7 Signs You May Have Clogged Arteries

None of these existed at the time of my stroke when my right carotid artery was 80% closed.

7 Signs You May Have Clogged Arteries

 

Heart disease is more common than most people realize; each year in the United States, more than 790,000 people suffer from heart attacks, and strokes account for one in 20 deaths. Preventing heart disease is the ultimate goal, but early detection is also crucial to stop its progression.

Changes in lifestyle and medical therapies can delay the onset of a heart attack, and the risk of heart disease can significantly decrease with simple daily changes. The following are seven signs that indicate a high possibility of clogged arteries that you should know.

7. Erectile Dysfunction

6. Baldness(Been bald since age 21)

5. Ear Crease

4. Calf Pain While Walking

3. Tight Jaw

2. Lower Back Pain

1. Smoking

Carotid stent occlusion after emergent stenting in acute ischemic stroke: Incidence, predictors and clinical relevance

I can see massive problems with stenting your carotid artery. Why do it if your Circle of Willis is complete?

1. Occlusion

2. Trying to snake mechanical thrombectomy thru that stent to get to a clot in the brain.

3. Tying to pull a grabbed clot back thru the stent without ripping the artery completely open. 

I'm not medically trained, don't listen to me. But have your doctor GUARANTEE NO COMPLICATIONS EVER!

Carotid stent occlusion after emergent stenting in acute ischemic stroke: Incidence, predictors and clinical relevance

• Arturo Renú ¹
• Jordi Blasco ¹
• Carlos Laredo
• 
  
• José David Guio
• Sergio Amaro
• Angel Chamorro
• Show all authors
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Published:September 10, 2020DOI:https://doi.org/10.1016/j.atherosclerosis.2020.09.002

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Highlights

• •
  Stent thrombosis occurs in one fifth of the patients treated with acute stenting.
• •
  Stent thrombosis is associated with specific procedural variables.
• •
  Stent thrombosis is associated with poor clinical outcome.
• •
  Further investigation of strategies aimed to prevent stent occlusion is needed.

Abstract

Background and aims

Emergent stent placement may be required during neurothrombectomy. Our aim was to investigate the incidence, predictors and clinical relevance of early extracranial carotid stent occlusion following neurothrombectomy.

Methods

We retrospectively analyzed a cohort of 761 consecutive neurothrombectomies performed at our center between May 2010 and August 2018, from whom a total of 106 patients had acute internal carotid artery occlusions. Early stent occlusion was defined as complete vessel occlusion within 24 h of neurothrombectomy. Clinical outcome was evaluated at day 90 with the modified Rankin Score scale (mRS). Pretreatment, procedural and outcome variables were recorded and analyzed using logistic regression.

Results

Carotid stenting was performed in 99 (13%) patients. Of those, 22 (22%) had early stent occlusion at follow-up. Stent occlusion was associated with a lower use of post-stenting angioplasty [adjusted OR (aOR) = 11.2, 95%CI = 2.49–50.78, p = 0.002)], increased residual intrastent stenosis (aOR = 2.1, 95%CI = 1.38–3.06, p < 0.001) and unsuccesful intracranial recanalization (modified TICI score 0-2a) (aOR = 13.5, 95%CI = 1.97–92.24, p = 0.008). Stent occlusion was associated with poor clinical outcome at day 90 (poorer mRS shift, aOR = 3.9, 95%CI = 1.3–11.3, p = 0.014; mRS>2, aOR = 6.3, 95%CI = 1.8–22.7, p = 0.005), and with an increased rate of symptomatic intracranial hemorrhage at 24 h (14% versus 1%, p = 0.033).

Conclusions

Early carotid stent occlusion occurred in one out of five neurothrombectomies and was associated with periprocedural factors that included increased residual intrastent stenosis, a lower use of post-stenting angioplasty and unsuccessful intracranial recanalization. Further investigation is warranted for the evaluation of strategies aimed to prevent carotid stent occlusion.

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Collateral Flow and White Matter Disease in Patients with Internal Carotid Artery Occlusion

I really question if there is any understanding of how carotid occlusion works and whether it leads to a stroke. My right carotid artery is fully occluded(closed up) and that is a good thing, I shouldn't have to worry about a stroke from that artery anymore. The closure of the artery is not the problem, if blood is still flowing thru it is the possible problem, a piece of the occlusion could break off and lodge in the brain causing a stroke. If your Circle of Willis is complete then you are getting enough blood to your brain even if some of the arteries feeding it are closed(2 vertebral and 2 carotid).
http://www.docguide.com/collateral-flow-and-white-matter-disease-patients-internal-carotid-artery-occlusion

Ishikawa M, Sugawara H, Nagai M, Kusaka G, Tanaka Y, Naritaka H; European Neurology 77 (1-2), 56-65 (Dec 2016)

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• Vascular Disorders

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BACKGROUND When an internal carotid artery (ICA) occludes, a patient may develop cerebral infarction (CI). We investigated whether CI caused by ICA occlusion (ICAO) is associated with collateral flow through the anterior and posterior communicating arteries (ACoA and PCoA).
METHODS In 100 patients with ICAO, we investigated CI and white matter disease by performing an MRI and the anatomy of the ACoA and PCoA were investigated by performing magnetic resonance angiography. All patients were divided into the symptomatic CI group or the no-CI group. The collateral flow pathway was estimated by the anterior cerebral artery (ACA)-PCoA score and the collateral flow volume after ICAO was estimated by the middle cerebral artery (MCA) flow score, based on how well the MCA was visualized.
RESULTS Of 100 patients with ICAO, the symptomatic CI group included 36 patients. ACA-PCoA score and white matter disease grades were significantly higher in the CI group (indicating poor collateral flow). More than 80% of patients with an ACA-PCoA score of 4 (poor collateral) experienced symptomatic CI. Thirty-one symptomatic CI patients (86%) had an MCA flow score of 1 or 2 (decreased MCA flow).
CONCLUSION The ACA-PCoA score and white matter disease grade may suggest an increased risk of CI following ICAO.

Prognosis of Asymptomatic Carotid Artery Occlusion

Way too many big medical words strung together to have any real understanding of this word salad. My right carotid artery is totally closed up and I'm extremely glad of that.

Prognosis of Asymptomatic Carotid Artery Occlusion

1. Daniel G. Hackam, MD, PhD

+ Author Affiliations

1. From the Division of Clinical Pharmacology, Departments of Medicine and Clinical Neurological Sciences and Stroke Prevention and Atherosclerosis Research Centre (SPARC), Robarts Research Institute, Western University, London, Ontario, Canada.

1. Correspondence to Daniel G. Hackam, MD, PhD, SPARC Unit, Room 100K-2, Siebens Drake Bldg, 1400 Western Rd, London, Ontario, Canada, N6G 2V2. E-mail dhackam@uwo.ca

Abstract

Background and Purpose—The aim of this systematic review was to quantify the risk of ipsilateral stroke in patients with asymptomatic carotid artery occlusion (ACAO).

Methods—Studies reporting ipsilateral stroke risk in ACAO were identified by a search of MEDLINE, EMBASE, and study bibliographies. Study estimates were pooled using a random effects model, and heterogeneity was quantified using the I² statistic. The primary outcome was the annual rate of ipsilateral stroke.

Results—Thirteen studies were identified, encompassing 718 patients with ACAO who were followed up for a median of 2.8 years. The annual rate of ipsilateral stroke was 1.3% (95% confidence interval, 0.4–2.1; I²=53%). The annual rate of ipsilateral transient ischemic attack was 1.0% (95% confidence interval, 0.3–1.8; I²=40%). The annual rate of death was substantially higher at 7.7% (95% confidence interval, 4.3–11.2; I²=83%). Correction for possible publication bias for the primary outcome suggested a lower risk of ipsilateral stroke (0.3% per year; 95% confidence interval, –0.4 to 1.1).

Conclusions—Stroke in ACAO is relatively infrequent, but patients face high mortality rates. This suggests the need for intensified medical therapy in ACAO.

Vessel occlusion, penumbra, and reperfusion – translating theory to practice

Read it and weep, for our doctors still have no idea what is going on with stroke or how to treat it.
http://journal.frontiersin.org/Journal/10.3389/fneur.2014.00194/full?utm_source=newsletter&utm_medium=email&
Bruce C. V. Campbell^1,2*, Geoffrey A. Donnan² and Stephen M. Davis¹

• ¹Department of Medicine, Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia
• ²Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia

The management of ischemic stroke is at a critical juncture. Administration of intravenous tPA is currently restricted to within 4.5 h from stroke onset with several trials in longer time windows proving neutral (1, 2). Revascularization success with tPA in major vessel occlusion is widely recognized as suboptimal (3). Alternative thrombolytic agents with theoretical efficacy advantages such as tenecteplase and desmoteplase are yet to show benefit in phase 3 trials. The promise of endovascular therapy has also yet to translate into positive randomized trials (4–6), although a new generation of devices is currently being studied. While it is possible that these therapeutic approaches are simply ineffective, the heterogeneity of stroke pathophysiology is likely to be contributing to the neutral results we often observe.

Imaging selection has been proposed as a means of reducing heterogeneity by identifying patients with the potential to benefit from revascularization and therefore enhancing the probability of success in trials of new therapies. However, whether it is sufficient to demonstrate an occluded artery as the target or to also require evidence of salvageable downstream tissue has been debated. The recent announcement of neutral results in DIAS 3 (7), a trial that compared desmoteplase versus placebo 3–9 h after stroke onset in patients with vessel occlusion, without reference to downstream tissue status other than what was visible on non-contrast CT, will no doubt further stimulate this discussion. It is, therefore, salient to consider the current methods to identify salvageable ischemic penumbra and the potential value of commonly used surrogates for clinical outcome, chiefly reperfusion, recanalization, and infarct growth.