Mild Luminal Stenosis of Parent Artery and Neurologic Deterioration After Acute Lacunar Stroke

 

Well congratulations, you described a problem BUT DID NOTHING TO SOLVE IT. You all need to be fired.

Mild Luminal Stenosis of Parent Artery and Neurologic Deterioration After Acute Lacunar Stroke

Dixon Yang

,

Jose Gutierrez

,

Shawna Cutting

,

Eytan Raz

,

Kursat Gurel

,

Jose Torres

,

Brian Mac Grory

,

Erica Scher

,

Sahnaz Pirooz

,

Adam de Havenon

,

Koto Ishida

,

Karen Furie

,

Mitchell S.V. Elkind

, and

Shadi Yaghi

Originally published22 Dec 2021https://doi.org/10.1161/SVIN.121.000132Stroke: Vascular and Interventional Neurology. 2021;0:e000132

Abstract

BACKGROUND

Early neurologic deterioration (END) occurs in a quarter of acute lacunar infarcts, but the underlying pathophysiological features are poorly understood. We sought to determine the association between luminal stenosis (<50%) of the parent artery and END.

METHODS

This observational study included consecutive patients with lacunar stroke from the ischemic stroke registries of New York University Langone Health and Brown University. All included patients were admitted for acute lacunar stroke, which was defined as a subcortical infarct <1.5 cm on computed tomography or <2 cm on diffusion‐weighted imaging without significant stenosis (>50%) in the parent vessel and no cardioembolic source. We defined END as any neurologic deterioration referable to the acute lacunar stroke and not related to a medical or noncerebrovascular neurological complication. We used univariate and logistic regression analyses to determine associations between luminal stenosis (<50%) and the odds of END. Furthermore, we attempted to validate findings using the Columbia University Medical Center stroke registry and perform a meta‐analysis combining the derivation and validation groups because of the expected small samples and event rates.

RESULTS

The New York University Langone Health and Brown University sample included 205 patients, of whom 41 (20%) had END. In adjusted models, we found no definite association between luminal stenosis (<50%) and END (adjusted odds ratio [OR], 1.74; 95% CI, 0.73–4.14). From Columbia University Medical Center, 361 total patients were included, of whom 59 (16%) had END. In adjusted models, we found an association between luminal stenosis (<50%) and END (adjusted OR, 2.28; 95% CI, 1.15–4.50). Meta‐analysis of both cohorts found luminal stenosis (<50%) associated with END (relative risk, 1.69; 95% CI, 1.17–2.43).

CONCLUSIONS

In this multicenter study, luminal stenosis (<50%) may be associated with END following an acute lacunar infarct. Larger studies using vessel wall imaging are needed to validate our findings.

Early neurologic deterioration (END) can occur in about a quarter of acute lacunar strokes within hours to days after initial deficit.¹ Although lacunar strokes generally have a more favorable prognosis,² END in lacunar stroke may especially involve motor function and increase risk for long‐term disability.^{3, 4} Diabetes, admission motor symptom severity, higher admission National Institutes of Health Stroke Scale, and larger lacune size have been shown to be associated with progressive deficits in lacunar stroke.^{4, 5, 6} However, the underlying pathologic mechanisms for END after lacunar stroke remain poorly understood.

Distinct from lipohyalinosis in intrinsic cerebral small‐vessel disease, Fisher and Caplan described branch atheromatous disease (BAD) as another mechanism of lacunar‐type infarcts that involves obstruction of penetrator artery orifices by atheroma of the parent vessel or microatheroma originating at the branch point.^{7, 8} END is frequently reported in lacunes with BAD, but the definition for BAD‐related lacune varied across studies and is often radiographically inferred by lacune characteristics, not direct evidence of atheroma.⁹

Therefore, a better understanding of clinical and radiographic risk factors for END in lacunar infarct may help elucidate the underlying pathophysiological features and predict patients at high risk for deterioration. In this present study, we sought to determine the association between radiographic parent vessel luminal stenosis (<50%) and END following an acute lacunar stroke.

 

Asymmetrical cortical vein sign predicts early neurological deterioration in acute ischemic stroke patients with severe intracranial arterial stenosis or occlusion

 Under what scenario did you think anything here is going to get survivors recovered? SOLVE STROKE YOU BLITHERING IDIOTS, PREDICTIONS ARE USELESS.  I would fire the lot of you.

Asymmetrical cortical vein sign predicts early neurological deterioration in acute ischemic stroke patients with severe intracranial arterial stenosis or occlusion

• Wei Li,
• Wei-Min Xiao,
• Gen-Pei Luo,
• Yong-Lin Liu,
• Jian-Feng Qu,
• Xue-Wen Fang,
• Fang Wang &
• Yang-Kun Chen 

BMC Neurology volume 20, Article number: 331 (2020) Cite this article

Abstract

Background

Susceptibility weighted imaging (SWI) provides an approximate assessment of tissue perfusion and shows prominent hypointense cortical veins in the ischemic territory because of the increased concentration of deoxyhemoglobin. We aimed to evaluate whether asymmetrical prominent cortical vein sign (APCVS) on SWI can predict early neurological deterioration (END) in acute ischemic stroke patients with severe intracranial arterial stenosis or occlusion (SIASO).

Methods

One hundred and nine acute ischemic stroke patients with SIASO who underwent SWI were retrospectively recruited. END was defined as an increase in the National Institutes of Health Stroke Scale score ≧2 points despite standard treatment in the first 72 h after admission. The APCVS was defined as more and/or large vessels with greater signal loss than those in the opposite hemisphere on SWI.

Results

Thirty out of the 109 (27.5%) patients developed END. Sixty (55.0%) patients presented with APCVS on SWI. APCVS occurred in 24 (80%) patients with END, whereas it only occurred in 36 (45.6%) patients without END (P = 0.001). Patients with APCVS were more likely to have END (40.0%, vs. 12.2%, P = 0.001) than those without END. Multivariate logistic regression indicated that APCVS (OR = 4.349, 95% C.I. = 1.580–11.970, P = 0.004) was a significant predictor of END in acute ischemic stroke patients with SIASO, adjusted for previous stroke history and acute infarct volume.

Conclusions

In acute ischemic stroke patients with SIASO, the APCVS might be a useful neuroimaging marker for predicting END, which suggests the importance of evaluation of perfusion status.

 

Asymmetrical cortical vein sign predicts early neurological deterioration in acute ischemic stroke patients with severe intracranial arterial stenosis or occlusion

 So fucking what? Predictions are useless to survivors, they want protocols that lead directly to recovery. If you can't even do the correct type of stroke research, get out and let better people in. Solve problems, don't just lazily describe them.

Oops, I'm not playing by the polite rules of Dale Carnegie,  'How to Win Friends and Influence People'. 

Politeness will never solve anything in stroke. Yes, I'm a bomb thrower and proud of it. Someday a stroke 'leader' will ream me out for making them look bad by being truthful , I look forward to that day.

Asymmetrical cortical vein sign predicts early neurological deterioration in acute ischemic stroke patients with severe intracranial arterial stenosis or occlusion

• Wei Li,
• Wei-Min Xiao,
• Gen-Pei Luo,
• Yong-Lin Liu,
• Jian-Feng Qu,
• Xue-Wen Fang,
• Fang Wang &
• Yang-Kun Chen 

BMC Neurology volume 20, Article number: 331 (2020) Cite this article

• 4 Accesses

• 10 Altmetric

• Metrics details

Abstract

Background

Susceptibility weighted imaging (SWI) provides an approximate assessment of tissue perfusion and shows prominent hypointense cortical veins in the ischemic territory because of the increased concentration of deoxyhemoglobin. We aimed to evaluate whether asymmetrical prominent cortical vein sign (APCVS) on SWI can predict early neurological deterioration (END) in acute ischemic stroke patients with severe intracranial arterial stenosis or occlusion (SIASO).

Methods

One hundred and nine acute ischemic stroke patients with SIASO who underwent SWI were retrospectively recruited. END was defined as an increase in the National Institutes of Health Stroke Scale score ≧2 points despite standard treatment in the first 72 h after admission. The APCVS was defined as more and/or large vessels with greater signal loss than those in the opposite hemisphere on SWI.

Results

Thirty out of the 109 (27.5%) patients developed END. Sixty (55.0%) patients presented with APCVS on SWI. APCVS occurred in 24 (80%) patients with END, whereas it only occurred in 36 (45.6%) patients without END (P = 0.001). Patients with APCVS were more likely to have END (40.0%, vs. 12.2%, P = 0.001) than those without END. Multivariate logistic regression indicated that APCVS (OR = 4.349, 95% C.I. = 1.580–11.970, P = 0.004) was a significant predictor of END in acute ischemic stroke patients with SIASO, adjusted for previous stroke history and acute infarct volume.

Conclusions

In acute ischemic stroke patients with SIASO, the APCVS might be a useful neuroimaging marker for predicting END(What the hell are you doing to fix this problem? Predictions are useless), which suggests the importance of evaluation of perfusion status.

 

 

Medical therapy may prevent strokes in asymptomatic carotid stenosis

 I personally think that the proper solution to this is:

1. Determine if Circle of Willis is complete.

2. If yes, then close up the offending artery, no chance of throwing clots to brain, no stroke risk from carotid endarterectomy.

But I'm not medically trained so don't listen to me, but have your doctor GUARANTEE NO STROKE FROM ANY INTERVENTION CHOSEN. 

'May' is way too wishy-washy.

Medical therapy may prevent strokes in asymptomatic carotid stenosis

Absolute risk reduction for fatal and nonfatal strokes in patients who underwent early carotid endarterectomy was less than half the risk difference from trials initiated 20 years ago, researchers found.

The study published in JAMA Neurology also determined that this absolute reduction was no longer statistically significant when accounting for the competing risk for nonstroke deaths.

 

“Given the upfront perioperative risks associated with carotid endarterectomy, initial medical therapy may be an equally acceptable treatment strategy for the management of patients with asymptomatic carotid stenosis,” Salomeh Keyhani, MD, MPH, professor of medicine at University of California, San Francisco, School of Medicine, and colleagues wrote.

In this comparative effectiveness study, researchers assessed data from 5,221 veterans aged at least 65 years who underwent carotid imaging from 2005 to 2009. Patients were excluded if they had carotid stenosis less than 50%, hemodynamically insignificant stenosis and a history of transient ischemic attack or stroke 6 months before imaging was performed.

Two cohorts were formed: patients assigned initial medical therapy (n = 2,509; mean age, 74 years; 99% men) and those assigned carotid endarterectomy (n = 2,712; mean age, 74 years; 99% men). Both treatment options were given within 1 year after index carotid imaging. Follow-up was conducted for 5 years. Analyses used in the Asymptomatic Carotid Surgery Trial were emulated in this trial to estimate the comparative effectiveness of carotid endarterectomy and initial medical therapy to prevent nonfatal and fatal strokes.

The rate of stroke or death within 30 days of carotid endarterectomy was 2.5% (95% CI, 2-3.1). At 5 years, the risk for fatal and nonfatal stroke was lower in the carotid endarterectomy group vs. the initial medical therapy group (5.6% vs. 7.8%; risk difference, 2.3%; 95% CI, 4 to 0.3).

When the competing risk for death was incorporated, the risk difference between patients assigned carotid endarterectomy and those assigned initial medical therapy was lower and not statistically significant (risk difference, 0.8%; 95% CI, 2.1 to 0.5).

In patients who met randomized controlled trial inclusion criteria, the risk for fatal and nonfatal strokes at 5 years was 5.5% (95% CI, 4.5-6.5) for the carotid endarterectomy group and 7.6% (95% CI, 5.7-9.5) for the initial medical therapy group (risk difference, 2.1%; 95% CI, 4.4 to 0.2). A risk difference of 0.9% resulted when accounting for competing risks (95% CI, 2.9 to 0.7).

“The decreased stroke risk in patients with carotid artery stenosis, the persistent upfront perioperative risks and the small difference in stroke risk between the two treatment strategies suggest that patients treated with carotid endarterectomy would now require a longer time to accrue enough stroke reduction benefit to justify the upfront risks of the surgical procedure,” Keyhani and colleagues wrote.

 

Prevalence of high-risk plaques and risk of stroke in patients with asymptomatic carotid stenosis: A meta-analysis

 Tells us nothing useful. If you are asymptomatic how would you even have a clue to get tested?  I was totally asymptomatic, yet I must have had high risk plaques since I broke one loose during a whitewater canoeing trip(common for me).  

Would this work? And how many hospitals/clinics have access to these?

Lasers used to detect risk of heart attack and stroke

New developments in the detection of vulnerable plaque 2001

 

The latest here:

Prevalence of high-risk plaques and risk of stroke in patients with asymptomatic carotid stenosis: A meta-analysis

A Meta-analysis

Joseph Kamtchum-Tatuene, MD¹; Jean Jacques Noubiap, MD²; Alan H. Wilman, PhD³; et al Maher Saqqur, MD⁴; Ashfaq Shuaib, MD⁴; Glen C. Jickling, MD⁴

Author Affiliations

JAMA Neurol. Published online August 3, 2020. doi:10.1001/jamaneurol.2020.2658

Key Points

Question  Is it relevant and feasible to use multimodal neurovascular imaging to perform a risk-oriented selection for revascularization in patients with asymptomatic carotid stenosis?

Findings  In this meta-analysis of 64 studies that enrolled 20 751 participants, high-risk plaques were common in patients with asymptomatic carotid stenosis, and the associated annual incidence of ipsilateral ischemic events (4 events per 100 person-years) was higher than the currently accepted estimates.

Meaning  This study’s findings indicate that extending the assessment of asymptomatic carotid stenosis beyond the grade of stenosis is needed in routine practice to improve risk stratification and optimize therapy; clinical trials using multimodal neurovascular imaging for risk stratification before randomization are warranted to evaluate optimal strategies for stroke prevention in patients with asymptomatic carotid stenosis.

Abstract

Importance  There is an ongoing debate regarding the management of asymptomatic carotid stenosis. Previous studies have reported imaging features of high-risk plaques that could help to optimize the risk-benefit ratio of revascularization. However, such studies have not provided an accurate estimate of the prevalence of high-risk plaques and the associated annual incidence of ipsilateral ischemic cerebrovascular events to inform the design of clinical trials using a risk-oriented selection of patients before randomization.

Objective  To assess the relevance and feasibility of risk-oriented selection of patients for revascularization.

Data Sources  A systematic search of PubMed and Ovid Embase from database inception to July 31, 2019, was performed.

Study Selection  Prospective observational studies that reported prevalence of high-risk plaques and incidence of ipsilateral ischemic cerebrovascular events were included.

Data Extraction and Synthesis  Aggregated data were pooled using random-effects meta-analysis. Data were analyzed from December 16, 2019, to January 15, 2020.

Main Outcomes and Measures  Prevalence of high-risk plaques and annual incidence of ipsilateral ischemic events.

Results  Overall, 64 studies enrolling 20 751 participants aged 29 to 95 years (mean age range, 55.0-76.5 years; proportion of men, 45%-87%) were included in the meta-analysis. Among all participants, the pooled prevalence of high-risk plaques was 26.5% (95% CI, 22.9%-30.3%). The most prevalent high-risk plaque features were neovascularization (43.4%; 95% CI, 31.4%-55.8%) in 785 participants, echolucency (42.3%; 95% CI, 32.2%-52.8%) in 12 364 participants, and lipid-rich necrotic core (36.3%; 95% CI, 27.7%-45.2%) in 3728 participants. The overall incidence of ipsilateral ischemic cerebrovascular events was 3.2 events per 100 person-years (22 cohorts with 10 381 participants; mean follow-up period, 2.8 years; range, 0.7-6.5 years). The incidence of ipsilateral ischemic cerebrovascular events was higher in patients with high-risk plaques (4.3 events per 100 person-years; 95% CI, 2.5-6.5 events per 100 person-years) than in those without high-risk plaques (1.2 events per 100 person-years; 95% CI, 0.6-1.8 events per 100 person-years), with an odds ratio of 3.0 (95% CI, 2.1-4.3; I² = 48.8%). In studies focusing on severe stenosis (9 cohorts with 2128 participants; mean follow-up period, 2.8 years; range, 1.4-6.5 years), the incidence of ipsilateral ischemic cerebrovascular events was 3.7 events per 100 person-years (95% CI, 1.9-6.0 events per 100 person-years). The incidence of ipsilateral ischemic cerebrovascular events was also higher in patients with high-risk plaques (7.3 events per 100 person-years; 95% CI, 2.0-15.0 events per 100 person-years) than in those without high-risk plaques (1.7 events per 100 person-years; 95% CI, 0.6-3.3 events per 100 person-years), with an odds ratio of 3.2 (95% CI, 1.7-5.9; I² = 39.6%).

Conclusions and Relevance  High-risk plaques are common in patients with asymptomatic carotid stenosis, and the associated risk of an ipsilateral ischemic cerebrovascular event is higher than the currently accepted estimates. Extension of routine assessment of asymptomatic carotid stenosis beyond the grade of stenosis may help improve risk stratification and optimize therapy.

Carotid artery calcification score and its association with cognitive impairment

I assume my calcification score would be off the charts since my right carotid artery is completely blocked. I don't think I'm cognitively impaired, but then if I truly am cognitively impaired I would think I'm ok.  Being so stupid you don't realize you are stupid.  Oh well, I'm happy in my stupidity and stroke impairments.

Carotid artery calcification score and its association with cognitive impairment

Clinical Interventions in Aging — Chu Z, et al. | January 22, 2019

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In carotid artery stenosis (CAS) patients, researchers retrospectively examined the possible relationship between carotid artery calcification score (CS) and cognitive impairment. Using Color Doppler ultrasound, multi-detector row spiral CT angiography and MRI scanning, carotid artery was measured in 102 patients with cervical carotid arteries. A significant correlation was found between carotid artery CSs and cognitive scores, making CS a possible risk factor for early screening of cognitive impairment in CAS patients. The possible mechanism could be linked to the effect of the calcification on the plaque burden.

Read the full article on Clinical Interventions in Aging

Transatlantic Differences in Management of Carotid Stenosis: BRIDGing the Gap in StrokE Management (BRIDGE) Project

You can't even discuss the options if your doctor doesn't identify it as a problem. My doctors never found the 80% blockage in my right carotid artery even though they told me that artery had dissected and thrown a clot into my brain. Not sure what orifice they pulled that knowledge out of. 

Transatlantic Differences in Management of Carotid Stenosis: BRIDGing the Gap in StrokE Management (BRIDGE) Project

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Clotilde Balucani, MD, PhD¹

Clotilde Balucani

1The Department of Neurology and Stroke Center, Downstate Medical Center, The State University of New York, SUNY, Brooklyn, New York, NY, USA
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, Vanessa Arnedo, MPH¹

Vanessa Arnedo

1The Department of Neurology and Stroke Center, Downstate Medical Center, The State University of New York, SUNY, Brooklyn, New York, NY, USA
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, Jeremy Weedon, PhD²

Jeremy Weedon

2The Department of Public Health, SUNY Downstate Medical Center, Brooklyn, New York, NY, USA
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,

Didier Leys, MD³

Didier Leys

3The Department of Neurology, Lille University Hospital, Lille, France
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, Jean-Louis Mas, MD⁴

Jean-Louis Mas

4Neurology Department and Stroke Unit, INSERM UMR S 894, Sainte-Anne Hospital, Paris Descartes University, Paris, France
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, Martin Brown, MD⁵

Martin Brown

5 The Stroke Research Group, UCL Institute of Neurology, London, UK
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, James C. Grotta, MD⁶

James C. Grotta

6Stroke Research, Memorial Hermann Hospital, Houston, TX, USA
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, Nicole R. Gonzales, MD⁷

Nicole R. Gonzales

7The Department of Neurology, UTHealth Medical School, Houston, TX, USA
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, Werner Hacke, MD⁸

Werner Hacke

8The Department of Neurology, Heidelberg, Germany
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, Thomas Brott, MD⁹

Thomas Brott

9The Department of Neurology, The Mayo Clinic, Jacksonville, FL, USA
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, Steven R. Levine, MD¹

Steven R. Levine

1The Department of Neurology and Stroke Center, Downstate Medical Center, The State University of New York, SUNY, Brooklyn, New York, NY, USA
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...

First Published January 17, 2018 Research Article

https://doi.org/10.1177/1941874417747772

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Article Information

Article first published online: January 17, 2018

https://doi.org/10.1177/1941874417747772

Clotilde Balucani, MD, PhD¹, Vanessa Arnedo, MPH¹, Jeremy Weedon, PhD², Didier Leys, MD³, Jean-Louis Mas, MD⁴, Martin Brown, MD⁵, James C. Grotta, MD⁶, Nicole R. Gonzales, MD⁷, Werner Hacke, MD⁸, Thomas Brott, MD⁹, Steven R. Levine, MD¹

¹The Department of Neurology and Stroke Center, Downstate Medical Center, The State University of New York, SUNY, Brooklyn, New York, NY, USA

²The Department of Public Health, SUNY Downstate Medical Center, Brooklyn, New York, NY, USA

³The Department of Neurology, Lille University Hospital, Lille, France

⁴Neurology Department and Stroke Unit, INSERM UMR S 894, Sainte-Anne Hospital, Paris Descartes University, Paris, France

⁵ The Stroke Research Group, UCL Institute of Neurology, London, UK

⁶Stroke Research, Memorial Hermann Hospital, Houston, TX, USA

⁷The Department of Neurology, UTHealth Medical School, Houston, TX, USA

⁸The Department of Neurology, Heidelberg, Germany

⁹The Department of Neurology, The Mayo Clinic, Jacksonville, FL, USA

Corresponding Author: Clotilde Balucani, Department of Neurology and Stroke Center, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, New York, NY 11203, USA. Email: clotilde.balucani@downstate.edu

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Abstract

Background and Purpose:

Management of carotid stenosis remains controversial despite several trials evaluating carotid endarterectomy (CEA) and carotid angioplasty/stenting (CAS). We compared attitudes in the management of carotid stenosis between selected experts within Europe and North America.

Methods:

A 3-phase Delphi survey was e-mailed to select stroke experts from Europe (n = 390) and North America (n = 289). Those completing the initial survey were shown all responses after each survey round. Consensus was defined as ≥80% agreement.

Results:

For phases 1, 2, and 3, response rates were 32%, 62%, and 73%, respectively. Overall, 100 (15%) of 679 participated in all 3 phases, 19% Europeans versus 9% North Americans (P = .0007). The European group reached consensus in 6 of 15 statements; The North American group reached consensus in 4 of 15. Ninety percentage of Europeans versus 70% of North Americans (P = .017) stated CEA is superior to CAS for symptomatic carotid stenosis. This difference was not significant in the final model (adjusted odds ratio: 3.72 [95% confidence interval: 0.95-14.5]). Sixty-nine percentage of North Americans agreed there is a stronger indication for CAS over CEA in patients younger than 65 years for symptomatic carotid stenosis, whereas 55% of Europeans (P = .023) disagreed. For asymptomatic carotid stenosis, when asked how likely they would recommend CAS, 62% North Americans said “sometimes” versus 60% of Europeans said “never” (P = .06).

Conclusion:

The majority of North American and European respondents did not consider the 2 procedures equivalent and seemed to indicate that CEA was preferred for the management of carotid stenosis. These findings need to be further explored to help establish evidence-based guidelines.

Carotid artery stenosis in people at high risk: treatment options.

My doctors never found my 80% blockage of my carotid artery so for three years I was at high risk for another stroke until that artery completely closed up.

Carotid artery stenosis in people at high risk: treatment options.

What is a Patient Decision Aid?

Patient decision aids are tools that help patients, care-givers and families become involved in decision making around difficult health care issues. They are designed to complement, rather than replace, the advice given by a health care practitioner.
Got It, Hide this

• Rating:

• Website: OHRI
• Resource type: Patient decision aid

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Summary - The message of this resource is:

This patient decision aid helps people with serious heart, lung or kidney problems or who are over 80 years old decide on the treatment methods for blocked or narrowed carotid arteries. It facilitates the process by outlining and comparing the three treatment options: taking medicines, stenting and taking medicines, and surgery and taking medicines.

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Keywords

Carotid artery stenosis, medicine, stenting, surgery

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Circulation conditio

Vigorous walking three to five times each week decreases the chance of recurrent stroke by fivefold in patients with narrowed arteries in the brain

So your doctor and therapists need to get you recovered well enough from your stroke to get you to vigorous walking. But I bet they have dumbed down goals of just getting you walking with assistance. Your patient centered goal is 100% recovery regardless of what your fucking doctor tells you can be accomplished. Don't pay her/him unless you achieve that goal. 

Vigorous walking three to five times each week decreases the chance of recurrent stroke by fivefold in patients with narrowed arteries in the brain

Research shows moderate to vigorous physical activity is by far the strongest predictor of an improved outcome in people who have suffered a stroke.

Vigorous walking three to five times each week decreases the chance of recurrent stroke by fivefold in patients with narrowed arteries in the brain, report investigators at the Medical University of South Carolina in an article in Neurology.

The results, published in the January 24 issue, involved patients with symptoms of intracranial stenosis, the narrowing of arteries in the brain, which is the most common cause of stroke worldwide. 

Dr. Tanya Turan tells patients with intracranial stenosis that exercise can have a big impact on improving their health.

The investigators analyzed three-year follow-up data for 227 patients who had been randomized to the intensive medical management arm of the MUSC-led Sammpris or stenting versus aggressive medical therapy for intracranial stenosis trial. Enrollment in the Sammpris trial, which was designed to evaluate whether stenting plus intensive medical management or intensive medical management alone was more effective at preventing recurrent stroke in these patients, was stopped early, in 2011, for safety reasons because patients in the stenting arm had a 2 ½ times higher 30-day rate of stroke or death than those in the intensive medical therapy arm. 

Follow-up continued, however, to evaluate the role of risk factor control in preventing recurrent stroke, and those findings are presented in the Neurology article. 

Reaching targets for systolic blood pressure (<140 mmHg, < 130 mmHg for diabetics) and low-density lipoprotein cholesterol (<70 mg/d) significantly reduced the risk of secondary stroke, myocardial infarction or a vascular event. Approximately half of the study participants met these targets on average during the study. Those who did not were about twice as likely to experience a recurrent stroke, heart attack or vascular event. 

However, moderate to vigorous physical activity was by far the strongest predictor of an improved outcome. Indeed, patients who did not regularly engage in moderate to vigorous exercise were up to five times as likely to experience a recurrent stroke or other vascular event. 

How much exercise was needed to attain benefit? “At least vigorous walking for about 30 minutes, three to five times each week,” says Tanya Turan, M.D., director of the MUSC Stroke Division and lead author of the article. 

Study participants self-reported exercise using the 6-point Patient-Centered Assessment and Counseling for Exercise, or PACE, score. Those who scored above 3 met the target for physical activity and received benefit. Moderate exercise was defined as brisk walking or slow cycling for at least 10 minutes at a time, and vigorous activity as jogging or fast cycling for at least 20 minutes at a time.

There was evidence for a dose-dependent effect with exercise, with greater protection from vascular events seen with more exercise. All study participants were enrolled free of charge in a commercially available lifestyle modification program, which included regular coaching on healthy lifestyle behaviors. 

Control of other risk factors, such as smoking, body mass index and glycated hemoglobin, did not significantly affect vascular outcomes.

This is the first report showing an association between exercise and prevention of recurrent stroke. The current American Heart guidelines for patients with intracranial stenosis recommend lowering blood pressure and cholesterol but do not mention exercise. Turan believes that, given these findings, the next version of the guidelines may be more supportive of exercise for secondary stroke prevention in patients with intracranial stenosis. 

“When I counsel my patients with this condition, I talk with them about those two primary risk factors, blood pressure and cholesterol, but also mention the impact of exercise and tell them that they can do it without having to take an extra pill and that it could have the biggest impact,” Turan says. 

While it is true that stroke patients can have physical or emotional barriers to exercise, including stroke-related disability or depression, this analysis demonstrates that access to a lifestyle modification program can substantially increase their willingness to exercise. The percentage of study participants who were at target for physical activity increased from 32 percent at study entry to 56 percent by the four-month follow-up visit.

Lifestyle modification programs, such as the one used in the study, are commercially available and can be used to help motivate stroke patients to meet exercise targets. These programs can cost $400 to $500 annually and may be out of the reach of some patients; however, insurance reimburses for these costs in some cases. For patients who cannot afford to participate in a formal lifestyle modification program, physicians and their health care staff can work toward the same goal by consistently encouraging exercise in order to prevent recurrent stroke. Many hospitals also offer cardiac and stroke rehabilitation services that promote exercise.

Turan has a simple message for physicians.

“Tell your patients to exercise,” she says. “Think outside of the pillbox.”

Systemic infusion and local irrigation with argatroban effective in preventing clot formation during carotid endarterectomy in a patient with heparin-induced thrombocytopenia.

What I don't understand is why with that blockage the solution isn't just to completely close it up as long as the Circle of Willis is complete rather than go through the risks of endarterectomy? But I have no medical training so someone with that could explain why I'm wrong.
http://dgcases.docguide.com/systemic-infusion-and-local-irrigation-argatroban-effective-preventing-clot-formation-during-carotid?overlay=2&

A therapeutic dilemma exists when patients with symptomatic carotid stenosis and concomitant heparin-induced thrombocytopenia (HIT) are advised to urgently undergo carotid endarterectomy (CEA) with heparin therapy. After a 63-year-old man with HIT and multiple medical comorbidities underwent emergent coronary artery bypass grafting, postoperative imaging revealed plaque at the origin of the left internal carotid artery with 80%-99% stenosis and minimal contralateral internal carotid artery disease. During the patient's evaluation to undergo CEA for symptomatic high-grade carotid stenosis, enzyme-linked immunosorbent assay revealed persistent platelet factor 4 antibodies. The endarterectomy was successfully performed while the patient received argatroban, both as a continuous infusion and intermittent irrigation during dissection of the plaque. Postoperatively, the drip was continued for 24 hours, and the patient was discharged day 2 on a daily dose of 325 mg of aspirin. At the 6-month examination, Doppler ultrasound revealed normal anterograde velocities with no evidence of stenosis, and the patient noted no subsequent ischemic events. We now recommend systemic intravenous and local argatroban irrigation to prevent thromboembolic complications in CEA cases with HIT and renal insufficiency. Bivalirudin for both systemic intravenous use and local irrigation may be safer in patients without renal insufficiency because of its shorter half-life.

from: Department of Neurosurgery, University of Cincinnati College of Medicine and Comprehensive Stroke Center at University of Cincinnati Neuroscience Institute, Cincinnati, Ohio, USA.

as reported in: Serrone JC, Andaluz N, Brink V, Zuccarello M, Ware SL. World Neurosurg. 2013 Jul-Aug:80(1-2):222.e15-8. doi: 10.1016/j.wneu.2013.01.037.

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TCAR procedure offers potentially safer method for high-risk stroke patients - carotid artery cleanout

Just in case you need to go down this route.

TCAR procedure offers potentially safer method for high-risk stroke patients - carotid artery cleanout

The carotid arteries supply oxygenated blood to the brain. Every year, more than 300,000 people in the United States are diagnosed with blockages, or plaques, in their carotid artery. When these arteries become blocked due to plaque build-up, an individual is at high risk for a stroke if the plaque ruptures and flows to the brain. Many individuals can manage carotid artery disease with medications and lifestyle changes. However, many may require carotid artery revascularization surgery to repair the blockage in the artery. Carotid endarterectomy has been the gold standard of treatment with carotid stenting reserved for those who are high risk for open surgery. While largely effective in some patients, carotid stenting from the transfemoral route has been found to carry a higher risk of stroke, with a significant amount of this risk felt to be related to the approach.
The FDA recently approved a new Transcarotid Artery Revascularization (TCAR) procedure that utilizes the ENROUTE® Transcarotid Neuroprotection and Stent System from Silk Road Medical. The TCAR procedure offers patients a potentially safer method of carotid stenting through a small cut down at the base of the neck and direct carotid artery access along with neuro-protective flow reversal during delivery of the stent. The Minneapolis Heart Institute Foundation® (MHIF) was selected as the only center in the four state area to participate in the ROADSTER 2 Study. Jessica Titus, MD, and Timothy Sullivan, MD, vascular surgeons at the Minneapolis Heart Institute® at Abbott Northwestern Hospital, will serve as Principal Investigator and Co-Investigator, respectively, for the trial. "We are excited to be able to bring this carotid artery revascularization option to our patients. It combines the advantages of a minimally invasive approach for high risk patients with a lower stroke risk than the standard method for carotid stent placement." said Dr. Titus.

The ENROUTE Transcarotid Neuroprotection System utilizes robust flow reversal during transcarotid stent placement to remove micro and macro emboli throughout the intervention. Erica Rogers, CEO of Silk Road Medical notes, "We selected the staff and researchers at MHIF as a key trial partner because they have the vascular surgery and research expertise we need to participate in this important study and provide this less invasive and more efficient TCAR procedure for their patients presenting with carotid artery disease." The first registry trial participant at MHIF is scheduled for first quarter 2016. In total, the ROADSTER2 study will assess the real world treatment of individuals at risk for stroke due to carotid artery disease with the ENROUTE® Transcarotid Neuroprotection (NPS) and Stent System with a minimum of 600 participants around the country.

Source:

Minneapolis Heart Institute Foundation

Meta-Analysis of Randomized Controlled Trials Comparing the Long-Term Outcomes of Carotid Artery Stenting Versus Endarterectomy

For those of you with partially blocked arteries. My right carotid is completely blocked and the left one is clear. It's all good because obviously my Circle of Willis is complete.
http://circoutcomes.ahajournals.org/content/8/6_suppl_3/S99.abstract?etoc

1. Sophie Vincent,
2. Maria Eberg, MSc,
3. Mark J. Eisenberg, MD, MPH and
4. Kristian B. Filion, PhD

+ Author Affiliations

1. From the Center for Clinical Epidemiology, Lady Davis Institute (S.V., M.E., M.J.E., K.B.F.) and Division of Cardiology (M.J.E.), Jewish General Hospital, Montreal, Quebec, Canada; and Faculty of Medicine (S.V., M.J.E., K.B.F.), Department of Epidemiology, Biostatistics, and Occupational Health (M.J.E., K.B.F.), Division of Cardiology (M.J.E.), and Division of Clinical Epidemiology, Department of Medicine (K.B.F.), McGill University, Montreal, Quebec, Canada.

1. Correspondence to Kristian B. Filion, PhD, Division of Clinical Epidemiology, Jewish General Hospital, McGill University, 3755 Cote Ste-Catherine Rd, Suite H416.1, Montreal, Quebec, Canada. E-mail kristian.filion@mcgill.ca

Abstract

Background—Stenting is an endovascular alternative to endarterectomy for the management of carotid stenosis, but its long-term safety and efficacy relative to endarterectomy remain unclear. Our objective was to compare the safety and efficacy of stenting with those of endarterectomy, with a particular focus on long-term outcomes, via meta-analysis of randomized controlled trials (RCTs).

Methods and Results—We systematically searched PubMed, EMBASE, MEDLINE, and the Cochrane Library for RCTs with ≥50 patients that compared stenting with endarterectomy in patients with carotid stenosis. Periprocedural and long-term outcomes were assessed, with data pooled across RCTs using random-effects models. Eight RCTs were included in our meta-analysis (n=7091), with follow-up ranging from 2.0 to 10.0 years. When compared with endarterectomy, stenting was associated with an increased risk of periprocedural stroke (relative risk, 1.49, 95% confidence interval [CI], 1.11 to 2.01; risk difference, 1.7%; 95% CI, 0.3 to 3.0) but a decreased risk of periprocedural myocardial infarction (relative risk, 0.47; 95% CI, 0.29 to 0.78; risk difference, −0.4%; 95% CI, −0.8% to 0.1%). During long-term follow-up, stenting was associated with an increased risk of stroke (relative risk, 1.36; 95% CI, 1.16 to 1.61) and a composite end point of ipsilateral stroke, periprocedural stroke, or periprocedural death (relative risk, 1.45; 95% CI, 1.20 to 1.75).

Conclusions—Although stenting has more favorable periprocedural outcomes with respect to myocardial infarction, the observed increased risk of stroke and death throughout follow-up with stenting suggests that endarterectomy remains the treatment of choice for carotid stenosis.

Use of Stent Increases Risk of Stroke in Patients With Intracranial Arterial Stenosis

Be careful out there.
http://dgnews.docguide.com/use-stent-increases-risk-stroke-patients-intracranial-arterial-stenosis?overlay=2&
Among patients with symptomatic intracranial arterial stenosis, the use of a balloon-expandable stent compared with medical therapy resulted in an increased risk of stroke or transient ischemic attack (TIA), according to a study published in the March 24/31 issue of JAMA.
Intracranial arterial stenosis is a common cause of stroke worldwide. The recurrent stroke risk with severe symptomatic intracranial stenosis may be as high as 23% at 1 year, despite medical therapy, according to Osama O. Zaidat, MD, Medical College of Wisconsin/Froedtert Hospital, Milwaukee, Wisconsin, and colleagues.

But they don't explain whether the strokes were downstream or close to the stent or in a completely different area. Don't these people know how to analyze cause and effect? If someone has stenosis it is probably throughout the brain so a stroke would be likely regardless of fixing one particular spot.

Stroke Rounds: USPSTF Says Carotid Screening Overused

Well the lack of information and vigorous thinking continues. After my dad had his carotid endarterectomy, his doctor should have known what the chances were that any children might have problems. My doctor who finally did an ultrasound on my carotids 3 years post stroke found that my right carotid had totally closed up. His thought was that it probably was 80% clogged at the time of the stroke. With the knowledge that maybe I should have had my carotids scanned, my stroke was totally preventable. In a complete failure of hospital procedures my carotid blockage was never found or looked for. So for 3 years I was at an extremely high risk of dissecting the exact same artery again.  But I managed to miss that bullet which is why I can be a complete pain in the ass right now to all things stroke related. But don't listen to me, I'm not medically trained and thus should just shut up and die. Have fun people, I am. This is probably more against those independent traveling clinics like Lifeline because they are outside of the normal medical channels.

Stroke Rounds: USPSTF Says Carotid Screening Overused

The U.S. Preventive Services Task Force (USPSTF) has reaffirmed its recommendation against screening asymptomatic adults(I was asymptomatic)  in the general population for carotid artery stenosis, draft guidance showed.
After an updated review of the evidence, the USPSTF concluded "with moderate certainty that the harms of screening for asymptomatic carotid artery stenosis outweigh the benefits."
The recommendation against screening is consistent with the task force's previous 2007 guidance on the topic, as well as guidelines from other major organizations, including the American Heart Association/American Stroke Association and the American College of Cardiology.
Several factors contribute to the consensus that routine screening isn't a good idea.
Studies indicate that the prevalence of carotid artery stenosis is low in the general population, at 1% or lower. When stenosis is present, few cases actually trigger a stroke, and there are no reliable ways to identify the problematic cases.(Has any research been done at all? With the correct amount of data this question could be easily solved. Stop throwing up your hands and accepting defeat at the slightest bump. In my organization you would be fired for that defeatist attitude.)

More at link

Early Detection for Maximizing Stroke Prevention

I couldn't really see what help this could be but your doctor should be subscribing to this and can tell you how it affects your case.

Early Detection for Maximizing Stroke Prevention

Only 1 page at this link, your doctor will have the rest.

Ischemic preconditioning tested in stroke patients

You'll have to question your doctor on why this works and if you might be a candidate.  What is the theory behind why this might work?
http://www.news-medical.net/news/20121010/Ischemic-preconditioning-tested-in-stroke-patients.aspx
Inducing repeated brief ischemia in the arms may reduce the rate of recurrent stroke in patients with symptomatic intracranial arterial stenosis, a small clinical study shows.
Recurrent stroke rates were just 5.0% after 90 days and 7.9% after 300 days of treatment, compared with 23.3% and 26.7%, respectively, in the control group, report Xunming Ji (Xuanwu Hospital, Beijing, China) and colleagues in Neurology.
Initially, 103 patients entered the study and were randomly assigned to active or control treatment. The device used was designed specifically for the study. It has two tourniquets, similar to blood pressure cuffs, which, once applied, inflate and deflate according to a preprogrammed schedule to induce five cycles of bilateral upper limb ischemia for 5 minutes followed by 5 minutes of reperfusion.

 More at link.

Juxtaluminal Black Area in Carotid Artery Plaques May Predict Strokes

I wish they would put a picture in here with pointer arrows.

Juxtaluminal Black Area in Carotid Artery Plaques May Predict Strokes

  Researchers from the Imperial College Faculty of Medicine in London in the United Kingdom (S Kakkos, M Griffin, A Nicolaides, E Kyriacou, M Sabetai, T Tegos, G Geroulakos) revealed that the presence and size of a juxtaluminal black (hypoechoic) area (JBA) on carotid ultrasound of asymptomatic carotid artery plaques can predict the occurrence of ipsilateral ischemic stroke. Their findings were explained today at the 66th Vascular Annual Meeting presented by the Society for Vascular Surgery®.


Co-author Stavros K. Kakkos, MD, MSc, PhD, RVT, who also is in the Department of Vascular Surgery at the University Hospital of Patras in Patras, Greece, said that the JBA is associated with a lipid core close to the lumen or a thrombus on the plaque surface and is defined as an area of carotid plaque pixels with gray scale median (GSM) value less than 25 which is adjacent to the vessel lumen and lacks a visible echogenic cap, after image normalization of the ultrasound plaque images.

This is the best I can find of images; unreadably pathetic.



The size of a JBA was measured in the carotid plaque images of 1,121 patients with asymptomatic carotid stenosis that was 50-99 percent in relation to the bulb which was followed for up to eight years. “We confirmed that JBA had a linear association with future stroke rate,” said Dr. Kakkos. “The area under the ROC curve was 0.816. Using Kaplan Meier curves, the mean annual stroke rate was 0.4 percent in 706 patients with a JBA size <4 mm2, 1.4 percent in 171 patients with JBA size 4-8 mm2, 3.2 percent in 46 patients with JBA size 8-10 mm2, and 5 percent in 198 patients with JBA size >10 mm2 with a highly significant statistical significance (P<.001).”


In multivariate analysis using a Cox model with ipsilateral ischemic events (amaurosis fugax, transient ischemic attack [TIA] or stroke) as the dependent variable, JBA (<4, 4-8, >8, in mm2) was still significant after adjusting for other plaque features known to be associated with increased risk. These include stenosis, GSM, presence of discrete white areas without acoustic shadowing (DWA) indicating neovascularization, plaque area and history of contralateral TIA or stroke. However, plaque area and GSM were not significant.


Using the significant variables (stenosis, DWA, JBA and history of contralateral TIA or stroke), this model predicted the annual risk of stroke (range 0.5-10.0 percent). The average annual stroke risk was <1 percent in 734 patients; 1-1.9 percent in 94; 2-3.9 percent in 134; 4-5.9 percent in 125; and 6-10 percent in 34.


“The size of JBA is linearly related to the risk of stroke and can be used in risk stratification models,” said Dr. Kakkos. “These findings need to be confirmed in future prospective studies or in the medical arm of randomized controlled studies in the presence of optimal medical therapy.”