Short-Term Risk of Ischemic Stroke After Detection of Left Ventricular Thrombus on Cardiac Magnetic Resonance Imaging.

BACKGROUND: The short-term risk of ischemic stroke in patients with left ventricular (LV) thrombus identified via delayed-enhancement cardiac magnetic resonance (DE-CMR) imaging is uncertain. METHODS: We performed a retrospective cohort study of patients who underwent DE-CMR for evaluation of LV systolic dysfunction at NewYork-Presbyterian Hospital/Weill Cornell between 2007 and 2016. We identified all hospitalized patients who had DE-CMR evidence of LV thrombus, and as controls, all hospitalized patients who had no DE-CMR evidence of LV thrombus; 2 control patients were randomly selected for each patient with LV thrombus. Our primary outcome was ischemic stroke prior to hospital discharge. Additionally, we compared the risk of stroke among patients with: (1) no LV thrombus, (2) LV thrombus by DE-CMR but not by echocardiography, and (3) LV thrombus by both DE-CMR and echocardiography. RESULTS: We identified 33 patients with LV thrombus and 66 patients without LV thrombus on DE-CMR. Of the 33 patients with LV thrombus on DE-CMR, 13 had echocardiographic evidence of thrombus. Ischemic stroke occurred in 3 of 33 (9.1%; 95% CI, 1.9%-24.3%) patients with LV thrombus on DE-CMR. Ischemic stroke occurred in 0 of 66 (0%; 95% CI, 0%-5.4%) patients without LV thrombus on DE-CMR, 1 of 20 (5.0%; 95% CI, .1%-24.9%) patients with thrombus on DE-CMR but not echocardiogram, and 2 of 13 (15.4%; 95% CI, 1.9%-45.4%) patients with thrombus on both DE-CMR and echocardiogram (P value for comparison among groups, .02). CONCLUSIONS: We found a 9% short-term risk of ischemic stroke in patients with LV thrombus detected on DE-CMR.

Clinical Impact of Thrombophilia Screening in Young Adults with Ischemic Stroke.

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.

Temporal Trends in the Use of Acute Recanalization Therapies for Ischemic Stroke in Patients with Cancer.

OBJECTIVE: We sought to characterize the US nationwide temporal trends in recanalization therapy utilization for ischemic stroke among patients with and without cancer. METHODS: We identified all acute ischemic stroke (AIS) hospitalizations in the National Inpatient Sample from January 1, 1998 to 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 (EVT). RESULTS: Among 9,508,804 AIS hospitalizations, 503,510 (5.3%) involved cancer patients. Intravenous thrombolysis use among ischemic stroke patients with cancer increased from .01% (95% confidence interval [CI], .00%-.02%) in 1998 to 4.91% (95% CI, 4.33%-5.48%) in 2015, whereas intravenous thrombolysis use among ischemic stroke patients without cancer increased from .02% (95% CI, .01%-.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). EVT use among ischemic stroke patients with cancer increased from .05% (95% CI, .02%-.07%) in 2006 to 1.90% (95% CI, 1.49%-2.31%) in 2015, whereas EVT use among ischemic stroke patients without cancer increased from .09% (95% CI, .00%-.18%) in 2006 to 1.88% (95% CI, 1.68%-2.09%) in 2015. CONCLUSIONS: Among 9.5 million AIS 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. EVT utilization was similar between cancer and non-cancer AIS patients.

Misdiagnosis of Cerebral Vein Thrombosis in the Emergency Department.

BACKGROUND AND PURPOSE: Rates of cerebral venous thrombosis (CVT) misdiagnosis in the emergency department and outcomes associated with misdiagnosis have been underexplored. METHODS: Using administrative data, we identified adults with CVT at New York, California, and Florida hospitals from 2005 to 2013. Our primary outcome was probable misdiagnosis of CVT, defined as a treat-and-release emergency department visit for headache or seizure within 14 days before CVT. In addition, logistic regression was used to compare rates of clinical outcomes in patients with and without probable CVT misdiagnosis. We performed a confirmatory study at 2 tertiary care centers. RESULTS: We identified 5966 patients with CVT in whom 216 (3.6%; 95% confidence interval [CI], 1.1%-4.1%) had a probable misdiagnosis of CVT. After adjusting for demographics, risk factors for CVT, and the Elixhauser comorbidity index, probable CVT misdiagnosis was not associated with in-hospital mortality (odds ratio, 0.14; 95% CI, 0.02-1.05), intracerebral hemorrhage (odds ratio, 0.97; 95% CI, 0.57-1.65), or unfavorable discharge disposition (odds ratio, 0.90; 95% CI, 0.61-1.32); a longer length of hospital stay was seen among misdiagnosed patients with CVT (odds ratio, 1.62; 95% CI, 1.04-2.50). In our confirmatory cohort, probable CVT misdiagnosis occurred in 8 of 134 patients with CVT (6.0%; 95% CI, 2.6%-11.4%). CONCLUSIONS: In a large, heterogeneous multistate cohort, probable misdiagnosis of CVT occurred in 1 of 30 patients but was not associated with the adverse clinical outcomes included in our study.

Association Between Unruptured Intracranial Aneurysms and Downstream Stroke.

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.

Modeling the Impact of Interhospital Transfer Network Design on Stroke Outcomes in a Large City.

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.

Population-Based Assessment of the Long-Term Risk of Seizures in Survivors of Stroke.

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 <65 years of age (IRR, 12.0; 95% CI, 11.9-12.2) than in patients ≥65 years of age (IRR, 5.5; 95% CI, 5.4-5.5) and in the multistate analysis, the association between stroke and seizure was stronger among nonwhite patients (IRR, 11.0; 95% CI, 10.8-11.2) than among white patients (IRR, 7.3; 95% CI, 7.2-7.4). Risks were especially elevated after intracerebral hemorrhage (IRR, 13.3; 95% CI, 13.0-13.6) and subarachnoid hemorrhage (IRR, 13.2; 95% CI, 12.8-13.7). Our study of Medicare beneficiaries confirmed these findings. 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.

Risk of Ischemic Stroke After Perioperative Atrial Fibrillation in Total Knee and Hip Arthroplasty Patients.

BACKGROUND: To determine if new-onset perioperative atrial fibrillation during arthroplasty represents a benign response to intraoperative cardiac stress or is a risk factor for stroke, we evaluated the subsequent risk of ischemic stroke in patients with new-onset atrial fibrillation occurring during primary total knee arthroplasty (TKA) and total hip arthroplasty (THA). METHODS: Discharge data of all adult patients undergoing primary TKA or THA from 1997 to 2013 were queried via the New York Statewide Planning and Research Cooperative System database to find patients with new-onset perioperative atrial fibrillation. These patients were then followed up over time to determine their risk of ischemic stroke. RESULTS: Of the 312,636 TKA and 215,610 THA unique patient admissions, 3646 (0.7%) had a diagnosis of new-onset perioperative atrial fibrillation. The cohort of patients with this finding was 58.9% female with an average age of 73.6 years and higher prevalence of vascular risk factors. Adjusting for validated stroke risk factors, the risk of ischemic stroke within 1 year after THA or TKA in patients with new-onset atrial fibrillation was 2.7 times higher than in those without a history of atrial fibrillation (odds ratio: 2.7, 95% confidence interval: 1.5-4.8). Hospital length of stay and charges for patients with new-onset atrial fibrillation were also greater than patients with either a prior diagnosis or no diagnosis of atrial fibrillation. CONCLUSION: New-onset atrial fibrillation during TKA and THA may indicate risk of ischemic stroke following surgery that should warrant medical follow-up and may increase hospital length of stay and charges.

Left Atrial Enlargement and Anticoagulation Status in Patients with Acute Ischemic Stroke and Atrial Fibrillation.

BACKGROUND: Despite anticoagulation therapy, ischemic stroke risk in atrial fibrillation (AF) remains substantial. We hypothesize that left atrial enlargement (LAE) is more prevalent in AF patients admitted with ischemic stroke who are therapeutic, as opposed to nontherapeutic, on anticoagulation. METHODS: We included consecutive patients with AF admitted with ischemic stroke between April 1, 2015, and December 31, 2016. Patients were divided into two groups based on whether they were therapeutic (warfarin with an international normalized ratio ≥ 2.0 or non-vitamin K oral anticoagulant with uninterrupted use in the prior 2 weeks) versus nontherapeutic on anticoagulation. Univariable and multivariable models were used to estimate associations between therapeutic anticoagulation and clinical factors, including CHADS2 score and LAE (none/mild versus moderate/severe). RESULTS: We identified 225 patients during the study period; 52 (23.1%) were therapeutic on anticoagulation. Patients therapeutic on anticoagulation were more likely to have a larger left atrial diameter in millimeters (45.6 ± 9.2 versus 42.3 ± 8.6, P = .032) and a higher CHADS2 score (2.9 ± 1.1 versus 2.4 ± 1.1, P = .03). After adjusting for the CHADS2 score, patients who had a stroke despite therapeutic anticoagulation were more likely to have moderate to severe LAE (odds ratio, 2.05; 95% confidence interval, 1.01-4.16). CONCLUSION: LAE is associated with anticoagulation failure in AF patients admitted with an ischemic stroke. This provides indirect evidence that LAE may portend failure of anticoagulation therapy in patients with AF; further studies are needed to delineate the significance of this association and improve stroke prevention strategies.

Left Atrial Appendage Morphology and Embolic Stroke of Undetermined Source: A Cross-Sectional Multicenter Pilot Study.

BACKGROUND: The left atrial appendage (LAA) is the main source of thrombus in atrial fibrillation, and there is an association between non-chicken wing (NCW) LAA morphology and stroke. We hypothesized that the prevalence of NCW LAA morphology would be higher among patients with cardioembolic (CE) stroke and embolic stroke of undetermined source (ESUS) than among those with noncardioembolic stroke (NCS). METHODS: This multicenter retrospective pilot study included consecutive patients with ischemic stroke from 3 comprehensive stroke centers who previously underwent a qualifying chest computed tomography (CT) to assess LAA morphology. Patients underwent inpatient diagnostic evaluation for ischemic stroke, and stroke subtype was determined based on ESUS criteria. LAA morphology was determined using clinically performed contrast enhanced thin-slice chest CT by investigators blinded to stroke subtype. The primary predictor was NCW LAA morphology and the outcome was stroke subtype (CE, ESUS, NCS). RESULTS: We identified 172 patients with ischemic stroke who had a clinical chest CT performed. Mean age was 70.1 ± 14.3 years and 51.7% were male. Compared with patients with NCS, the prevalence of NCW LAA morphology was higher in patients with CE stroke (58.7% versus 46.3%, P = .1) and ESUS (58.8% versus 46.3%, P = .2), but this difference did not achieve statistical significance. CONCLUSION: The prevalence of NCW LAA morphology may be similar in patients with ESUS and CE, and may be higher than that in those with NCS. Larger studies are needed to confirm these associations.

Timing of Incident Stroke Risk After Cervical Artery Dissection Presenting Without Ischemia.

BACKGROUND AND PURPOSE: Cervical artery dissection is a common cause of stroke in young people. The temporal profile of stroke risk after cervical artery dissection presenting without ischemia remains uncertain. METHODS: We performed a crossover cohort study using administrative claims data on all emergency department visits and acute care hospitalizations from 2005 to 2011 in CA, 2006 to 2013 in NY, and 2005 to 2013 in FL. Using previously validated International Classification of Diseases, Ninth Revision, Clinical Modification codes, we identified patients with a cervical artery dissection and no previous or concurrent stroke or transient ischemic attack diagnosis. We compared the risk of stroke in successive 2-week periods during the 12 weeks after dissection versus the corresponding 2-week period 1 year later. Absolute risk increases were calculated using McNemar test for matched data. In a sensitivity analysis, we limited our population to patients presenting with typical symptoms of cervical artery dissection. RESULTS: We identified 2791 patients with dissection without ischemia. The absolute increase in stroke risk was 1.25% (95% confidence interval, 0.84-1.67%) in the first 2 weeks after dissection compared with the same time period 1 year later. The absolute risk increase was 0.18% (95% confidence interval, 0.02-0.34%) during weeks 3 to 4 and was no longer significant during the remainder of the 12-week postdissection period. Our findings were similar in a sensitivity analysis identifying patients who presented with typical symptoms of acute dissection. CONCLUSIONS: The risk of stroke after cervical artery dissection unaccompanied by ischemia at time of diagnosis seems to be limited to the first 2 weeks.

Timing of Carotid Revascularization Procedures After Ischemic Stroke.

BACKGROUND AND PURPOSE: In 2006, the American Heart Association recommended that carotid revascularization generally occurs within 2 weeks of stroke based on data from 2 trials of carotid endarterectomy (CEA). We aimed to determine whether the time between stroke and CEA or carotid artery stenting (CAS) has decreased and whether the proportion of procedures occurring within 14 days has increased. METHODS: Using validated International Classification of Diseases, Ninth Revision, Clinical Modification codes and administrative claims data from nonfederal hospitals in CA, FL, and NY, we identified patients with ischemic stroke who underwent CEA or CAS within 90 days of an ischemic stroke from 2005 to 2013. Our outcomes were the number of days between stroke and CEA/CAS and the proportion of patients undergoing CEA/CAS within the recommended 14-day period. We assessed temporal trends using nonparametric correlation, the χ2 test for trend, and logistic regression. RESULTS: We identified 16 298 patients with ischemic stroke who underwent CEA/CAS within 90 days. The time from stroke to CEA/CAS decreased from 25 days (interquartile range, 5-48 days) in 2005 to 6 days (interquartile range, 3-17 days) in 2013 (P<0.001). The proportion of patients who underwent CEA/CAS within 14 days of stroke increased from 40% (95% confidence interval, 37%-43%) in 2005 to 73% (95% confidence interval, 71%-76%) in 2013 (P<0.001). These temporal trends remained significant after adjustment for patient demographics and comorbidities. CONCLUSIONS: Since 2005, revascularization for symptomatic carotid disease has been occurring progressively sooner after ischemic stroke.

Safety Outcomes After Percutaneous Transcatheter Closure of Patent Foramen Ovale.

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.

Safety Outcomes After Thrombolysis for Acute Ischemic Stroke in Patients With Recent Stroke.

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.

Risk of Pulmonary Embolism After Cerebral Venous Thrombosis.

BACKGROUND AND PURPOSE: Cerebral vein thrombosis (CVT) is a type of venous thromboembolism. Whether the risk of pulmonary embolism (PE) after CVT is similar to the risk after deep venous thrombosis (DVT) is unknown. METHODS: We performed a retrospective cohort study using administrative data from all emergency department visits and hospitalizations in California, New York, and Florida from 2005 to 2013. We identified patients with CVT or DVT and the outcome of PE using previously validated International Classification of Diseases, Ninth Revision, Clinical Modification codes. Kaplan-Meier survival statistics and Cox proportional hazards models were used to compare the risk of PE after CVT versus PE after DVT. RESULTS: We identified 4754 patients with CVT and 241 276 with DVT. During a mean follow-up of 3.4 (±2.4) years, 138 patients with CVT and 23 063 with DVT developed PE. CVT patients were younger, more often female, and had fewer risk factors for thromboembolism than patients with DVT. During the index hospitalization, the rate of PE was 1.4% (95% confidence interval [CI], 1.1%-1.8%) in patients with CVT and 6.6% (95% CI, 6.5%-6.7%) in patients with DVT. By 5 years, the cumulative rate of PE after CVT was 3.4% (95% CI, 2.9%-4.0%) compared with 10.9% (95% CI, 10.8%-11.0%; P<0.001) after DVT. CVT was associated with a lower adjusted hazard of PE than DVT (hazard ratio, 0.26; 95% CI, 0.22-0.31). CONCLUSION: The risk of PE after CVT was significantly lower than the risk after DVT. Among patients with CVT, the greatest risk for PE was during the index hospitalization.

Neutrophil-Lymphocyte Ratio and Perihematomal Edema Growth in Intracerebral Hemorrhage.

BACKGROUND AND PURPOSE: Although preclinical studies have shown inflammation to mediate perihematomal edema (PHE) after intracerebral hemorrhage, clinical data are lacking. Leukocyte count, often used to gauge serum inflammation, has been correlated with poor outcome but its relationship with PHE remains unknown. Our aim was to test the hypothesis that leukocyte count is associated with PHE growth. METHODS: We included patients with intracerebral hemorrhage admitted to a tertiary-care stroke center between 2011 and 2015. The primary outcome was absolute PHE growth during 24 hours, calculated using semiautomated planimetry. Linear regression models were constructed to study the relationship between absolute and differential leukocyte counts (monocyte count and neutrophil-lymphocyte ratio) and 24-hour PHE growth. RESULTS: A total of 153 patients were included. Median hematoma and PHE volumes at baseline were 14.4 (interquartile range, 6.3-36.3) and 14.0 (interquartile range, 5.9-27.8), respectively. In linear regression analysis adjusted for demographics and intracerebral hemorrhage characteristics, absolute leukocyte count was not associated with PHE growth (ß, 0.07; standard error, 0.15; P=0.09). In secondary analyses, neutrophil-lymphocyte ratio was correlated with PHE growth (ß, 0.22; standard error, 0.08; P=0.005). CONCLUSIONS: Higher neutrophil-lymphocyte ratio is independently associated with PHE growth. This suggests that PHE growth can be predicted using differential leukocyte counts on admission.

Rates of Spinal Cord Infarction After Repair of Aortic Aneurysm or Dissection.

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<0.001) of unruptured aneurysm. 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.

The Association between Carotid Artery Atherosclerosis and Silent Brain Infarction: A Systematic Review and Meta-analysis.

BACKGROUND: Carotid atherosclerosis is responsible for ~20% of ischemic strokes, but it is unclear whether carotid disease is associated with the presence of downstream silent brain infarction (SBI). We performed a systematic review and meta-analysis to study the relationship between SBI and 2 separate manifestations of carotid atherosclerosis, carotid intima-media thickening (IMT) and luminal stenosis. METHODS: Ovid MEDLINE, Ovid Embase, and the Cochrane Library Database were searched with an additional search of references and citing articles of target studies. Articles were included if they reported an association between carotid IMT or stenosis and magnetic resonance imaging-defined SBI, excluding SBIs found after carotid intervention. RESULTS: We pooled 7 studies of carotid IMT reporting on 1469 subjects with SBI and 5102 subjects without SBI. Subjects with SBI had a larger mean IMT than subjects without SBI (pooled standardized mean difference, .37; 95% confidence interval [CI], .23-.51; P < .0001). We pooled 11 studies of carotid stenosis reporting on 12,347 subjects (2110 subjects with carotid stenosis and 10,237 subjects without carotid stenosis). We found a higher prevalence of SBI among subjects with carotid stenosis (30.4% versus 17.4%). Our pooled random-effects analysis showed a significant positive relationship between carotid stenosis and SBI (odds ratio, 2.78; 95% CI, 2.19-3.52; P < .0001). CONCLUSIONS: Two forms of atherosclerotic disease, carotid IMT and stenosis, are both significantly associated with SBI. This review highlights a lack of consistent definitions for carotid disease measures and little evidence evaluating SBI prevalence downstream from carotid stenosis.

Cryptogenic Stroke and Nonstenosing Intracranial Calcified Atherosclerosis.

OBJECTIVE: Because some cryptogenic strokes may result from large-artery atherosclerosis that goes unrecognized as it causes <50% 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. METHODS: 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. RESULTS: 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. CONCLUSION: In patients with strokes of undetermined etiology, the burden of calcified intracranial large-artery plaque was associated with downstream cerebral infarction.

Biomarkers of Atrial Cardiopathy and Atrial Fibrillation Detection on Mobile Outpatient Continuous Telemetry After Embolic Stroke of Undetermined Source.

BACKGROUND: Biomarkers of atrial dysfunction or "cardiopathy" are associated with embolic stroke risk. However, it is unclear if this risk is mediated by undiagnosed paroxysmal atrial fibrillation or flutter (AF). We aim to determine whether atrial cardiopathy biomarkers predict AF on continuous heart-rhythm monitoring after embolic stroke of undetermined source (ESUS). METHODS: This was a single-center retrospective study including all patients with ESUS undergoing 30 days of ambulatory heart-rhythm monitoring to look for AF between January 1, 2013 and December 31, 2015. We reviewed medical records for clinical, radiographic, and cardiac variables. The primary outcome was a new diagnosis of AF detected during heart-rhythm monitoring. The primary predictors were atrial biomarkers: left atrial diameter on echocardiography, P-wave terminal force in electrocardiogram (ECG) lead V1, and P wave - R wave (PR) interval on ECG. A multiple logistic regression model was used to assess the relationship between atrial biomarkers and AF detection. RESULTS: Among 196 eligible patients, 23 (11.7%) were diagnosed with AF. In unadjusted analyses, patients with AF were older (72.4 years versus 61.4 years, P < .001) and had larger left atrial diameter (39.2 mm versus 35.7 mm, P = .03). In a multivariable model, the only predictor of AF was age ≥ 60 years (odds ratio, 3.0; 95% CI, 1.06-8.5; P = .04). CONCLUSION: Atrial biomarkers were weakly associated with AF after ESUS. This suggests that previously reported associations between these markers and stroke may reflect independent cardiac pathways leading to stroke. Prospective studies are needed to investigate these mechanisms.