American Heart Association

Monthly Archives: August 2015

Dabigatran is safe to use in small ischemic strokes initiated within 24 hours from stroke onset

Jay Shah, MD

Kate M, Gioia L, Buck B, Sivakumar L, Jeerakathil T, Shuaib A, and Butcher K. Dabigatran Therapy in Acute Ischemic Stroke Patients Without Atrial Fibrillation. Stroke. 2015 

Balancing risk of ischemic stroke and hemorrhage risk is a particular challenge in vascular neurology. It has been well established that patients with transient ischemic attack (TIA) are at greater risk for recurrent stroke, particularly within days and weeks following TIA. Strategies to ameliorate this risk depend on the stroke mechanism. For example, dual anti-platelet therapy would be adequate for intracranial atherosclerosis but insufficient for atrial fibrillation (AF) where anticoagulation is required. However, safety of dabigatran, a direct oral anticoagulant, prescribed within 2 weeks of minor stroke is unknown as previous safety trials excluded such patients. Anticoagulation, if safe, can help reduce stroke risk during a period of increased stroke recurrence rate in selected populations.

In this study, the authors designed a single-arm treatment trial to assess the safety of dabigatran initiated within 24 hours of ischemic stroke in patients without AF. Patients with National Institutes of Health Stroke Scale (NIHSS) less than 3 were screened and only included if magnetic resonance imaging (MRI) revealed diffusion restriction. All patients underwent MRI at baseline, 7, and 30 days assessing for ischemia and hemorrhage.

53 patients were enrolled with a median NIHSS of 1 and median infarct volume of 0.8mL. Three patients had evidence of asymptomatic hemorrhagic transformation on MRI at day 7. In 2 of these patients, petechial hemorrhage was evident at baseline and remained unchanged. However, there was one patient death of unknown etiology. There was no incidence of systemic bleeding or recurrent ischemic stroke but 7 patients had asymptomatic diffusion restriction at day 7. The most common stroke etiology was cardioembolism as 15 patients were identified to have AF.

While dabigatran cannot be recommended for use in this setting based on this small non-randomized trial, this trial does suggest the feasibility and safety of dabigatran use in minor stroke within 24 hours of infarct and supports a design for a future randomized trial. The authors suggest short-term use of AC following minor ischemic infarct in all patients while stroke etiology investigation is underway. This strategy would expose patients without AF to unnecessary hemorrhage risk, albeit short term. Future trials should focus on patients with AF and also assess timing of anticoagulation as this is a continuing dilemma in clinical practice.

By |August 31st, 2015|treatment|0 Comments

Blood pressure variability and acute stroke.

Russell Mitesh Cerejo, MD 

Manning LS, Rothwell PM, Potter JF, and Robinson TG. Prognostic Significance of Short-Term Blood Pressure Variability in Acute Stroke: Systematic Review. Stroke. 2015 

Appropriate management of blood pressure in acute stroke has always a moving target. In a meta-analysis of 18 studies, Dr. Manning and her group evaluated the effect of blood pressure variability within the first seven days after a stoke on short and long term outcomes. None of the studies were randomized controlled trials (RCT) but seven studies were of a prospective observational nature, five were observational analyses of prospective stroke registry data and six were observational analyses of previous RCT data. Seven studies were deemed suitable for the final meta-analysis of blood pressure variability on functional outcome. 


The group found that greater variability in blood pressure early after acute stroke might be associated with an increased risk of death and disability. Early on, systolic blood pressure variation was also associated with hemorrhagic complications after thrombolysis. However no effect was seen on short-term functional or neurological outcomes.

There was considerable heterogeneity in the studies that were reviewed by the group. The authors stress the importance of standardized practice for reporting of blood pressure measurements, blood pressure medications and timing with respect to the stroke onset. This will help draw robust conclusion in the future with regards to blood pressure management in acute stroke care.

By |August 28th, 2015|prognosis|0 Comments

Unlocking the Genetics of Lacunar Stroke through Genome-wide Association Studies

Danny R. Rose, Jr., MD

Traylor M, Bevan S, Baron JC, Hassan A, Lewis CM, and Markus HS. The Genetic Architecture of Lacunar Stroke. Stroke. 2015
 
The identification of genetic risk factors has opened new avenues for understanding disease pathogenesis. With the advent of genome-wide association studies (GWAS) over the last decade, insights have been gained into the contribution of single nucleotide polymorphisms (SNPs) to a variety of disease states. The potential for these types of studies to identify therapeutic targets and implicate particular biological pathways has made them particularly enticing to researchers, but previous GWAS for lacunar stroke have been inconclusive. It has been suggested through pathologic and radiographic analyses that lacunar stroke is not a pathologically homogeneous disease, and this phenotypic heterogeneity could obscure potential genetic association in GWAS analyses. In particular, it has been suggested that there may be two distinct lacunar subtypes: isolated lacunar infarcts (ILI) associated with microatheroma and multiple lacunar infarcts and leukoaraiosis (MLA/LA) associated with diffuse small vessel arteriopathy. Traylor et al. investigated the potential heritability of lacunar stroke and its subtypes by conducting a GWAS using a highly phenotyped cohort of MRI confirmed lacunar strokes.

This study included 1,029 Caucasian subjects less than 70 years of age with a clinical lacunar syndrome related to an anatomically compatible lesion on MRI.
Subjects with other potential causes of stroke were excluded, which included those with >50% stenosis of intracranial or extracranial vessels, previous carotid endarterectomy, moderate to high probability of cardioembolic stroke by TOAST criteria, cortical infarcts and subcortical infarcts >15mm in diameter, an identified etiology of their stroke (dissection, vasculitis, hypercoagulable state) and with NOTCH3 CADASIL or Fabry mutations.Those with lacunar disease were compared to age and sex stratified controls free of clinical cerebrovascular disease. Lacunar subjects were subtyped into two groups based on the presence and severity of leukoaraiosis using the semiquantitative Fazekas scale. Both subjects with lacunar disease and controls were assessed for known risk factors associated with lacunar stroke including hypertension, diabetes, hyperlipidemia, and smoking status.

Heritability was determined using genetic restricted maximum likelihood (GREML) analyses to estimate the proportion of phenotypic variance explained by the genetic relationships among subjects with common SNPs. This was performed versus controls for all MRI defined lacunar strokes as well as the two subtypes described previously. The authors also analyzed identified SNPs using information from a database of genotype-tissue expression studies that seeks to identify “functional” sites in the genome that influence expression, as well as sites where regulatory factors are thought to bind to the genome as evidenced by matched transcription factor binding sites and DNAse footprints. Lastly, the authors tested for the potential polygenic contribution from rare variation by calculating the ratio of risk to protective variants for all lacunar stroke cases and both subtypes versus controls.

It was found that lacunar stroke verified by MRI in the selected subjects was highly heritable for the population in aggregate (h2=0.2 0-0.25, p=0.00054) as well as the ILI (h2=0.15-0.18, p=0.029) and MLI/LA subtypes (h2=0.23-0.28, p=0.0035). The point estimate suggested a higher degree of heritability for the MLI/LA subtype, suggesting an increased contribution of genetic factors as compared to the ILI subtype, although this was viewed as speculative and needs to be confirmed. The heritability of lacunar stroke from this study is comparable to other neurologic diseases with strong genetic influences such as Alzheimer’s Disease and multiple sclerosis and should prompt additional research into using GWAS to gain more insights into the pathophysiology and genetic risk factors for this disease. This is further strengthened by the finding that a significant portion of the SNPs identified were found to have roles in either gene expression or regulation. Their analysis regarding polygenic contribution of rare variation showed an increase in the ratio of risk variants to protective variants at low allele frequencies in both subtypes of lacunar stroke, but not in both subgroups combined. This suggests a distinct role for the variants implicated for each of the pathologic subtypes.

This study represents a significant step forward in our understanding of the genetic basis of lacunar stroke and leukoaraiosis. The authors’ choice of including only MRI confirmed disease as well as the decision to divide lacunar stroke into distinct pathologic subtypes for analysis appears to be a large contributing factor to the success of this study compared to previous GWAS evaluating the genetic component of lacunar stroke. Additionally, their findings showing significant contribution of rare variants to both subtypes individually, but not as a whole, provides more evidence that these do represent distinct subtypes with potentially different pathologic mechanisms. Their successful precedent for separating lacunar strokes into these groups will likely influence future study design when evaluating the lacunar stroke population as a whole to determine novel associations and findings that may be specific to one group. Although this study was limited by a somewhat small sample size and the inherently incomplete nature of functional genetic databases, it represents a promising glimpse into the genetic basis of small vessel disease.

F-FACE identifies brain tissue at-risk

Peggy Nguyen, MD

Yamauchi H, Kagawa S, Kishibe Y, Takahashi M, Nishii R, Mizuma H, et al. Increase in [18F]-Fluoroacetate Uptake in Patients With Chronic Hemodynamic Cerebral Ischemia. Stroke. 2015

2-18F-fluoracetate (F-FACE) metabolites inhibit one of the key enzymes in the mitochondrial tricarboxylic acid cycle, leading to accumulation of metabolized substances in aerobic conditions. F-FACE uptake is therefore posited to reflect glial acetate metabolism, and consequently correlate with areas of ischemia. In this study, the authors use this compound to evaluate areas of the brain at-risk for ischemia in patients with atherosclerotic large vessel disease.


In 9 patients with unilateral symptomatic atherosclerotic occlusion or stenosis of the internal carotid artery (ICA) or middle cerebral artery (MCA), F-FACE uptake on PET increased ipsilateral to the occluded/stenosed artery. F-FACE uptake increased in areas where cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CRMO2) were decreased, and decreased in areas with increased oxygen extraction fraction (OEF). The strongest associations were seen with decreased CBF and increased OEF.

This study is limited in size, but does give evidence that F-FACE uptake is increased in tissue at-risk for ischemia. The authors suggest that F-FACE uptake could potentially help identify tissue at most risk for ischemic damage, and may select patients who need immediate treatments. The use of this modality for patient selection for acute intervention would likely be very limited given time constraints for intervention and availability of the imaging modality, but may have a role in patient selection for carotid stents, endarterectomies, or surgical bypass, which is more congruent with the study population. For example, patients being considered for bypass may undergo perfusion studies with an acetazolamide challenge; it would be of interest to see whether F-FACE might better identify which patients would benefit from intervention compared to conventional imaging.

By |August 26th, 2015|treatment|0 Comments

Patient-Centered Outcome Analysis for Stroke Trials

Mark N. Rubin, MD

Chaisinanunkul N, Adeoye O, Lewis RJ, Grotta JC, Broderick J, Jovin TG, et al. Adopting a Patient-Centered Approach to Primary Outcome Analysis of Acute Stroke Trials Using a Utility-Weighted Modified Rankin Scale. Stroke. 2015
 
The modified Rankin Scale (mRS) is the unequivocal reigning champion of outcome measurement in acute stroke trials, at least in North America but seemingly internationally. It represents a digestible, easy to understand scale that, decades of use later, is the common outcome parlance in the acute stroke treatment literature. The premise of the gradations, however, are based on an evaluation by a trained healthcare professional and the point-by-point changes on the scale are arbitrary; does jumping from a 0 to 1 have the same relative meaning to a patient as jumping from a 3 to a 4?

Many of the titans of acute stroke treatment trials came together in this project to suggest a relative weight to different mRS grades from a patient perspective, and apply these to various acute stroke trials spanning the last twenty years to see how this new scale compares to the more typically employed strategies of dichotomized and/or ordinal shift in mRS. The scale itself was given its patient-centered bona fides by being derived from mapping mRS scales against patient-provided quality of life measurements from the European Quality of Life Scale (EQ-5D) and medical-professional-determined disability weighting from the World Health Organization Global Burden of Disease (WHO-GBD) project. Overall, they found the Utility Weighted mRS (UW-mRS) to perform well, with similar “statistical efficiency” as ordinal analysis of mRS and even better than mRS dichotomization to recognize the benefit (or lack thereof) of the trialed interventions. An added bonus is that statistical analysis was straightforward with t-tests.

The authors present an important point here. Trial outcome reporting has to mirror the shared goals of the patient, clinician and researcher: “how much better will mom do if she undergoes _____?” All discussions are predicated on goals of care, and no one knows the goal better than the patient or surrogate, and it is reasonable to suggest that our studied outcome measures should be weighted with generally accepted views of quality of life and disability.

By |August 25th, 2015|clinical|0 Comments

First ever stroke in Sickle Cell Disease: What different in adults?

Michelle Christina Johansen, MD

Calvet D, Bernaudin F, Gueguen A, Hosseini H, Habibi, Galactéros F, and Bartolucci P. First Ischemic Stroke in Sickle-Cell Disease: Are There Any Adult Specificities? Stroke. 2015

Extensive exposure to Sickle cell Disease (SCD) is not a common occurrence for the general adult neurologist, but cerebrovascular specialists must treat SCD patients appropriately and know how to respond when they present with an ischemic stroke. Literature dictates that exchange transfusions are essential in preventing both recurrent and first ever stroke when paired with transcranial doppler in the pediatric population. For the adult patient however, there is little data to guide treatment. What is the best way to treat these patients? What are the common presenting symptoms?

26 children and 29 adults (>18yo) with a first ever ischemic stroke were identified from a prospective cohort (1985-2014) based at a sickle cell referral center in France. The aim of the study was to assess characteristics of first ischemic stroke in adults and compare those characteristics to child patients. Mechanisms of the ischemic stroke was determined by consensus meeting held with a neurologist, internist, neuroradiologist and pediatrician when appropriate. The patients were grouped according to prespecified etiologies: Vasculopathy, Cardioembolism, other defined causes and undetermined. Stroke recurrence was also monitored. Of the 29 adult patients identified, 2 suffered a fatal stroke, 25 were homozygous for SC, 3 were heterozygous and 1 had S-β0 thalassemia. All 26 children were homozygous.

Calvet et al. found that vasculopathy was more frequently the cause of ischemic stroke in SCD children (24/26) than adults (12/29). The remaining adults had cardioembolism (7), antiphospholipid syndrome (1), cocaine (1) and undetermined (8) as mechanisms. Both adults and children with vasculopathy as an etiology were treated with exchange transfusion yet adults still had a higher risk of recurrent stroke (23.1%) when compared to the children (1 occurrence).

The results of this study are limited by referral bias as well as the small number of patients in each cohort but the authors are to be applauded for their important investigation into the presenting characteristics of adult patients with sickle cell. Despite the limitations, what conclusions can the practicing neurologist draw? Vasculopathy, as would be expected, remains the leading cause of ischemic stroke in SC adults. As the authors point out in their discussion, the physician must avoid tunnel vision when treating these patients and consider other, more frequently encountered etiologies. What role does exchange transfusion play in the adult? It is important to note that all children were homozygous for SC while 4 adult patients were not. How does this influence the results? Should the SCD clinical phenotype play a more important role in guiding our acute stroke care? There are many remaining unanswered questions but larger epidemiologic cohort studies should in the future more accurately guide our care.

    

 

By |August 24th, 2015|clinical|0 Comments

The intransient effects of a stroke are borne by many

 
In this issue of Stroke, Persson and colleagues seek to establish the long-term impact of stroke on a stroke survivor’s spouse. They ask whether a patient’s stroke impacts his or her spouse beyond the short-term or if perhaps improvements in a patient’s stroke deficits or the general adaptability of the human spirit attenuate the consequences for the spouse over the long-term.

They derived their cohort from a Swedish ischemic stroke study that enrolled 600 consecutive patients under the age of 70 with ischemic stroke. After seven years, spouses of stroke survivors and age- and sex-matched controls were identified for comparison. The unit of analysis was survivor and spouse dyad and control and spouse dyad. 248 stroke survivor and 245 control dyads were included after excluding stroke survivors who had deceased or become single. Importantly, those who were excluded had greater disability at 3 months than those who were included. The outcome was self-reported health-related quality of life measured by the multidimensional Short Form 36 tool after controlling for multiple demographic and stroke outcome variables.

Notably, the median NIHSS for stroke survivors had been zero and the median mRS had been only 2. Regardless, even after 7 years, spouses of stroke survivors suffered significantly lower health in multiple domains as compared to spouses of controls. Attributes of the stroke survivor that predicted poor spousal health included the survivor’s levels of disability, depression and cognitive impairment. Perceived lack of social support also predicted poorer spousal mental and emotional health.

It is surprising that minor strokes in young persons with relatively good functional outcomes lead to persistent spousal health consequences. Patients who have strokes before 70 likely have predisposing vascular risk factors (some of which, such as diabetes, can require continued, laborious management) that may be responsible for this study’s findings; there is possible significant residual confounding as the dyads are only matched for age and sex.

If we are to believe the findings, it is worth noting that Sweden has a nationalized healthcare system with near universal coverage, excellent literacy and a high GDP per capita. Extrapolating their findings to developing nations where healthcare and social resources are scant underscores the importance of stroke prevention.

Standard-dose NOACs preferred to Vitamin K Antagonists in Asian Patients with AFib

Ilana Spokoyny, MD

Wang KL, Lip GYH, Lin SJ, and Chiang CE. Non–Vitamin K Antagonist Oral Anticoagulants for Stroke Prevention in Asian Patients With Nonvalvular Atrial Fibrillation: Meta-Analysis. Stroke. 2015
 

For Asian patients with atrial fibrillation, there has been hesitation to treating with Vitamin K antagonists due to increased rates of intracranial hemorrhage in Asians. NOACs may represent a safer alternative, but this has not been studied on a large scale in Asian patients until now. The authors performed a meta-analysis using data from recent clinical trials, to assess for differences in safety and efficacy of NOACs in Asian patients. Trials were included if they had more than 500 patients, followed for at least a year, and reported long term efficacy and safety in Asian patients. On literature review, 78 studies were identified but only 5 were included (RE-LY, ROCKET AF, J-ROCKET-AF, ARISTOTLE, ENGAGE AF-TIMI 48.) 8,928 Asian patients (5250 NOAC, 3678 VKA) and 64,033 Non-Asians (37800 NOAC, 26233 VKA) were included. The NOACs included were dabigatran, rivaroxaban, apixaban, and edoxaban. Two separate meta-analyses were performed to compare low- and high-dose NOACs to VKAs. 

Standard Dose NOACs
Efficacy
NOAC vs VKA
Better in Asians? (p-interaction)
stroke or systemic embolism               
better in NOAC
better in Asians
(p int 0.045)       
ischemic stroke                
same in NOAC vs VKA
MI
same in NOAC vs VKA
All-cause mortality                         
better in NOAC
same effect in both groups
Safety
NOAC vs VKA
Better in Asians? (p-interaction)
major bleeding                                
better in NOAC
better in Asians
(p int 0.004)
ICH                                                        
better in NOAC
slightly better in Asians
(p int 0.059)
hemorrhagic stroke                       
better in NOAC
better in Asians
(p int 0.046)
GI bleeding                                        
Mixed picture
less in Asians on NOAC vs VKA – OR 0.79
more in non-Asians on NOAC vs VKA – OR 1.44

Low dose NOACs
Efficacy
NOAC vs VKA
Better in Asians? (p-interaction)
stroke or systemic embolism
same in NOAC vs VKA
ischemic stroke
same in NOAC vs VKA
MI                                                                                         
Mixed picture
same in Asians on NOAC vs VKA
more events in non-Asians on NOAC than VKA (OR 1.28, p=0.01)
All-cause mortality
Better in NOACs
significant reduction in non-Asians, trend for reduction in Asians
Safety
NOAC vs VKA
Better in Asians? (p-interaction)
Major Bleeding
better in NOAC
same in Asians vs non-Asians
Hemorrhagic stroke
better in NOAC
same in Asians vs non-Asians
ICH        
better in NOAC
same in Asians vs non-Asians
GI bleeding        
Trend toward better in NOAC
same in Asians vs non-Asians

One of the limitations addressed by the authors is that they could not determine the actual ethnicity of patients, just their country of residence. Three sensitivity analyses were performed to mitigate these factors, with largely the same results.

A common criticism of standard dose NOACs is their increased risk of GI bleeding – this was only shown to be significant in non-Asians.

So, what explains the differences between Asian and non-Asian patients? We still don’t know. There are likely multiple factors which affect a patient’s or group’s sensitivity to NOACs versus VKAs. The authors note that there may be different genetic polymorphisms in VKA metabolism accounting for higher hemorrhagic stroke in Asians treated with VKAs, with a lower rate by comparison in Asians treated with NOACs. Additional factors in Asians which may contribute to higher hemorrhagic stroke rates with VKAs include: lower body weight and lower creatinine clearance. Other variables identified in Asian patients which are less clearly linked are less prior VKA use (likely due to perception of higher risk of bleed), lower rates of prior MI, less common concomitant use of GI ppx, higher rates of renal impairment, higher rates of prior stroke and non-paroxysmal AFib, and more antiplatelet use.

Overall, the advent of NOACs was a game changer. They provide an easier-to-monitor alternative to Vitamin K Antagonists. This meta-analysis shows that standard dose NOACs are preferred in Asian patients, with regard to both safety and efficacy outcomes. Lower dose NOACs may be an effective and safe alternative in Asian patients with an especially high risk of bleeding, but do not have better efficacy than VKAs. This study can reassure providers in Asian countries (and probably providers in non-Asian countries treating Asian patients) that there are safe and efficacious drugs for stroke prevention in atrial fibrillation. It is likely that many Asian patients are placed on antiplatelets in lieu of VKAs, due to perceived risk of intracerebral bleed. These patients will benefit from anticoagulation, and now have a good alternative to VKAs.

By |August 20th, 2015|prevention|0 Comments

Presence of cerebral microbleeds is not associated with an increased risk of poor 3-month outcomes after tPA for acute ischemic stroke

Alexander E. Merkler, MD 

Turc G, Sallem A, Moulin S, Tisserand M, Machet A, Edjlali M, Baron JC, et al. Microbleed Status and 3-Month Outcome After Intravenous Thrombolysis in 717 Patients With Acute Ischemic Stroke. Stroke. 2015

Patients who receive intravenous tPA within 3 hours are 30% more likely to have minimal or no disability at 3 months – but does this hold true for every patient with an acute ischemic stroke? What if a patient’s initial MRI has cerebral microbleeds – are these patients at higher risk for hemorrhage and poor functional outcome?


Cerebral microbleeds are small areas of signal void seen on T2*, SWI, or SWAN imaging often due to hypertensive vasculopathy, amyloid angiopathy, or a combination thereof. Cerebral microbleeds are present on pre-treatment MRIs in 15-35% of patients with acute ischemic stroke. Whether or not cerebral microbleeds are associated with an increased risk of symptomatic hemorrhage or poor functional outcome at 3 months is uncertain and prior studies have conflicting results.

In the current study, Turc et al evaluated whether presence of cerebral microbleeds was associated with poor 3 month functional outcome in 717 patients who received IV tPA for acute ischemic stroke and who received a pre-treatment MRI. The authors assessed whether presence or burden of cerebral microbleeds was associated with poor functional 3 month outcome, whether underlying etiology of cerebral microbleeds (amyloid versus hypertensive) was associated with poor functional 3 month outcome, and as a secondary outcome, whether cerebral microbleeds were associated with symptomatic ICH.

On pre-treatment imaging, 20.9% of patients had at least one cerebral microbleed, 33 patients (4.6%) had 2-4 microbleeds, and 25 (3.5%) had ≥ 5 microbleeds. Amyloid was thought to be the etiology of the cerebral microbleeds in 40% of patients, hypertension in 22.7% of patients, and undetermined in 37.3% of patients.

The authors found no significant association between either presence or burden of cerebral microbleeds and poor 3-month outcome. Neither etiology of cerebral microbleed nor microbleed location was associated with poor 3 month outcome. In addition, there was no association between cerebral microbleeds and increased rates of symptomatic hemorrhage.

Two noteworthy limitations included 1) the fact that T2*/1.5 T MRIs were performed and perhaps newer modalities such as SWI or SWAN could have detected cerebral microbleeds in patients who were thought to have none and 2) the number of patients with a high burden of cerebral microbleeds was low, and perhaps the study was underpowered to detect a relationship in this subgroup of patients previously found to be at very high risk for poor functional outcome after IV tPA.

Overall, previous data regarding the association between cerebral microbleeds and poor functional outcome after IV tPA is conflicting. This large study supports the practice of not withholding tPA in an otherwise eligible patient with an acute ischemic stroke even in the presence of cerebral microbleeds on a pre-treatment MRI. However, as the authors mention, future studies are needed to detect whether there is a subset of patients with cerebral microbleeds who may be at higher risk of hemorrhage or poor functional outcome after tPA.

Patient Selection for Endovascular Thrombectomy

Russell Mitesh Cerejo, MD

Espinosa de Rueda M, Parrilla G, Manzano-Fernández S, García-Villalba B,  Zamarro J, Hernández-Fernández F, et al. Combined Multimodal Computed Tomography Score Correlates With Futile Recanalization After Thrombectomy in Patients With Acute Stroke. Stroke. 2015 

Dr. Mariano Espinosa de Rueda and colleagues couldn’t have chosen a better time to publish this paper. With the positive endovascular trials, we can move beyond the age old question – does this work? As this paper aptly points out, it is now time to determine who best benefits from endovascular therapy. Their study over a 2 year period, analyzed 150 patients who underwent endovascular recanalization for ischemic stroke. Patients were divided into a good outcome (mRS ≤2) and a futile recanalization (mRS >2) group at 3 months. The authors analyzed different modalities of imaging data. Fifty seven percent patients had a bad outcome and were noted to have a higher NIHSS, were older and had hypertension. With regards to imaging, the bad outcome group had a lower Alberta Stroke Program Early CT Score (ASPECTS) score on the non-contrast head CT, CT Angiogram Source Imaging (CTA-SI), cerebral blood volume (CBV), cerebral blood flow (CBF), and mismatch CBV-CBF ASPECTS. They also found a higher proportion of bad collaterals in this population. In univariate analysis low ASPECTS and poor-collaterals were associated with futile recanalization. However in the multivariate analysis CTA-SI, CBV ASPECTS and poor collaterals were associated with poor outcomes. Based on this they created a 3 variable scoring system with CTA-SI, CBV and Collaterals (see figure) to predict futile recanalization. In the reclassification analysis this scoring method added complimentary information to their test model. 

This study sheds light on the current issue of appropriate patient selection for endovascular thrombectomy for ischemic stroke. Given the myriad of variables that account for a good or bad outcome in ischemic stroke, we need to streamline our efforts to evaluate which are the most reliable. Another challenge in acute stroke treatment is the race against time – these variables should be easily calculated, precise and leave no room for ambiguity. Most centers today use CT and CTA technology to identify candidates for acute stroke therapy and this scoring may be a useful, quick step to help triage the patient. Further prospective studies with a control arm would be useful.