American Heart Association

Monthly Archives: November 2014

Here’s a way to stop those annoying aneurysms from growing!

Daniel Korya, MD

Bor ASE, Groenestege ATT, terBrugge KG, Agid R, Velthuis BK, Rinkel GJE, and Wermer MJH. Clinical, Radiological, and Flow-Related Risk Factors for Growth of Untreated,Unruptured Intracranial Aneurysms. Stroke. 2014

Over a year has passed since Dr. Villablanca from UCLA taught us the rate of growth of aneurysms is more important with regard to risk of rupture than the size of the aneurysm. So, needless to say, an understanding of the elements that contribute to the growth of aneurysms has been in greater demand. Researchers from Finland provided some clues about 13 years ago when they published their findings in Stroke (2001) concluding that women are more likely to have aneurysms and smoking cigarettes made their aneurysms grow faster. That study comprised of 87 patients with a total of 111 unruptured aneurysms. 



Dr. Bor from the Netherlands and her colleagues expanded significantly on the previous number of patients and aneurysms by analyzing 363 patients with a total of 468 aneurysms. They followed these patients for a median of 2.1 years (total of 1372 patient-years) and performed multivariate Cox regression analysis to come up with their conclusions. Their efforts are commendable and the level of information gathered on these aneurysms is important.

First, they separated the patients into two groups: small aneurysms (< 7mm) and larger ones (≥7mm). They then evaluated the number of aneurysms with and without growth at 2-year intervals and performed analysis to find risk factors for growth. The risk factors they assessed were: sex, age, smoking and hypertension at the time of diagnosis, previous SAH (SAH predating or at the time of diagnosis), presence of multiple aneurysms (ruptured or unruptured), family history of SAH (≥ 2 first degree relatives with an (un)ruptured intracranial aneurysm), initial aneurysm size (maximum aneurysm height or dome width), aneurysm location (posterior versus anterior circulation), multilobarity (multilobar versus unilobar shape), dome>neck ratio (aneurysm dome width larger than aneurysm neck width versus aneurysm dome width smaller than aneurysm neck width), aspect ratio≥median (aspect ratio larger than the median versus aspect ratio smaller than the median), flow direction into the aneurysm (highest versus lowest tertile) and bifurcation angles (highest versus lowest tertile).

In order to increase the level discrimination, the researchers also inserted age (<50, 50-60, >60 years at initial diagnosis), initial aneurysm size (< 2mm, 2-4 mm, 4-7 mm, 7-15 mm and > 15mm), aneurysm location in the anterior circulation: middle cerebral artery versus carotid artery, and anterior communicating/cerebral artery versus carotid artery into the multivariate analysis.

Some of the results were not surprising and were essentially expected since they have been previously shown to be true. For example, the researchers once again confirmed that smoking causes aneurysms to grow faster. They found that about 10% of all aneurysms grow and the initial dome-to-neck ratio was a risk factor as was multilobularity. The greater the dome-to-neck ratio, the more likely the aneurysms were to grow and more lobes meant more growth as well.

However, unlike previous studies that showed female sex to be associated with aneurysm development and growth, Dr. Bor and her colleagues did not find an association. They also did not find any relationship with age, hypertension, familial history of SAH, previous SAH, flow direction into the aneurysm or bifurcation angles.

That was interesting and unexpected. Most clinicians who deal with aneurysms try to avoid hypertension and we were all taught that a previous SAH in a patient who has an aneurysm is a risk for growth and rupture of new aneurysms. But, this study says otherwise. That is why this study is important and deserves discussion.

By |November 28th, 2014|clinical|Comments Off on Here’s a way to stop those annoying aneurysms from growing!

High Sensitivity of Diffusion- and Perfusion-Weighted Imaging for Diagnosing Acute Stroke

Rizwan Kalani, MD

Simonsen CZ, Madsen MH, Schmitz ML, Mikkelsen IK, Fisher M, and Andersen G. Sensitivity of Diffusion- and Perfusion-Weighted Imaging for Diagnosing Acute Ischemic Stroke Is 97.5%. Stroke. 2014

Diffusion-weighted imaging (DWI) can sometimes be negative in the setting of acute stroke. This is most notably seen with small infarct size, early timing of scan, and brainstem location. In this study, Simonsen et al retrospectively evaluated DWI magnetic resonance imaging (MRI) and the contribution of perfusion-weighted imaging (PWI) for diagnosing ischemic stroke from a database of intravenous tissue plasminogen activator (IV-TPA) treated patients.



At the center where this study was conducted, MRI (including DWI & PWI) was performed as the initial preferred imaging modality prior to acute stroke thrombolysis. Patients received IV-TPA according to standard guidelines. DWI and PWI lesion evaluation was done by a neuroradiologist and neurologist blinded to final diagnosis. Patient follow-up at 90 days established functional outcomes (modified Rankin scale [mRS]) and etiologic subtype (per TOAST criteria).

569 IV-TPA treated patients were included from 2004-2010 for this study. Four of them ended up having stroke mimics based on clinical and imaging follow-up. Of the 565 patients with clinically diagnosed stroke, 518 had a DWI positive lesion. The sensitivity of DWI for ischemic stroke was 92% with specificity of 75% and positive predictive value of 99.8%. 47 patients had MRIs that were DWI negative, 43 of which had PWI completed. Hypoperfusion in the location corresponding to symptoms was seen in 33. In effect, the combination of DWI and PWI increased sensitivity for detection of hyperacute stroke to 97.5%. DWI negative MRI was associated with less severe stroke (NIHSS 4 vs 7, p=0.0008), improved outcome (80.9% vs 61.8% with mRS 0-1), posterior circulation location (34.9% vs 15.3%, p=0.0019), higher prevalence of small vessel disease (36.2% vs 18.0%, p=0.0047), and longer time from symptom onset to imaging (120 min vs 109 min, p=0.047).

Consistent with prior studies, this manuscript re-demonstrates the high sensitivity of DWI for acute infarct. The addition of PWI can improve the sensitivity further. The authors argue that visualizing the lesion on MRI can assist in decision making about IV-TPA. Furthermore, they suggest that PWI may be of diagnostic utility in DWI negative patients with suspected ischemic stroke who are outside of the acute treatment window (or as part of research study).

Completing MRI prior to thrombolytic treatment decision making is not universal practice. With accumulating evidence supporting earlier IV-TPA administration improving patient outcomes as well as relative safety of thrombolysis demonstrated in stroke mimics, a role for MRI prior to acute stroke treatment is likely to be limited. Results from DEFUSE, EPIPHET, and MR-RESCUE have shown that perfusion imaging does not clearly assist with patient selection for IV-TPA or endovascular treatment.

With continual improvement in PWI techniques, ongoing and future studies will have to further define its role in etiologic diagnosis, management, prognostication, and clinical outcomes after stroke.

By |November 26th, 2014|diagnosis and imaging|Comments Off on High Sensitivity of Diffusion- and Perfusion-Weighted Imaging for Diagnosing Acute Stroke

Back Again: Hospital Readmissions after Stroke

Mark L. McAllister, MD


Evaluating an acute ischemic stroke patient in the inpatient setting, our concerns are often focused on determination of stroke etiology and secondary prevention measures, evaluating and treating early complications, and preparing patients for rehabilitation. What happens after the patient leaves the hospital is often a secondary concern. Readmission to the hospital is a common and deleterious outcome for many stroke patients.



The authors here investigated the rates of readmission among stroke patients in Dijon, France. Of 519 patients with first time stroke who survived initial hospitalization, 32% had a hospitalization in the first year after their discharge. The leading cause of admission was neurologic complaints, with stroke or TIA being the most frequent in that category. Unsurprisingly, patients who were older, had more comorbidities, and more severe initial strokes were most likely to have readmission in the year following stroke.

What is not clear in this study is what proportion of hospitalizations were due to preventable causes, and especially causes that were preventable based on actions taking place during the acute hospitalization for stroke. Readmission adversely affects patients’ general level of health and independence, emphasizing the need to minimize preventable readmissions. Finally, the correlation with initial stroke severity and rehospitalization further underscores the need for aggressive primary prevention measures in stroke to avoid these patients’ initial hospitalization.  

By |November 25th, 2014|prognosis|Comments Off on Back Again: Hospital Readmissions after Stroke

Stroke controversy: Should a patient with a severe stroke be transferred from a primary to a comprehensive stroke center?

Early Transfer of Stroke Patients to Comprehensive Stroke Centers: David and Goliath


This month’s Stroke controversy addresses whether patients with moderately severe stroke should be transferred to a comprehensive stroke center (CSC) in the acute stage or whether the transfer can be done later if complications develop or more complex issues arise.  Drs. Kevin Sheth and Peter Langhorne, the two panelists, present their views on the need to transfer a 55 year old man with 75% left carotid artery stenosis who presents with a left MCA syndrome and NIHSS score of 20 five hours after symptom onset.



Dr. Seth argues for early transfer even if the patient is outside the time window for a reperfusion therapy because he is at high risk for neurologic deterioration and the staff at a CSC may closely monitor him to identify any complications and intervene in a timely manner if necessary. The staff at a CSC may also implement secondary stroke prevention strategies early on, including carotid endarterectomy for this patient. Dr. Langhorne, on the other hand, maintains that an ambulance ride will not help the patient and that many small hospitals can care for the patient as long as they have a well-run stroke unit. He reminds us that a stroke unit admission is the only intervention proven to improve survival after stroke and maintains that staff in a stroke unit should be able to monitor for complications and institute secondary prevention measures. If carotid endarterectomy is not available at the smaller hospital, the patient may be transferred to a larger center within the first two weeks after the stroke.

Both authors address the possible need for a hemicraniectomy if the patient develops significant brain swelling but disagree in terms of the  risk in a patient with an NIHSS score of 20 and, if an intervention is needed, the timing when the neurosurgical team should get involved.

In a Solomonic discussion, Drs. Molina and Selim, the moderators of the debate, acknowledge the validity of the issues raised by the debaters. They conclude that system and patient factors play a role in the decision to transfer a patient, and suggest that telemedicine is a way to make the decision easier. I agree with them. Well organized primary stroke centers must have the infrastructure required for managing most patients in the acute stage. The decision to transfer a patient to a comprehensive stroke center must take into account availability of local resources, the condition of the patient, the expertise of the treatment team and, ideally, the advice of the stroke specialists at the CSC. The way forward cannot be prescriptive.


– José G. Merino, MD

By |November 25th, 2014|controversy|1 Comment

“You can observe a lot just by watching:” more clinical data is better when diagnosing childhood stroke.

Mark N Rubin, MD

Wintermark M, Hills NK, deVeber GA, Barkovich AJ, Elkind MSV, Sear K, et al. Arteriopathy Diagnosis in Childhood Arterial Ischemic Stroke: Results of the Vascular Effects of Infection in Pediatric Stroke Study. Stroke. 2014


“You can observe a lot just by watching.”
~Yogi Berra

Thankfully, acute ischemic stroke is fairly rare in the pediatric population. However, when it occurs, arteriopathy of some kind – be it inflammatory, traumatic, or iatrogenic – is a major cause thereof. Estimates of incidence vary widely by reports, in part because of heterogeneous populations and diagnostic resources, and the inherent difficulty in diagnosing an arteriopathy in the first place. That being the case, a NIH-funded international group of pediatric investigators sought to clarify the diagnostic process by adjudicating consecutive stroke patients. They studied the test performance of diagnoses of arteriopathy based on baseline imaging alone, baseline imaging and clinical data, and the combination of baseline imaging, clinical data and follow up imaging.



Their cohort consisted of 355 cases, and 45% (161 patients) were thought to have definite (36%, 127 patients) or possible (9.6%, 34 patients) arteriopathy. As one might expect, sensitivity grew with each “step” of additional data, from 79% with baseline vascular imaging alone to 90% with both vascular imaging and clinical data and up to 94% with the former elements plus follow up imaging. Agreement was excellent at each step (κ ~ 0.8). Cases were clearly diagnosed conservatively as specificity was essentially 100% for any amount of data provided.  

The results of this study can be a bit difficult to generalize given the heterogeneity of everything from the diagnosis of arteriopathy to the clinical means of coming to that conclusion. However, and important take-away from their investigation is that “more is better” as regards difficult diagnoses. As is the case with much of clinical neurology, results of diagnostics must be contextualized within a pattern of illness to be of most use to the patient and the provider.

By |November 24th, 2014|diagnosis and imaging|Comments Off on “You can observe a lot just by watching:” more clinical data is better when diagnosing childhood stroke.

Antithrombotic therapy after Ischemic Stroke in Atrial Fibrillation

A. Kaleel, MD, MSc 

McGrath ER, Kapral MK, Fang J, Eikelboom JW, Conghaile AO, Canavan M, et al. Antithrombotic Therapy After Acute Ischemic Stroke in Patients With Atrial Fibrillation. Stroke. 2014

Management of patients with atrial fibrillation following an ischemic stroke is a frequent and yet, at times, challenging scenario in many stroke units and outpatient clinics. While the consensus guidelines currently recommend anticoagulation alone following an ischemic event in patients with atrial fibrillation, actual management differs among clinicians. 



This large prospective cohort study contained 2,162 consecutive patients from the Ontario Stroke Registry between July 2003 and March 2008 who were hospitalized with acute ischemic stroke and atrial fibrillation. It sought to examine the relationship between antithrombotic regimen upon discharge and the ensuing risk of major vascular events as well as major bleeding on follow up, giving particular attention to patients with severe stroke as well as those with coronary heart disease. The primary outcomes included death or hospital readmission for recurrent stroke, myocardial infarction, or major bleeding while secondary outcomes included hospital admission for stroke, myocardial infarction, major bleeding, intracerebral hemorrhage, all cause mortality, and a combination of these outcomes. Among the 2162 patients with atrial fibrillation, 8% were discharged without any antithrombotic therapy, 21.6% were prescribed antiplatelets alone, 39.3% were prescribed anticoagulation alone, and 31.1% were prescribed combination therapy with anticoagulation and antiplatelet. Comparing populations, it was seen that actual management of these patients differed, and patients with a higher risk of bleeding were less likely to be prescribed anticoagulation while patients discharged on combination therapy had a higher cardiovascular risk profile and higher risk of severe strokes.

After statistical analysis, it was discovered that combination anticoagulation and antiplatelet were associated with a trend towards a reduced risk of the primary outcome while no antithrombotic therapy or antiplatelet therapy alone were associated with an increased risk. Those patients not given antithrombotic therapy or given antiplatelet therapy alone were associated with a reduced risk of admission for major bleeding while combination therapy was associated with an increased risk. Of note, there was not an association with increased risk of admission for ICH over the four years on those patients with combination therapy. In assessing those patients found to have severe stroke, identified as those with mRS 4-5 on discharge, as well as those with coronary heart disease, it was found that those patients given no antithrombotic therapy or given antiplatelet therapy alone were associated with an increased risk of death or admission for stroke, myocardial infraction, or major bleeding. An interesting observation from this study is that over 60% of patients with atrial fibrillation discharged after acute stroke are not managed according to current antithrombotic guideline recommendations. Finally, the authors recommended further clinical trials to determine the efficacy of antithrombotic therapy in patients with severe stroke and high cardiovascular risk.




By |November 21st, 2014|treatment|Comments Off on Antithrombotic therapy after Ischemic Stroke in Atrial Fibrillation

The FePASS Playground: Using the FePASS Web Portal for Clinical Trial Planning

Vikas Pandey, MD

Minnerup J, Trinczek B, Storck M, Hohenberger M, Wilpsbaumer S, Abdul-Rahim A, et al. Feasibility Platform for Stroke Studies: An Online Tool to Improve Eligibility Criteria for Clinical Trials. Stroke. 2014

The planning of clinical trials is an arduous task that requires painstaking detail and numerous revisions to ensure that the highest quality trial design is achieved to obtain useful clinical data. The usual rate-limiting step to the time and effort involved in clinical trials is the number of patients that can be enrolled. Rather obviously, stricter limits placed on patient enrollment will allow for more uniform patient population however this data may not be as generalizable to the general population and patient enrollment will take more time whereas less strict inclusion criteria will lead to faster patient enrollment and better generalizability however leaves the door open for confounders in the data. The group from Europe devised a plan to make an online tool (the web portal FePASS) to estimate proportions of eligible patients in acute stroke trials in order to optimize eligibility criteria for a certain trial as well as allow for better estimation of potential recruitment rate. 



The group conglomerated 61 eligibility criteria derived from 30 trials on acute ischemic stroke (treatment initiation within 24 hours after stroke onset) and retrospectively analyzed data of all ischemic stroke patients admitted in Switzerland (1 month period), United Kingdom (7 month period) and Germany (2 year period). They entered these patients’ data (multiple data points: age, NIHSS, time of onset, etc.) into the FePASS web portal to determine using the web interface if the patient would be eligible for two trials recently completed (ALIAS part 2, AXIS 2) and two ongoing (EuroHYP-1, SWIFT PRIME) based on their inclusion and exclusion criteria. Overall, 1537 patients were included in the database. By using the database, the proportions of trial-eligible patients for ALIAS part 2, AXIS 2, EuroHYP-1 and SWIFT PRIME were 4.3%, 3.3%, 11.3% and 2.1%, respectively. They found that small changes in the search parameters i.e. variation of time of onset by 1 hour would increase the amount of eligible patients from 2.33 to 3.54% exemplifying the potential impact of rather minor modifications in trial design.

The FePASS web portal can be found at https://fepass.uni-muenster.de/. The interface was well-designed and the website is user friendly. I am unsure if the website is fully functional currently as any search I conducted yielded 0% patient match and a “Search for patients” message in the middle of the page, but this may be because I am not a registered user. The included results images from the authors show an efficient results output screen for the user when properly functional. The website is a brilliant concept and may be the future of clinical trial study design given that it provides an excellent forecasting playground for the predicted percent of patients that will be eligible for a given trial and provide better allocation of resources for a trial and less trial closures due to poor planning. This, in turn, will eventually lead to more published clinical data and expansion of our field so the natural next step would be to build up the database with further modifying search parameters.

@DrVikasNeuro

By |November 20th, 2014|treatment|Comments Off on The FePASS Playground: Using the FePASS Web Portal for Clinical Trial Planning

Early Rehab – It leads to better outcomes!

Rajbeer Singh Sangha, MD

Liu N, Cadilhac DA, Andrew NE, Li Z, Li J, et al. Randomized Controlled Trial of Early Rehabilitation After Intracerebral Hemorrhage Stroke: Difference in Outcomes Within 6 Months of Stroke. Stroke. 2014


Current evidence suggests that early physical rehabilitation (VER) of stroke survivors in the acute stage may result in better motor recovery, reduced mental, functional and neurological disability, and improved quality of life. The previous studies that have been conducted regarding this topic have analyzed a small proportion of patients with ICH and there still remains a need for a larger phase three trial. According to the authors, the current general consensus that exists is that patients with ICH should be mobilized later than those with ischemic stroke, despite a lack of evidence to support this view. They aimed to compare Very Early Rehabilitation (VER) with standard care in patients with ICH and hypothesized that VER within 48 hours of ICH onset would result in reduced mortality, morbidity, and better quality of life outcomes compared to standard care at 3- and 6- months following stroke.



The study was a prospective, multi-centre, randomized controlled study, with 2 parallel groups followed for 6-months with blinded assessment of outcomes. Both groups received standard care, but participants in the VER group commenced rehabilitation as soon as practical after randomization but within 48 hours of ICH onset. In contrast, the standard care group commenced rehabilitation after 7 days. Out of 326 patients that were eligible, 243 patients were randomized (mean age 59 years; 56% male). At 6-months, patients receiving standard care were more likely to have died (aHR: 4.44, 95%CI: 1.24, 15.87). Further analysis of the morbidity outcomes showed a 6-point difference in the Physical Component Summary score of the SF-36 (95%CI 4.2, 8.7); a 7-point difference for the Mental Component Summary score (95%CI: 4.5, 9.5); a 13-point difference in Modified Barthel Index scores (95%CI: 6.8, 18.3), and a 6-point difference in SAS scores (95%CI: 4.4, 8.3) was reported in favor of the intervention groups.

The findings in this study point strongly towards ICH patients who were randomized to VER more likely to be alive at 6-months than those who received standard care alone. Patients who received VER also had a shorter length of hospital stay and reported significantly greater quality of life, independence with activities of daily living, and improved mental health outcomes at 6-months following stroke compared to those randomized to standard care. These results are in conjunction with previous smaller trials that have been conducted including the VERITAS trial in the UK and the AVERT phase II trial. While the authors could not account for the exact pathophysiological mechanism that lead to the improved outcomes, it should mean a significant change in the dogma towards rehabilitation in centers that wait for a period of 7 days or greater prior to starting. Further trials should focus on the specific techniques that would improve outcomes in a more efficient manner as well as more sensitive scales of measuring outcomes including the Neuro QOL which is a validated self-reported neurological assessment of quality of life.

By |November 19th, 2014|hemorrhage|1 Comment

Genetic underpinnings of renal dysfunction associated with large vessel stroke: genetics as a window to understand stroke pathophysiology

Chirantan Banerjee, MD

Holliday EG, Traylor M, Malik R, Bevan S, Maguire J, Koblar SA, et al. Polygenic Overlap Between Kidney Function and Large Artery Atherosclerotic Stroke. Stroke. 2014

The human genome project was arguably one of the most important scientific advances of the last decade. It revolutionized our understanding of single nucleotide polymorphisms (SNPs or “snips”) which act as markers of disease genes, as well as help us study their inheritance. Genome wide association studies (GWAS) use DNA microarrays to compare SNPs across thousands of people with and without disease, and have the ability to identify novel associations.




As stroke pathophysiology is heterogeneous, studies have reported the need to study heritability of stroke subtypes separately. The International Stroke Genetics Consortium (ISGC) was formed to study the genetic basis of stroke, and has identified genes associated with large vessel stroke and cardioembolic stroke.
Kidney dysfunction has been associated with ischemic stroke in several epidemiologic cohorts. In the current study by Holliday et al, the ISGC authors investigate whether this association is secondary to underlying shared genetic polymorphisms. One of the major issues with GWAS is that the single SNPs they identify only explain a small portion of the heritability, as individual risk variants have effects too small to be significant statistically. 

The authors of this study try to clarify this issue in the study by aggregating numerous SNPs that pass apriori p-value thresholds into polygenic scores via GWAS. They derived polygenic scores for 3 renal traits: eGFR using serum creatinine, eGFR using cystatin C, and urine albumin to creatinine ratio. The performances of the polygenic scores for these traits were then tested in stroke GWAS datasets. One of the major strengths of the analysis is that they classified stroke cases into three subtypes, large vessel atherosclerosis, cardioembolic, and small vessel disease and tested them separately. 

Polygenic scores associated with higher eGFRcrea were associated with decreased risk of large vessel atherosclerotic stroke, and polygenic scores for higher urine albumin to creatinine ratio were also associated with higher risk of large vessel atherosclerotic stroke.  Subclassifying into stroke subtypes led to decreased power in the study, and the authors believe that the effect estimates are markedly underestimated. 

There are some other interesting hypothesis-generating findings. One such finding is that although CKD is associated with atrial fibrillation epidemiologically, kidney trait polygenic scores in the study were not associated with cardioembolic stroke. Also, there was a trend for association of polygenic score for higher urine albumin to creatinine ratio with small vessel strokes, which may be attributed to underlying heritable small vessel arteriopathy.

These findings are important, as they demonstrate a way to test polygenic genetic variants, which may arguably be more important in a complex heterogeneous entity like ischemic stroke as opposed to individual SNPs. Also, they provide some insight into underlying shared genetic basis of renal dysfunction and large vessel stroke.

As more stroke GWAS datasets become available, these findings will have to be replicated. But stroke genetics will surely be a fascinating area of research over the next several years, as it slowly unravels the underlying genetic underpinnings of cerebrovascular disease, as well as atherosclerosis at large.
By |November 18th, 2014|epidemiology and genetics|Comments Off on Genetic underpinnings of renal dysfunction associated with large vessel stroke: genetics as a window to understand stroke pathophysiology

Circumferential Aneruysmal Wall Enhancement on MRI as a Marker of Aneurysm Instability

Duy Le, MD

Edjlali M, Gentric JC, Régent-Rodriguez C, Trystram D, Ben Hassen W, Lion S, et al. Does Aneurysmal Wall Enhancement on Vessel Wall-MRI Help to Distinguish Stable From Unstable Intracranial Aneurysms? Stroke. 2014


As exciting as acute treatment is in the stroke world, just as much energy should be focused on prevention. As with any disease, if we can appropriately risk stratify in order to prevent catastrophic events from ever happening, then the battle will have been won. Although much work has been done to risk stratify cerebral aneurysms based on size (International Study of Unruptured Intracranial Aneurysms), Edjlali et al attempt to quantify another parameter of measuring aneurysm rupture risk: circumferential aneurysmal wall enhancement (CAWE). 




It has been known that arterial wall enhancement indicates evidence of inflammatory disease. This study evaluated 87 patients harboring 108 intracranial aneurysms. These patients were followed out for 6 months. Prospectively within 6 months, aneurysms were determined as unstable if it ruptured, became symptomatic or had undergone morphologic changes.

Patients underwent Vessel Wall MRI’s which consisted of a 3T MRI with gadolinium administration. The MRI’s were reviewed by 2 radiologist with excellent inter-reader and intra-reader agreement for CAWE (k=0.85 and k=0.90 respectively). CAWE was significantly more frequently seen in unstable aneurysms (27/31; 87%), as compared to stable aneurysms (22/77; 28.5%). Multivariate logistic regression including CAWE, size, location, multiplicity of aneruysms and daily aspirin intake revealed that CAWE was the only independent factor associated with unstable aneurysm (OR, 9.20; 95% CI; p=0.0002)

While it does appear that CAWE is seen more often in unstable aneurysms, it is also seen in about 30% in stable aneurysms. There is good sensitivity, but evidence of CAWE is not necessarily specific for an unstable aneurysm. Weaknesses of the study includes that patients were only followed patients out for 6 months; it would be important track these patients out over a number of years as well. Additionally, there may be a referral bias.

Taken together, from this limited data, it would be difficult to determine management of aneurysms solely based on CAWE. Stratifying aneurysmal rupture risk according to size is quite ingrained in our common practice. On the bright side however, evaluation for CAWE does not require any post imaging processing and appears easy to identify. This risk stratifying method is promising, but more work remains to be done. With a strong, positive, longitudinal cohort study evaluating CAWE, this method may prove useful in identifying those who are at high risk of bleeding; thus being able to classify and manage a patient as a high risk bleed without having to suffer the sequela of an actual bleed.

By |November 17th, 2014|diagnosis and imaging|Comments Off on Circumferential Aneruysmal Wall Enhancement on MRI as a Marker of Aneurysm Instability