Background and Purpose- There has been a recent sharp rise in opioid-related deaths in the United States. Intravenous opioid use can lead to infective endocarditis (IE) which can result in stroke. ...There are scant data on recent trends in this neurological complication of opioid abuse. We hypothesized that increasing opioid abuse has led to a higher incidence of stroke associated with IE and opioid use. Methods- We used the 1993 to 2015 releases of the National Inpatient Sample and validated International Classification of Diseases, Ninth Revision, Clinical Modification codes ( ICD-9-CM) to identify hospitalizations with the combination of opioid abuse, IE, and stroke (defined as ischemic stroke, intracerebral hemorrhage, or subarachnoid hemorrhage). Survey weights provided by the National Inpatient Sample were used to calculate nationally representative estimates and population estimates from the United States. Census data were used to calculate annual hospitalization rates per 10 million person-years. Joinpoint regression was used to assess trends. Results- From 1993 through 2015, there were 5283 hospitalizations with stroke associated with IE and opioid use. Across this period, the rate of such hospitalizations increased from 2.4 (95% CI, 0.5-4.3) to 18.8 (95% CI, 14.4-23.3) per 10 million US residents. Joinpoint regression detected 2 segments: no significant change in the hospitalization rate was apparent from 1993 to 2008 (annual percentage change, 1.9%; 95% CI, -2.2% to 6.1%), and then rates significantly increased from 2008 to 2015 (annual percentage change, 20.3%; 95% CI, 10.5%-30.9%), most dramatically in non-Hispanic white patients in the Northeastern and Southern United States. Conclusions- US hospitalization rates for stroke associated with IE and opioid use were stable for ≈2 decades but then sharply increased starting in 2008, coinciding with the emergence of the opioid epidemic.
The rate of spinal cord infarction (SCI) after surgical or endovascular repair of an aortic aneurysm or dissection is unclear.
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).
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%;
=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%;
<0.001) of unruptured aneurysm.
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.
We aimed to estimate the risk of ischemic stroke after intracranial hemorrhage in patients with atrial fibrillation.
Using discharge data from all nonfederal acute care hospitals and emergency ...departments in California, Florida, and New York from 2005 to 2012, we identified patients at the time of a first-recorded encounter with a diagnosis of atrial fibrillation. Ischemic stroke and intracranial hemorrhage were identified using validated diagnosis codes. Kaplan-Meier survival statistics and Cox proportional hazard analyses were used to evaluate cumulative rates of ischemic stroke and the relationship between incident intracranial hemorrhage and subsequent stroke.
Among 2,084,735 patients with atrial fibrillation, 50,468 (2.4%) developed intracranial hemorrhage and 89,594 (4.3%) developed ischemic stroke during a mean follow-up period of 3.2 years. The 1-year cumulative rate of stroke was 8.1% (95% CI, 7.5-8.7%) after intracerebral hemorrhage, 3.9% (95% CI, 3.5-4.3%) after subdural hemorrhage, and 2.0% (95% CI, 2.0-2.1%) in those without intracranial hemorrhage. After adjustment for the CHA2DS2-VASc score, stroke risk was elevated after both intracerebral hemorrhage (hazard ratio HR, 2.8; 95% CI, 2.6-2.9) and subdural hemorrhage (HR, 1.6; 95% CI, 1.5-1.7). Cumulative 1-year rates of stroke ranged from 0.9% in those with subdural hemorrhage and a CHA2DS2-VASc score of 0, to 33.3% in those with intracerebral hemorrhage and a CHA2DS2-VASc score of 9.
In a large, heterogeneous cohort, patients with atrial fibrillation faced a substantially heightened risk of ischemic stroke after intracranial hemorrhage. The risk was most marked in those with intracerebral hemorrhage and high CHA2DS2-VASc scores.
Stroke frequently complicates infective endocarditis (IE). However, the temporal relationship between these diseases is uncertain.
We performed a retrospective study of adult patients hospitalized ...for IE between July 1, 2007, and June 30, 2011, at nonfederal acute care hospitals in California. Previously validated diagnosis codes were used to identify the primary composite outcome of ischemic or hemorrhagic stroke during discrete 1-month periods from 6 months before to 6 months after the diagnosis of IE. The odds of stroke in these periods were compared with the odds of stroke in the corresponding 1-month period 2 years earlier, which was considered the baseline risk of stroke.
Among 17,926 patients with IE, 2,275 strokes occurred within the 12-month period surrounding the diagnosis of IE. The risk of stroke was highest in the month after diagnosis of IE (1,640 vs 17 strokes in the corresponding month 2 years prior). This equaled an absolute risk increase of 9.1% (95% confidence interval 8.6%-9.5%) and an odds ratio of 96.5 (95% confidence interval 60.1-166.0). Stroke risk was significantly increased beginning 4 months before the diagnosis of IE and lasting 5 months afterward. Similar temporal patterns were seen when ischemic and hemorrhagic strokes were considered separately.
The association between IE and stroke persists for longer than previously reported. Most diagnoses of stroke and IE are made close together in time, but a period of heightened stroke risk becomes apparent several months before the diagnosis of IE and lasts for several months afterward.
Elevated cardiac troponin is a marker of cardiac disease and has been recently shown to be associated with embolic stroke risk. We hypothesize that early elevated troponin levels in the acute stroke ...setting are more prevalent in patients with embolic stroke subtypes (cardioembolic and embolic stroke of unknown source) as opposed to noncardioembolic subtypes (large-vessel disease, small-vessel disease, and other).
We abstracted data from our prospective ischemic stroke database and included all patients with ischemic stroke during an 18-month period. Per our laboratory, we defined positive troponin as ≥0.1 ng/mL and intermediate as ≥0.06 ng/mL and <0.1 ng/mL. Unadjusted and adjusted regression models were built to determine the association between stroke subtype (embolic stroke of unknown source and cardioembolic subtypes) and positive and intermediate troponin levels, adjusting for key confounders, including demographics (age and sex), clinical characteristics (hypertension, hyperlipidemia, diabetes mellitus, renal function, coronary heart disease, congestive heart failure, current smoking, and National Institutes of Health Stroke Scale score), cardiac variables (left atrial diameter, wall-motion abnormalities, ejection fraction, and PR interval on ECG), and insular involvement of infarct.
We identified 1234 patients, of whom 1129 had admission troponin levels available; 10.0% (113/1129) of these had a positive troponin. In fully adjusted models, there was an association between troponin positivity and embolic stroke of unknown source subtype (adjusted odds ratio, 4.46; 95% confidence interval, 1.03-7.97;
=0.003) and cardioembolic stroke subtype (odds ratio, 5.00; 95% confidence interval, 1.83-13.63;
=0.002).
We found that early positive troponin after ischemic stroke may be independently associated with a cardiac embolic source. Future studies are needed to confirm our findings using high-sensitivity troponin assays and to test optimal secondary prevention strategies in patients with embolic stroke of unknown source and positive troponin.
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 .
Magnetic resonance imaging of carotid plaque can aid in stroke risk stratification in patients with carotid stenosis. However, the prevalence of complicated carotid plaque in patients with ...cryptogenic stroke is uncertain, especially as assessed by plaque imaging techniques routinely included in acute stroke magnetic resonance imaging protocols. We assessed whether the magnetic resonance angiography-defined presence of intraplaque high-intensity signal (IHIS), a marker of intraplaque hemorrhage, is associated with ipsilateral cryptogenic stroke.
Cryptogenic stroke patients with magnetic resonance imaging evidence of unilateral anterior circulation infarction and without hemodynamically significant (≥50%) stenosis of the cervical carotid artery were identified from a prospective stroke registry at a tertiary-care hospital. High-risk plaque was assessed by evaluating for IHIS on routine magnetic resonance angiography source images using a validated technique. To compare the presence of IHIS on the ipsilateral versus contralateral side within individual patients, we used McNemar's test for correlated proportions. A total of 54 carotid arteries in 27 unique patients were included. A total of 6 patients (22.2%) had IHIS-positive nonstenosing carotid plaque ipsilateral to the side of ischemic stroke compared to 0 patients who had IHIS-positive carotid plaques contralateral to the side of stroke (P=0.01). Stroke severity measures, diagnostic evaluations, and prevalence of vascular risk factors were not different between the IHIS-positive and IHIS-negative groups.
Our findings suggest that a proportion of strokes classified as cryptogenic may be mechanistically related to complicated, nonhemodynamically significant cervical carotid artery plaque that can easily be detected by routine magnetic resonance imaging/magnetic resonance angiography acute stroke protocols.
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.
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.
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.
Optimizing acute stroke transfer networks resulted in clinically small changes in population-level stroke outcomes in a dense, urban area.
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