identified patients hospitalized with a diagnosis of cervicocephalic artery dissection and no prior stroke diagnosis. Possible misdiagnosis of cervicocephalic artery dissection was defined as having a treat-and-release ED visit for headache, facial pain, neck pain, or Horner syndrome in the 14 days prior to a hospitalization for cervicocephalic artery dissection. Multivariable logistic regression was used to compare adverse clinical outcomes (stroke or death at the time of cervicocephalic artery dissection diagnosis) in patients with and without a possible misdiagnosis. Results: Among 8,874 patients diagnosed with cervicocephalic artery dissection (mean age 52.7 years, 44.1% women), 300 (3.4%; 95% CI, 3.0-3.8%) had a possible ED misdiagnosis. Patients with a possible misdiagnosis of cervicocephalic artery dissection were younger and more often women than those not misdiagnosed. Stroke occurred in 128 (42.7%; 95% CI, 37.0-48.5%) patients with a possible misdiagnosis of dissection and in 3,908 (44.0%; 95% CI, 43.0-45.1%, P =0.63) patients without a possible misdiagnosis of cervicocephalic artery dissection. After adjustment for demographics and vascular risk factors, there were no differences in rates of hospital death (OR 0.48; 95% CI, 0.20-1.9) or stroke (OR 0.94; 95% CI, 0.74-1.2). Conclusion: We found a low rate of possible misdiagnosis of cervicocephalic artery dissection in the ED. Possible misdiagnosis was not associated with stroke or death at the time of subsequent hospitalization for cervicocephalic artery dissection.

Introduction: Patients presenting to emergency departments (ED) with TIA and minor strokes (TIAMS) are often admitted for expedited evaluation, though outpatient care models have been proposed. We piloted a rapid outpatient evaluation protocol for patients presenting with TIAMS within 24 hours of ED discharge. We hypothesized that this approach would reduce hospital costs and length of stay (LOS). Methods: This analysis looked at patients presenting to our institution’s ED with TIAMS (NIHSS < 5) in calendar year 2017. We compared hospitalization LOS, costs and expected revenues between admitted patients and those referred for rapid outpatient evaluation. Patients eligible for outpatient evaluation were without disabling deficits, recurrent symptoms, new-onset atrial fibrillation, prior carotid imaging with >50% stenosis, and not receiving thrombolysis. Disabling deficits were defined as new gait impairments, significant motor weakness, hemianopia, dysphagia or severe aphasia. Cost data was obtained from our finance department and expected revenue was estimated using Medicare reimbursement data, assuming Medicare-Fee for Service as the primary payer for all patients. Results: We identified 92 patients referred to our rapid outpatient clinic and 90 admitted patients (mean NIHSS 0.8 vs 1.8 respectively). In comparison to patients who were admitted, patients referred to outpatient evaluation had shorter hospital stays, lower total hospitalization costs, and decreased net-losses after accounting for expected revenue (Table). Only one patient in the outpatient cohort was readmitted for further management. Overall, the one-year pilot cohort averted approximately 138 bed-days and $950,000 in hospitalization costs. Conclusions: For patients who presented to our ED with TIAMS without disabling deficits, rapid outpatient evaluation reduced hospital LOS and total costs. Further research is needed to incorporate costs to payers and patients.

Background: Retrospective studies have reported an association between cancer and arterial thromboembolism risk. We sought to confirm this in a prospective cohort with adjudicated cardiovascular outcomes. Methods: We analyzed data from participants enrolled in the REasons for Geographic and Racial Differences in Stroke (REGARDS) study who had Medicare coverage for 365 days before their baseline study visit in 2003-2007. Participants with prevalent cancer, coronary heart disease, or cerebrovascular disease were excluded. Medicare claims were used to identify new cancer diagnoses during follow-up. Using incidence-density sampling, participants who developed cancer were matched by age, sex, race, and education level 1:4 to participants who hadn’t developed cancer. Participants were prospectively followed through September 30, 2015 for an adjudicated arterial thromboembolic event, defined as fatal or nonfatal acute myocardial infarction or ischemic stroke. Cox regression was performed to evaluate the association between incident cancer and subsequent arterial thromboembolic events. To fulfill the proportional hazard assumption, follow-up time was modeled in discrete time periods. Results: In this analysis, 836 REGARDS participants with incident cancer were matched to 3,339 participants without cancer. During median follow-up of 3 years, 63 (7.5%) participants with cancer and 216 (6.5%) participants without cancer had an arterial thromboembolic event. Compared to non-cancer controls, participants with incident cancer had an increased risk of arterial thromboembolic events in the first 30 days after diagnosis (HR, 5.2; 95% CI, 2.1-12.7). This association persisted after adjustment for demographics, region of residence, and cardiovascular risk factors (HR, 5.8; 95% CI, 2.1-15.9). Cancers with known metastases and types considered high-risk for venous thromboembolism had the strongest associations with arterial thromboembolic events. There was no association between cancer diagnosis and arterial thromboembolic event risk beyond 30 days. Conclusions: Incident cancer, particularly when metastatic, is associated with an increased short-term risk of arterial thromboembolic events independent of vascular risk factors.

Background: Given the time-sensitivity of endovascular stroke therapy (EST), an increased availability of these treatments to lower-volume centers may improve patient outcomes. However, clinical trials demonstrating efficacy of EST were performed at larger volume centers, and our understanding of outcomes at lower volume centers is lacking. Methods: Using validated diagnosis codes from administrative data on all discharges from hospitals in Florida (2005-2016), and New York (2006-2014) we identified patients with acute stroke treated with EST. Primary endpoint was good outcome defined as discharge home without intracerebral hemorrhage. Descriptive statistics were used to calculate the number of EST performed. Multivariate logistic regressions adjusted for age, sex, and comorbidities were used to evaluate the association between year of treatment and hospital volume with outcome. Results: Among 5,699 patients (at 439 hospitals) treated with EST, median age was 72[60-81], 52% were female, and 54% received IV tPA. Annual EST procedures increased from 158 in 2007 to 423 in 2010 to 925 in 2014, as did the number of hospitals performing EST, from 30 in 2007 to 50 in 2010 to 68 in 2014. During the study period, an increasing proportion of total EST procedures were performed at lower volume centers ( Figure 1a ). Adjusting for age and comorbidities, the likelihood of good outcome increased yearly (OR 1.1 [1.05 -1.14]). Adjusting for age, comorbidities and year of treatment, increasing annual hospital EST volume was associated with increasing likelihood of good outcome ( Figure 1b ). Conclusions: In two large and diverse states, clinical outcomes with EST improved over time. Higher volume centers performed better than lower volume centers, a finding that persisted despite the overall trend towards improvement. These findings support the need for further study on the efficacy of EST outside of specialized centers.

Introduction: The recent Insulin Resistance Intervention after Stroke trial found that pioglitazone decreased the risk of stroke and myocardial infarction in patients with insulin resistance and a recent cerebrovascular event. However, by 5 years, patients receiving pioglitazone had a significantly increased risk of bone fracture requiring surgery or hospitalization compared to patients who received placebo (5.1% versus 3.2%). Data is lacking on the long-term real-world risk of bone fracture among patients with ischemic stroke. Methods: We performed a retrospective cohort study using inpatient and outpatient claims data between 2008-2015 from a nationally representative 5% sample of Medicare beneficiaries. We included patients who were ≥65 years old and hospitalized with ischemic stroke, defined by validated International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis codes. We excluded patients who had a prior or concurrent hip fracture diagnosis at the time of ischemic stroke. The primary outcome was hip fracture requiring hospitalization. Survival statistics were used to calculate incidence rates and Kaplan-Meier statistics were used to calculate cumulative rates of hip fracture. Results: Among the 1,952,305 beneficiaries in our sample, 60,099 patients developed an ischemic stroke in the absence of a prior or concomitant hip fracture. During 4.5 (±2.2) years of follow-up, the incidence of hip fracture was 1.6 (95% CI, 1.5-1.6) per 100 person-years in the patients with ischemic stroke versus 0.6 (95% CI, 0.6-0.6) per 100 person-years in patients without ischemic stroke. The cumulative 5-year rate of hip fracture was 7.6% (95% CI, 7.2-8.0%) among patients with ischemic stroke compared to 2.8% (95% CI, 2.8-2.9%) among the remaining Medicare beneficiaries. Conclusions: We found that the 5-year cumulative risk of hip fracture in the overall population of Medicare beneficiaries with ischemic stroke was approximately 7.5%.

Background: About one-fifth of ischemic strokes lack a determined etiology and can be classified as embolic strokes of undetermined source (ESUS). Lambl’s excrescences are commonly seen on cardiac valves during echocardiography, and only a few studies have addressed whether they may be a source of thrombus formation and subsequent embolization. We therefore evaluated whether Lambl’s excrescences are associated with ESUS. Methods: We performed a case-control analysis using data from the Cornell AcutE Stroke Academic Registry (CAESAR), a prospective registry of all patients with stroke at our hospital since 2011. Stroke etiologies were adjudicated by a panel of neurologists using the TOAST and ESUS criteria. We included only patients who underwent transthoracic (TTE) or transesophageal (TEE) echocardiography within 6 months of hospital discharge. Cases were all ESUS patients and controls were all patients with non-cardioembolic stroke (small- or large-vessel strokes). Multiple logistic regression was used to evaluate the association between Lambl’s excrescence and ESUS after adjustment for demographics, comorbidities, and mode of echocardiography (TTE vs TEE). Results: Among 2,116 patients registered in CAESAR from 2011-2016, 923 patients met the criteria for this analysis, including 530 with ESUS and 393 with small- or large-vessel strokes. Patients with ESUS were more often women and had fewer stroke risk factors. Lambl’s excrescences were identified in 47 (8.9%) patients with ESUS and 11 (2.8%) patients with small- or large-artery strokes. The majority (54/58) of Lambl’s excrescences were visualized on TEE, and ESUS patients were much more likely to undergo TEE. After adjustment for demographics, comorbidities, and mode of echocardiography, we found no association between the presence of Lambl’s excrescences and ESUS (OR 0.9; 95% CI 0.4-2.3). Conclusion: While Lambl’s excrescences are commonly seen on echocardiograms performed to evaluate ischemic stroke, we found no association between Lambl’s excrescences and ESUS. These results do not support the hypothesis that Lambl’s excrescences are an occult cause of ESUS.

Background: Mobile stroke units (MSUs) reduce time to thrombolytic treatment in acute ischemic stroke. It is unclear whether this time advantage persists in densely-populated urban areas with many readily-accessible hospitals. Methods: We collected clinical data, treatment times, numbers of nearby designated stroke centers (DSC), and distances traveled from suspected stroke patients transported by a single-institution MSU operating in Manhattan, New York from October 2016-September 2017. For comparison, we collected information on patients transported to our institution via conventional ambulance for acute stroke during the same hours of MSU operation (Monday-Friday, 9AM-5PM). Our exposure was MSU care, and our coprimary outcomes were dispatch-to-scene arrival and scene arrival-to-thrombolysis times. We estimated mean differences in each primary outcome between both groups, adjusting for clinical, demographic, and geographic factors. Results: We identified 66 patients transported by MSU, of whom 29 (44%) were treated with IV thrombolysis, and 19 patients transported by conventional ambulance, of whom 9 (48%) were treated with IV thrombolysis. Patients treated in the MSU traveled longer to accepting hospitals and were picked up closer to a greater number of DSCs in a 1 mile radius than non-MSU patients (Table). Despite longer median dispatch-to-ambulance arrival and ambulance arrival-to-hospital arrival times than non-MSU patients, MSU patients had shorter mean dispatch-to-thrombolysis and ambulance arrival-to-thrombolysis times. In multivariable analysis, MSU care was associated with a mean increase in dispatch-to-ambulance arrival time of 6.5 minutes (95% CI, 2.3-10.6) that was offset by a mean decrease in ambulance arrival-to-thrombolysis time of 42.2 minutes (95% CI, 31.1-53.4). Conclusions: In a densely populated urban area, MSU care was associated with substantially quicker time-to-thrombolysis when compared to conventional care.

Introduction: Elevations in cardiac troponin in the absence of a clinically recognized acute myocardial infarction are typically seen in patients with acute ischemic stroke, though their significance remains unclear. Visceral infarcts appear to be more common in patients with embolic stroke subtypes, but their relation to troponin elevation remains uncertain. Methods: Among patients with acute ischemic stroke enrolled in the Cornell AcutE Stroke Academic Registry (CAESAR) from 2011 through 2016, we included those with troponin measured within 24 hours from stroke onset and a contrast-enhanced abdominal computed tomographic scan within 1 year of admission. A troponin elevation was defined as a value exceeding our laboratory’s upper limit of normal (0.04 ng/mL) in the absence of a clinically recognized acute ST-segment elevation myocardial infarction. Visceral infarction was defined as a renal or splenic infarction as ascertained by a single radiologist blinded to patients’ other characteristics including troponin levels. Multiple logistic regression was used to evaluate the association between elevated troponin and visceral infarction after adjustment for demographics and comorbidities. Results: Among 2,116 patients registered in CAESAR from 2011-2016, 153 patients had a troponin assay and underwent a contrast-enhanced abdominal computed tomographic scan, of whom 33 (21%) had an elevated troponin and 22 (14%) had a visceral infarct. The prevalence of visceral infarction was higher among patients with an elevated troponin (30%; 95% CI, 16-49%) than among patients without an elevated troponin (10%; 95% CI, 5-17%) ( P = 0.003). After adjustment for demographics and comorbidities, we found a significant association between elevated troponin and visceral infarct (OR, 3.8; 95% CI, 1.2-11.7). Conclusions: Among patients with acute ischemic stroke, elevated troponin in the absence of a clinically recognized acute ST-segment elevation myocardial infarction was associated with visceral infarction, which is typically caused by embolism. Our results support the hypothesis that post-stroke troponin elevation indicates the presence of underlying embolic sources.

Background: Evidence of visceral infarction is often found in patients with acute ischemic stroke, and appears to be more common among patients with embolic stroke subtypes. It remains uncertain whether there exists a relationship between visceral infarction and functional outcomes among patients with stroke. Methods: Among patients with acute ischemic stroke enrolled in the Cornell AcutE Stroke Academic Registry (CAESAR) from 2011 through 2016, we included those with a contrast-enhanced abdominal computed tomographic scan within 1 year of admission. Our outcome was ambulatory status at discharge from the acute stroke hospitalization, defined as walking without assistance, walking with assistance, and unable to walk. We used ordinal logistic regression to examine the association between visceral infarction and discharge ambulatory status after adjustment for demographics, stroke risk factors, stroke severity (NIH Stroke Scale score) and stroke subtype. Results: Among 2,116 ischemic stroke patients registered in CAESAR from 2011-2016, 228 had contrast-enhanced abdominopelvic computed tomographic imaging, of whom 40 (18%) had evidence of visceral infarction. Among the 188 patients without visceral infarction, 125 (66%) patients were discharged walking without assistance, 34 (18%) patients could walk with assistance, and 29 (15%) patients could not walk. In comparison, among the 40 patients with visceral infarction, 18 (45%) patients were discharged walking without assistance, 9 (23%) patients could walk with assistance, and 13 (33%) patients could not walk. After adjustment for demographics, stroke risk factors, stroke severity and stroke subtype, the presence of visceral infarction was associated with a worse ambulatory status (global OR for better ambulatory status, 0.3; 95% CI, 0.1-0.8). Conclusions: We found that the presence of visceral infarction, which is often incidentally detected on imaging among stroke patients, was associated with poor functional outcomes at the time of hospital discharge. These findings suggest that such incidental findings are not benign and are at the least a marker of poor outcomes.

Introduction: We examined the association between prior antiplatelet therapy and outcomes in patients with lobar versus deep intracerebral hemorrhage (ICH) versus intraventricular hemorrhage (IVH). Methods: We performed a retrospective cohort study using data from patients with lobar and deep ICH registered in the Virtual International Stroke Trials Archive (VISTA-ICH), and patients with IVH enrolled in the Clot Lysis: Evaluating Accelerated Resolution of Intraventricular Hemorrhage (CLEAR) III trial. We excluded patients in the intervention arms of the trials, and those on prior anticoagulation therapy. The exposure was antiplatelet therapy prior to ICH/IVH. Primary outcomes were hematoma expansion and death/major disability in the VISTA-ICH cohort, and ventriculostomy tract hemorrhage, hematoma expansion, and death/major disability in the CLEAR III cohort. We used separate sets of logistic regression models in each group—lobar ICH, deep ICH, and IVH—to examine the association between antiplatelet therapy and our outcomes. Results: Among 548 ICH patients in the VISTA-ICH cohort, there were 416 (75.9%) lobar and 121 (22.1%) deep hematomas. Median baseline ICH volumes were 19 ml (IQR, 11-26) in lobar and 8 ml (IQR, 4-13) in deep bleeds. Prior antiplatelet therapy was reported in 92 patients with lobar (22.1%) and 26 patients (20.8%) patients with deep ICH. After adjustment for demographics, comorbidities, and hematoma characteristics, antiplatelet therapy was not associated with hematoma expansion or poor functional outcomes after lobar (OR, 0.8; 95% CI, 0.5-1.8) or deep (OR, 1.3; 95% CI, 0.4-3.8) ICH. In the CLEAR cohort, the 62 of 222 IVH patients (27.9%) with prior antiplatelet therapy had similar odds of hematoma expansion (OR, 0.6; 95% CI, 0.2-1.7) or poor functional outcomes (OR, 0.9; 95% CI, 0.4-2.1), but higher odds of ventriculostomy tract hemorrhage (OR, 3.2; 95% CI, 1.3-7.7). Conclusions: Prior antiplatelet therapy was not associated with hematoma expansion or functional outcomes after lobar or deep ICH or IVH, but was associated with ventriculostomy tract hemorrhage.

Introduction: Anaphylaxis has been reported as a potential adverse event after intravenous thrombolysis in patients with acute ischemic stroke, but the magnitude of risk remains unclear. Methods: We performed a retrospective cohort study using inpatient and outpatient claims between 2008-2015 from a nationally representative 5% sample of Medicare beneficiaries. We included patients who were ≥65 years old and hospitalized with ischemic stroke, defined by validated ICD-9-CM diagnosis codes. Our exposure was treatment with an intravenous thrombolytic agent during the index hospitalization ( ICD-9-CM code 99.10). Our primary outcome was anaphylaxis, defined using an accepted ICD-9-CM code algorithm (989.5, 995.0-4, 995.6x, E905, E905.3, E905.5, or E905.8-9). Our secondary outcome was anaphylactic shock (995.0 or 995.6x). Multiple logistic regression was used to evaluate the association between intravenous thrombolysis and anaphylaxis after adjustment for demographics, vascular risk factors, the Charlson comorbidity index, exposure to intravenous contrast dye, treatment with mechanical thrombectomy, and history of allergic reactions. Results: Among 66,989 patients with acute ischemic stroke, the 3,176 (4.7%) who underwent intravenous thrombolysis more often had atrial fibrillation (47.7% vs 37.4%) and more often received intravenous contrast dye (44.3% vs 21.9%), but were otherwise similar in terms of demographics and comorbidities. Anaphylaxis developed in 17 (0.54%; 95% CI, 0.31-0.86%) patients who received intravenous thrombolysis versus 45 (0.07%; 95% CI, 0.05-0.09%) who did not. After adjustment for demographics, comorbidities, contrast dye, mechanical thrombectomy, and history of allergies, there was a significant association between receipt of intravenous thrombolysis and anaphylaxis (OR, 7.3; 95% CI, 4.1-13.0). We found a similar association for anaphylactic shock. Conclusions: Although a rare occurrence, the risk of anaphylaxis among patients with acute ischemic stroke was significantly higher among those who received intravenous thrombolysis.

Introduction: Mechanical thrombectomy has recently been proven to improve outcomes in selected patients with acute ischemic stroke, prompting concerns about equitable access to this treatment. Methods: We performed a retrospective cohort study using inpatient and outpatient claims between 2008-2015 from a nationally representative 5% sample of Medicare beneficiaries. We included patients who were ≥65 years old and hospitalized with ischemic stroke, defined by validated ICD-9-CM diagnosis codes. Our exposure variable was county-level socioeconomic advantage, defined by a validated summary score of income, wealth, education, and occupation data from the U.S. Census Bureau’s American Community Survey. Our outcome was mechanical thrombectomy, ascertained using CPT codes. Multiple logistic regression was used to evaluate the association between socioeconomic status and thrombectomy while adjusting for demographics, vascular risk factors, Charlson comorbidities, calendar year, intravenous thrombolysis, and mechanical ventilation (included as proxy for stroke severity). Results: Among 66,989 patients with acute ischemic stroke, the 459 (0.69%; 95% CI 0.62-0.75%) patients who underwent thrombectomy during their index hospitalization were younger (77.7 versus 79.9 years), more often had atrial fibrillation (65.1% versus 37.7%), and more often received intravenous thrombolysis (43.7% versus 4.5%). The likelihood of thrombectomy increased across increasing quartiles of the county-based socioeconomic advantage score: 0.46%, 0.59%, 0.70%, and 0.97% ( P Conclusions: We found an association between increasing socioeconomic status and higher odds of thrombectomy for acute ischemic stroke.

Introduction: It is unknown how the clinical characteristics of stroke mimics treated on Mobile Stroke Units (MSUs) compare to confirmed acute strokes treated on these units. Methods: We retrospectively analyzed all patients transported by the NewYork-Presbyterian MSU in New York City from October 2016-May 2018. A vascular neurologist assigned a final diagnosis after comprehensive medical record review. Clinical data were abstracted, including comorbidities, presenting symptoms, stroke severity, acute treatments, and short-term outcomes. We compared characteristics of patients with a stroke mimic diagnosis versus those with acute ischemic or hemorrhagic stroke using targeted minimum loss-based estimation to adjust for demographics, comorbidities, NIH Stroke Scale (NIHSS) score, and intravenous tPA administration. Results: Among 92 suspected stroke patients transported by MSU, 56 (61%) had confirmed acute stroke (77% ischemic, 23% hemorrhagic) and 36 (39%) had a stroke mimic. Mimics consisted of seizure (n=8), metabolic encephalopathy (n=6), somatoform disorders (n=4), and others (n=18). The mean NIHSS score was 8 (SD 7) among mimics versus 11 (SD 8) among confirmed strokes (p=0.14). The top presenting symptoms among mimics were unilateral weakness (n=8), aphasia (n=6), confusion (n=6), and decreased consciousness (n=6). Nine mimics (25%) received tPA and none had hemorrhagic conversion; while 30 (53%) confirmed strokes received tPA and 2 (7%) had hemorrhagic conversion. There was no difference in MSU arrival-to-tPA time between groups (46 vs. 44 minutes, p=0.70). In multivariable analyses, compared to patients with confirmed stroke, mimics had significantly lower NIHSS scores, higher initial blood pressures, and shorter lengths-of-stay. Rates of death and discharge disposition were similar between groups. Conclusions: Among patients transported by a MSU for suspected stroke, two-fifths were stroke mimics. Seizure, metabolic encephalopathy, and somatoform disorders were the most common mimic diagnoses. Patients with stroke mimics had lower NIHSS scores and less often were treated with tPA.

Introduction: Liver disease is associated with inflammation and coagulopathy. We hypothesized that liver fibrosis, a frequently subclinical precursor of cirrhosis, is associated with outcomes in intracerebral hemorrhage (ICH). Methods: We performed a retrospective cohort study using the Virtual International Stroke Trials Archive - ICH database. We included adult patients with primary ICH who presented within 24 hours of symptom onset. Patients with alcohol abuse and known liver disease were excluded. The exposure variables were three validated fibrosis indices calculated at the time of admission: the Aspartate aminotransferase Platelet Ratio Index (APRI), the Non-alcoholic Fatty Liver Disease Fibrosis Score (NFS), and the Fibrosis-4 (Fib-4) score. Our outcomes were hematoma expansion (HE) over 96 hours, perihematomal edema expansion, 90-day mortality, and 90-day disability (modified Rankin Scale scores 4-6). Multiple logistic regression models assessing the relationship between each 1.0 unit change in fibrosis indices and outcomes were adjusted for age, baseline ICH volume, Glasgow Coma Scale, location, intraventricular hemorrhage, and use of antithrombotic drugs. Patients with antithrombotic use and thrombocytopenia were excluded in sensitivity analyses. Results: Of 588 patients with ICH, mean age was 66 years (SD, 12), and mean baseline hematoma volume was 22.8 milliliters (SD, 21.6). Antithrombotic use was noted in 165 patients (28%). The mean APRI, NFS, and FIB-4 values were 0.4 (SD, 0.4), -0.8 (SD, 1.3), and 1.9 (SD, 1.4), respectively; the means reflect intermediate probabilities of fibrosis. HE was seen in 212 patients (36%). After adjusting, APRI was associated with HE (OR 2.00; 95% CI 1.09-3.67) and 90-day mortality (OR 1.75; 95% CI 1.04-2.97). NFS was also associated with HE (OR 1.20; 95% CI 1.04-1.46) and mortality (OR 1.34; 95% CI 1.02-1.75). Similarly, FIB-4 was associated with HE (OR 1.28; 95% CI 1.05-1.56) and mortality (OR 1.9; 95% CI 1.04-1.60). Indices were not associated with perihematomal edema expansion or 90-day disability. Sensitivity analysis results were similar. Conclusion: Liver fibrosis may be associated with HE and 90-day mortality after ICH. The implications of liver fibrosis for ICH warrant further investigation.

Objective: We evaluated the ability of genetic and serological testing to diagnose clinically relevant thrombophilias in young adults with ischemic stroke. Methods: We performed a retrospective cohort study of patients aged 18-65 years diagnosed with acute ischemic stroke at a comprehensive stroke center between 2011 and 2015 with laboratory testing for thrombophilia. The primary outcome was any positive thrombophilia screening test. The secondary outcome was a change in clinical management based on thrombophilia testing results. Logistic regression was used to assess whether the prespecified risk factors of age, sex, prior venous thromboembolism, family history of stroke, stroke subtype, and presence of patent foramen ovale were associated with outcomes. Results: Among 196 young ischemic stroke patients, at least 1 positive thrombophilia test was identified in 85 patients (43%; 95% CI, 36%-51%) and 16 (8%; 95% CI, 5%-13%) had a resultant change in management. Among 111 patients with cryptogenic strokes, 49 (44%) had an abnormal thrombophilia test and 9 (8%) had a change in management. After excluding cases of isolated hyperhomocysteinemia or methylenetetrahydrofolate reductase or Factor V Leiden gene mutation heterozygosity, the proportion of patients with an abnormal thrombophilia screen decreased to 24%. Prespecified risk factors were not significantly associated with positive thrombophilia testing or a change in management. Conclusions: Two-of-five young patients with ischemic stroke who underwent thrombophilia screening at our institution had at least 1 positive test but only one-in-twelve had a resultant change in clinical management. Neither cryptogenic stroke subtype nor other studied clinical factors were associated with a prothrombotic state.

Background The duration of heightened stroke risk after acute myocardial infarction ( MI ) remains uncertain. Methods and Results We performed a retrospective cohort study using claims between 2008 and 2015 from a nationally representative 5% sample of Medicare beneficiaries aged ≥66 years. Both acute MI and ischemic stroke were ascertained using previously validated International Classification of Diseases, Ninth Revision, Clinical Modification ( ICD‐9‐CM ), diagnosis codes. To exclude periprocedural strokes from percutaneous coronary intervention, we did not count strokes occurring during an acute MI hospitalization. Patients were censored at the time of ischemic stroke, death, end of Medicare coverage, or September 30, 2015. We fit Cox regression models separately for the groups with and without acute MI to examine its association with ischemic stroke after adjustment for demographics, stroke risk factors, and Charlson comorbidities. We used the corresponding survival probabilities to compute the hazard ratio in each 4‐week interval after discharge. Confidence intervals were computed using the nonparametric bootstrap method. Among 1 746 476 eligible beneficiaries, 46 182 were hospitalized for acute MI and 80 466 for ischemic stroke. After adjustment for demographics, stroke risk factors, and Charlson comorbidities, the risk of ischemic stroke was highest in the first 4 weeks after discharge from the MI hospitalization (hazard ratio: 2.7; 95% confidence interval, 2.3–3.2), remained elevated during weeks 5 to 8 (hazard ratio: 2.0; 95% confidence interval, 1.6–2.4) and weeks 9 to 12 (hazard ratio: 1.6; 95% confidence interval, 1.3–2.0), and was no longer significantly elevated afterward. Conclusions Acute MI is associated with an elevated risk of ischemic stroke that appears to extend beyond the 1‐month window that is currently considered the at‐risk period.

Background Visceral infarctions appear to be more common in patients with embolic stroke subtypes, but their relation to troponin elevation remains uncertain. Methods Among patients with acute ischemic stroke enrolled in the Cornell AcutE Stroke Academic Registry (CAESAR) from 2011 to 2016, we included those with troponin measured within 24 hours from stroke onset and a contrast-enhanced abdominal computed tomographic scan within 1 year of admission. A troponin elevation was defined as a value exceeding our laboratory's upper limit of normal (.04 ng/ mL) in the absence of a clinically recognized acute ST-segment elevation myocardial infarction. Visceral infarction was defined as a renal or splenic infarction as ascertained by a single radiologist blinded to patients’ other characteristics. Multivariable logistic regression was used to evaluate the association between elevated troponin and visceral infarction. Results Among 2116 patients registered in CAESAR from 2011 to 2016, 153 patients had both a troponin assay and a contrast-enhanced abdominal computed tomographic scan, of whom 33 (21%) had an elevated troponin and 22 (14%) had a visceral infarction. The prevalence of visceral infarction was higher among patients with an elevated troponin (30%; 95% confidence interval [CI], 16%-49%) than among patients without an elevated troponin (10%; 95% CI, 5%-17%) (P = .003). After adjustment for demographics and comorbidities, we found a significant association between elevated troponin and visceral infarction (odds ratio, 3.9; 95% CI, 1.5-10.4). Conclusions Among patients with acute ischemic stroke, elevated troponin was associated with visceral infarction. Our results demonstrate that poststroke troponin elevation may indicate the presence of underlying embolic sources.

Background Myocardial infarction (MI) is a known cause of cerebral infarction. We assessed whether the size and location of MI is associated with the risk of cerebral infarction. Methods and results We performed a cross-sectional study of adults who underwent both brain MRI and delayed-enhancement cardiac MRI (DE-CMR) within 365 days of each other at Weill Cornell Medicine between 2014 and 2017 and had evidence of MI on DE-CMR. We used multiple logistic regression to evaluate associations between MI size and any cerebral infarction, apical MI location and any cerebral infarction, and MI size/location and cortical versus subcortical cerebral infarction. Models were adjusted for demographics, and the total number of vascular risk factors. Among 234 patients who underwent both DE-CMR and brain MRI within 365 days, 76 had evidence for MI on DE-CMR. Among these 76 patients, 51 (67.1%) had evidence of cerebral infarction. The size of MI (global MI burden) was not associated with any cerebral infarction (OR per 5% increase in MI size, 1.12; 95% CI, 0.85–1.47), but was associated with cortical cerebral infarction (OR per 5% increase in MI size, 1.30; 95% CI, 1.00.-1.68). Similarly, apical MI location was not associated with any cerebral infarction (OR 2.63, 95% CI, 0.78–8.87), but was associated with cortical cerebral infarction (OR, 3.67; 95% CI, 1.19–11.33). Conclusion Among patients with MI on cardiac MRI, both size and apical location of MI were associated with cortical cerebral infarction. Our results may help stratify cardioembolic risk and inform antithrombotic treatment algorithms among patients with MI.

Importance The etiology and significance of diffusion-weighted imaging (DWI) lesions in patients with acute intracerebral hemorrhage (ICH) remain unclear. Objective To evaluate which factors are associated with DWI lesions, whether associated factors differ by ICH location, and whether DWI lesions are associated with functional outcomes. Design, Setting, and Participants This analysis pooled individual patient data from 3 randomized clinical trials (Minimally Invasive Surgery Plus Alteplase for Intracerebral Hemorrhage Evacuation phase 3 trial, Antihypertensive Treatment of Acute Cerebral Hemorrhage trial, and Intracerebral Hemorrhage Deferoxamine phase 2 trial) and 1 multicenter prospective study (Ethnic/Racial Variations of Intracerebral Hemorrhage). Patients were enrolled from August 1, 2010, to September 30, 2018. Of the 4782 patients, 1788 who underwent magnetic resonance imaging scans of the brain were included. Data were analyzed from July 1 to December 31, 2019. Main Outcomes and Measures The primary outcome consisted of factors associated with DWI lesions. Secondary outcomes were poor functional outcome, defined as a modified Rankin score (mRS) of 4 to 6, and mortality, both assessed at 3 months. Mixed-effects logistic regression was used to evaluate the association between exposures and outcomes. Subgroup analyses stratified by hematoma location were performed. Results After exclusion of 36 patients with missing data on DWI lesions, 1752 patients were included in the analysis (1019 men [58.2%]; mean [SD] age, 60.8 [13.3] years). Diffusion-weighted imaging lesions occurred in 549 patients (31.3%). In mixed-effects regression models, factors associated with DWI lesions included younger age (odds ratio [OR] per year, 0.98; 95% CI, 0.97-0.99), black race (OR, 1.64; 95% CI, 1.17-2.30), admission systolic blood pressure (OR per 10–mm Hg increase, 1.13; 95% CI, 1.08-1.18), baseline hematoma volume (OR per 10-mL increase, 1.12; 95% CI, 1.02-1.22), cerebral microbleeds (OR, 1.85; 95% CI, 1.39-2.46), and leukoaraiosis (OR, 1.59; 95% CI, 1.67-2.17). Diffusion-weighted imaging lesions were independently associated with poor mRS (OR, 1.50; 95% CI, 1.13-2.00), but not with mortality (OR, 1.11; 95% CI, 0.72-1.71). In subgroup analyses, similar factors were associated with DWI lesions in lobar and deep ICH. Diffusion-weighted imaging lesions were associated with poor mRS in deep but not lobar ICH. Conclusions and Relevance In a large, heterogeneous cohort of prospectively identified patients with ICH, results were consistent with the hypothesis that DWI lesions represent acute sequelae of chronic cerebral small vessel disease, particularly hypertensive vasculopathy. Diffusion-weighted imaging lesions portend a worse prognosis after ICH, mainly deep hemorrhages.

Background Recent literature suggests that acute rises in blood pressure may precede intracerebral hemorrhage. We therefore hypothesized that patients discharged from the emergency department with hypertension face an increased risk of intracerebral hemorrhage in subsequent weeks. Methods Using administrative claims data from California, New York, and Florida, we identified all patients discharged from the emergency department from 2005 to 2011 with a primary diagnosis of hypertension ( ICD-9-CM codes 401-405). We excluded patients if they were hospitalized from the emergency department or had prior histories of cerebrovascular disease at the index visit with hypertension. We used the Mantel–Haenszel estimator for matched data to compare each patient's odds of intracerebral hemorrhage during days 8-38 after emergency department discharge to the same patient's odds during days 373-403 after discharge. This cohort-crossover design with a 1-week washout period enabled individual patients to serve as their own controls, thereby minimizing confounding bias. Results Among the 552,569 patients discharged from the emergency department with a primary diagnosis of hypertension, 93 (.017%) were diagnosed with intracerebral hemorrhage during days 8-38 after discharge compared to 70 (.013%) during days 373-403 (odds ratio 1.33, 95% confidence interval .96-1.84). The odds of intracerebral hemorrhage were increased in certain subgroups of patients (≥60 years of age and those with secondary discharge diagnoses besides hypertension), but absolute risks were low in all subgroups. Conclusions Patients with emergency department discharges for hypertension do not face a substantially increased short-term risk of intracerebral hemorrhage after discharge.

In this study, models based on quantitative imaging biomarkers of post-stroke structural connectome disruption were used to predict six-month outcomes in various domains. Demographic information and clinical MRIs were collected from 40 ischemic stroke subjects (age: 68.1 ± 13.2 years, 17 female, NIHSS: 6.8 ± 5.6). Diffusion-weighted images were used to create lesion masks, which were uploaded to the Network Modification (NeMo) Tool. The NeMo Tool, using only clinical MRIs, allows estimation of connectome disruption at three levels: whole brain, individual gray matter regions and between pairs of gray matter regions. Partial Least Squares Regression models were constructed for each level of connectome disruption and for each of the three six-month outcomes: applied cognitive, basic mobility and daily activity. Models based on lesion volume were created for comparison. Cross-validation, bootstrapping and multiple comparisons corrections were implemented to minimize over-fitting and Type I errors. The regional disconnection model best predicted applied cognitive (R(2) = 0.56) and basic mobility outcomes (R(2) = 0.70), while the pairwise disconnection model best predicted the daily activity measure (R(2) = 0.72). These results demonstrate that models based on connectome disruption metrics were more accurate than ones based on lesion volume and that increasing anatomical specificity of disconnection metrics does not always increase model accuracy, likely due to statistical adjustments for concomitant increases in data dimensionality. This work establishes that the NeMo Tool's measures of baseline connectome disruption, acquired using only routinely collected MRI scans, can predict 6-month post-stroke outcomes in various functional domains including cognition, motor function and daily activities. Hum Brain Mapp, 2016. © 2016 Wiley Periodicals, Inc.

Background and Purpose— Although chronic hypertension is a well-established risk factor for stroke, little is known about stroke risk after hypertensive encephalopathy (HE), when neurologic sequelae of hypertension become evident. Therefore, we evaluated the risk of stroke after a diagnosis of HE. Methods— We identified all patients discharged from California, New York, and Florida emergency departments and acute care hospitals between 2005 and 2012 with a primary International Classification of Diseases , Ninth Edition, Clinical Modification discharge diagnosis of HE (437.2). Patients discharged with a primary diagnosis of seizure (345.x) served as negative controls, whereas patients with a primary diagnosis of transient ischemic attack (435.x) were positive controls. Our primary outcome was the composite of subsequent ischemic stroke or intracerebral hemorrhage. Kaplan–Meier survival statistics were used to calculate cumulative outcome rates, and Cox proportional hazard analysis was used to examine the association between index disease types and outcomes while adjusting for vascular risk factors. Results— We identified 8233 patients with HE, 191 091 with seizure, and 308 680 with transient ischemic attack. The 1-year cumulative rate of ischemic stroke or intracerebral hemorrhage after HE was 4.90% (95% confidence interval [CI], 4.45–5.40) when compared with 0.92% (95% CI, 0.88–0.97) after seizure and 4.49% (95% CI, 4.42–4.57) after transient ischemic attack. The risk of intracerebral hemorrhage was significantly elevated in those with HE (hazard ratio, 2.0; 95% CI, 1.7–2.5) but not in those with transient ischemic attack (hazard ratio, 1.0; 95% CI, 0.9–1.1), when compared with seizure patients. Conclusions— Patients discharged with a diagnosis of HE face a high risk of future cerebrovascular events, particularly intracerebral hemorrhage.

To evaluate the cost-effectiveness of a decision-making rule based on the magnetic resonance (MR) imaging assessment of intraplaque hemorrhage (IPH) in patients with asymptomatic carotid artery stenosis.Two competing stroke prevention strategies were compared: (a) an intensive medical therapy-based management strategy versus (b) an imaging-based strategy in which the subset of patients with asymptomatic carotid artery stenosis with IPH on MR images would undergo immediate carotid endarterectomy in addition to ongoing intensive medical therapy. Patients in the medical therapy-only group could undergo carotid endarterectomy only with substantial carotid artery stenosis disease progression. Lifetime quality-adjusted life years (QALYs) and costs were modeled for patients with asymptomatic carotid artery stenosis with 70%-89% and 50%-69% carotid artery stenosis at presentation. Risks of stroke and complications from carotid endarterectomy, costs, and quality of life values were estimated from published sources.The medical therapy-based strategy had a lower life expectancy (12.65 years vs 12.95 years), lower lifetime QALYs (9.96 years vs 10.05 years), and lower lifetime costs ($13 699 vs $15 297) when compared with the MR imaging IPH-based strategy. The incremental cost-effectiveness ratio (ICER) for the MR imaging IPH strategy compared with the medical therapy-based strategy was $16 000 per QALY by using a base-case 70-year-old patient. When using starting patient ages of 60 and 80 years, the ICERs for the MR imaging IPH strategy were $3100 per QALY and $73 000 per QALY, respectively. The ICERs for the MR imaging IPH strategy were slightly higher at all ages for 50%-69% stenosis but remained below a willingness-to-pay threshold of $100 000 per QALY for starting ages of 60 and 70 years.MR imaging IPH can be used as a cost-effective tool to identify patients with asymptomatic carotid artery stenosis most likely to benefit from carotid endarterectomy.

Background and Purpose— It is uncertain whether previous ischemic stroke within 3 months of receiving intravenous thrombolysis (tPA [tissue-type plasminogen activator]) for acute ischemic stroke (AIS) is associated with an increased risk of adverse outcomes. Methods— Using administrative claims data, we identified adults with AIS who received intravenous tPA at California, New York, and Florida hospitals from 2005 to 2013. Our primary outcome was intracerebral hemorrhage, and our secondary outcomes were unfavorable discharge disposition and inpatient mortality. We used logistic regression to compare rates of outcomes in patients with and without previous ischemic stroke within 3 months of intravenous tPA for AIS. Results— We identified 36 599 AIS patients treated with intravenous tPA, of whom 568 (1.6%) had a previous ischemic stroke in the past 3 months. Of all patients who received intravenous tPA, the rate of intracerebral hemorrhage was 4.9% (95% confidence interval [CI], 4.7%–5.1%), and death occurred in 10.7% (95% CI, 10.4%–11.0%). After adjusting for demographics, vascular risk factors, and the Elixhauser Comorbidity Index, previous ischemic stroke within 3 months of thrombolysis for AIS was not associated with an increased risk of intracerebral hemorrhage (odds ratio, 0.9; 95% CI, 0.6–1.4; P =0.62), but was associated with an increased risk of death (odds ratio, 1.5; 95% CI, 1.2–1.9; P =0.001) and unfavorable discharge disposition (odds ratio, 1.3; 95% CI, 1.0–1.7; P =0.04). Conclusions— Among patients who receive intravenous tPA for AIS, recent ischemic stroke is not associated with an increased risk of intracerebral hemorrhage but is associated with a higher risk of death and unfavorable discharge disposition.

e13537 Background: Patients with cancer have an increased risk of arterial thromboembolic events (ATE). Clinical characteristics such as medical comorbidities, cancer type, cancer stage and a history of smoking are established risk factors for ATE, but scant data exist about the effect of cancer-specific genomic alterations. We aimed to determine whether individual tumor mutations influence ATE risk. Methods: We performed a retrospective cohort study using tumor mutational data from adults with solid cancers who had MSK-IMPACT testing at Memorial Sloan Kettering Cancer Center between 2014 and 2016. MSK-IMPACT is an FDA-authorized DNA sequencing panel targeting 341+ oncogenes and tumor suppressor genes identifying mutations, copy number alterations, and gene fusions in solid malignancies. The primary ATE outcome was defined as ischemic stroke, myocardial infarction or coronary revascularization and detected by systematic electronic health record assessments. Patients were followed up to one year from the date of tissue-matched blood control sampling to the first ATE or death. We used Cox proportional hazards regression adjusting for age, cancer type, cytotoxic chemotherapy treatment (time-dependent) and tobacco use to determine hazard ratios (HR) of individual genes for ATE risk. We adjusted for multiple comparisons using the Benjamini-Hochberg method. Results: Among 11,317 patients, mean age was 59 years (SD = 14 years) and 55% were women. The most frequent cancers were lung (16%), breast (15%), and colorectal (10%), and 73% were metastatic. During a median follow-up of 253 days, 151 patients had an ATE (1.3%). In multivariable analysis, genomic alterations in KRAS (HR, 2.11; CI, 1.41-3.16), STK11 (HR, 2.62; 95% CI, 1.49-4.59), and ROS1 (HR, 5.3; 95% CI, 1.93-14.58) were independently associated with an increased risk of ATE. Presence of clonal hematopoiesis was not found to be associated with an increased risk of ATE in this cohort (HR, 0.96; 95% CI, 0.63-1.47). Conclusions: In a large genomic tumor-profiling registry of patients with solid cancers, alterations in KRAS, STK11, and ROS1 were associated with an increased risk of ATE independent of cancer type. [Table: see text]

Background and Purpose— It is unclear whether atrial fibrillation/flutter (AF) newly diagnosed after ischemic stroke represents a preexisting risk factor that led to stroke, an arrhythmia triggered by poststroke autonomic dysfunction, or an incidental finding. Methods— We compared AF incidence after hospitalizations for ischemic stroke, hemorrhagic stroke, and nonstroke conditions using inpatient and outpatient claims between 2008 and 2015 from a nationally representative 5% sample of Medicare beneficiaries. We used validated International Classification of Diseases, Ninth Revision, Clinical Modification ( ICD-9-CM ) codes to identify AF-free patients hospitalized with ischemic or hemorrhagic stroke and matched them in a 1:1 ratio by age, sex, race, calendar year, vascular risk factors, and Charlson comorbidities. We then matched the combined stroke cohort in a 1:1 ratio to patients hospitalized for nonstroke diagnoses. We used survival statistics and Cox regression to compare postdischarge AF incidence among groups. Results— We matched 2580 patients with ischemic stroke, 2580 with hemorrhagic stroke, and 5160 patients with other conditions. The annual postdischarge AF incidence was 3.4% (95% CI, 3.1%–3.7%) after ischemic stroke, 2.2% (95% CI, 1.9%–2.4%) after hemorrhagic stroke, and 2.9% (95% CI, 2.6%–3.1%) after nonstroke hospitalization. Ischemic stroke was associated with a somewhat higher risk of AF than hemorrhagic stroke (hazard ratio, 1.5; 95% CI, 1.3–1.8) or nonstroke conditions (hazard ratio, 1.2; 95% CI, 1.1–1.3). The latter association attenuated in sensitivity analyses limiting the outcome to AF diagnoses made by cardiologists (hazard ratio, 1.1; 95% CI, 0.8–1.5) or limiting the outcome to a minimum of 2 AF claims on separate dates (hazard ratio, 1.2; 95% CI, 1.0–1.5; P =0.09). Conclusions— New diagnoses of AF were more common after hospitalization for ischemic stroke than after hospitalization for hemorrhagic stroke or nonstroke conditions, but all hospitalized patients had a substantial incidence of new AF diagnoses after discharge and differences were attenuated when using more stringent definitions.

Background and Purpose— Case reports suggest that unruptured intracranial aneurysms may serve as a nidus for thrombus formation and downstream embolic stroke. However, few data exist to support an association between unruptured aneurysms and ischemic stroke. Methods— We conducted a within-subjects case-control study of acute ischemic stroke patients prospectively enrolled in the Cornell Acute Stroke Academic Registry who had magnetic resonance imaging of the brain and arterial imaging of the head within 14 days of admission. Reviewers blinded to the study hypothesis ascertained the presence of aneurysms from the neuroradiologist’s clinical report of the arterial imaging findings. McNemar test for paired data was used to compare the prevalence of unruptured aneurysms ipsilateral versus contralateral to the side of anterior circulation infarcts. Aneurysms of the anterior communicating artery or in the posterior circulation were not counted in the analysis. Results— Among 2116 patients registered in the Cornell Acute Stroke Academic Registry during 2011 to 2016, 1541 met our inclusion criteria, of whom 176 (11.4%; 95% CI, 9.8–13.0%) had an intracranial aneurysm. The prevalence of aneurysms did not differ on the side ipsilateral versus contralateral to the infarction (risk ratio [RR], 1.2; 95% CI, 0.9–1.5). There was no significant association between aneurysms and ipsilateral stroke in secondary analyses of the 1244 patients with stroke in a single anterior circulation territory (RR, 1.2; 95% CI, 0.8–1.9), the 619 patients with cryptogenic stroke (RR, 1.4; 95% CI, 0.9–2.0), or the 485 patients with cryptogenic stroke in a single anterior circulation territory (RR, 1.7; 95% CI, 0.8–3.3). Results were unchanged when counting only aneurysms >3 mm (RR, 1.2; 95% CI, 0.8–1.9) or 5 mm in diameter (RR, 1.2; 95% CI, 0.9–1.5). Conclusions— Contrary to our hypothesis, we found no significant association between unruptured intracranial aneurysms and ipsilateral ischemic stroke.

Introduction: Atrial fibrillation (AF) is often newly diagnosed during heart-rhythm monitoring after ischemic stroke. It is unclear whether this represents pre-existing AF that led to stroke, AF that was triggered by stroke, or AF that would also be seen in stroke-free patients with comparable vascular risk factors. Methods: We compared AF incidence after hospitalization for ischemic stroke, hemorrhagic stroke, and non-stroke conditions. We used inpatient and outpatient claims data from 2008-2015 from a nationally representative 5% sample of Medicare beneficiaries. We used validated ICD-9-CM codes for AF and stroke to identify patients hospitalized with a first-recorded ischemic or hemorrhagic stroke and no documented AF, and matched them in a 1:1 ratio by age, sex, race, calendar year, vascular risk factors, and Charlson comorbidities. We then matched these stroke patients in a 1:1 ratio to patients hospitalized for non-stroke diagnoses. We used survival statistics and Cox regression to compare post-discharge AF incidence among the three matched groups. Results: We matched 2,650 patients with ischemic stroke, 2,650 with hemorrhagic stroke, and 5,300 controls. The post-discharge incidence of AF was 3.4% (95% CI, 3.1-3.7%) per year after ischemic stroke, 2.2% (95% CI, 1.9-2.5%) per year after hemorrhagic stroke, and 2.6% (2.4-2.8%) per year after non-stroke hospitalization. Compared to non-stroke controls, hemorrhagic stroke was associated with a similar risk of AF (HR, 0.9; 95% CI, 0.8-1.0; P = 0.13) and ischemic stroke was associated with a higher risk of AF (HR, 1.4; 95% CI, 1.2-1.6). These findings were unchanged in sensitivity analyses censoring at the time of post-discharge heart-rhythm monitoring or limiting the outcome to AF diagnoses made by a cardiologist. Conclusions: AF was diagnosed more often after hospitalization for ischemic stroke than hemorrhagic stroke or non-stroke conditions.

Introduction: Given recent advances in diagnostic and therapeutic tools, delivery of stroke care has become more complex. We sought to investigate what proportion of patients with stroke are evaluated by neurologists, and specifically by vascular neurologists. Methods: Using 2008-2015 claims data from a 5% nationally representative sample of Medicare beneficiaries, we identified all patients >65 years of age who were hospitalized for ischemic stroke, as defined by previously validated ICD-9-CM codes. Our primary outcome was the proportion of patients evaluated during the stroke hospitalization or within 90 days of discharge by a neurologist, as determined from evaluation and management CPT codes and Medicare provider specialty codes. To ascertain which of these neurologists were vascular neurologists, we used a Python script and National Provider Identifier numbers to merge in publicly available data from the American Board of Psychiatry and Neurology on all board-certified vascular neurologists in the U.S. As a comparison, we used previously validated diagnosis codes to identify patients hospitalized with acute myocardial infarction (MI) and determined the proportion seen by a cardiologist during the hospitalization or within 90 days of discharge. Statistical analysis involved descriptive statistics with exact confidence intervals (CI)s and the chi-square test. Results: Among 66,989 patients with ischemic stroke, 49,335 (73.7%; 95% CI, 73.1-74.0%) were evaluated by a neurologist. A board-certified vascular neurologist evaluated 11,001 patients, equating to 16.4% (95% CI, 16.1-16.7%) of all stroke patients and 22.3% (95% CI, 21.9-22.7%) of stroke patients seen by a neurologist. In comparison, a cardiologist evaluated 53,481 of 61,232 patients with acute MI (87.3%; 95% CI, 87.1-87.6%), a proportion significantly higher than the proportion of stroke patients seen by a neurologist ( P Conclusions: In a nationally representative cohort of Medicare beneficiaries, we found that approximately 75% of patients with ischemic stroke were evaluated by a neurologist, a proportion significantly lower than the comparable metric for acute MI. Furthermore, about one of every six stroke patients was evaluated by a vascular neurologist.

Background: It is uncertain whether history of prior ischemic stroke is associated with an increased risk of adverse outcomes in diabetic patients treated with intravenous tissue plasminogen activator (IV-tPA) for acute ischemic stroke. Methods: Using administrative claims data, we identified all diabetic adults with acute ischemic stroke who received IV-tPA at California, New York, or Florida hospitals between 2005-2013. Our exposure of interest was prior ischemic stroke. Our primary outcome was intracerebral hemorrhage (ICH) and our secondary outcomes were inpatient mortality and unfavorable discharge disposition (skilled nursing facility, subacute care center, chronic rehabilitation center, hospice, or death). We used multivariable logistic regression to compare the rate of outcomes in diabetic patients with and without a history of prior ischemic stroke. Results: We identified 12,786 diabetic patients (mean age 70.7 [±13.1] years) who received IV-tPA for AIS, of whom 1,112 (8.6%) had a history of prior ischemic stroke. Among all patients, 699 (5.5%; 95% confidence interval [CI] 5.1-5.9%) developed ICH and in-hospital death occurred in 11.9% (95% CI, 11.3-12.5%). After adjusting for demographics, stroke risk factors, and the Elixhauser comorbidity index, history of prior ischemic stroke was not associated with an increased risk of ICH (OR, 0.8; 95% CI, 0.6-1.1, P = 0.26), inpatient mortality (OR, 0.9; 95% CI, 0.7-1.1, P =0.22), or unfavorable discharge disposition (OR, 1.1; 95% CI, 0.9-1.2, P= 0.57). Conclusion: Among diabetic patients who received IV-tPA for acute ischemic stroke at three large states in the U.S., history of prior ischemic stroke was not associated with an increased risk of ICH, inpatient death, or unfavorable discharge disposition. Further evaluation is necessary to assess whether administration of IV-tPA within the extended 3-4.5 hour window for acute ischemic stroke is safe for diabetic patients with prior stroke.