Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label antithrombotic therapy. Show all posts
Showing posts with label antithrombotic therapy. Show all posts

Monday, May 27, 2019

Cerebral Microbleeds Should Not Deter Antithrombotics in Stroke

Do you prefer your hospital incompetence to be: Not knowing? OR not doing? Or maybe you prefer stroke survivors running a stroke hospital, they can't do any worse than stroke medical professionals.  This should prompt a change in the next week, test your hospital on that responsibility.

Cerebral Microbleeds Should Not Deter Antithrombotics in Stroke

May 23, 2019
The presence of cerebral microbleeds should not deter the use of antithrombotic treatment in patients with recent ischemic stroke or transient ischemic attack (TIA), new data from a pooled analysis of cohort studies suggest.
The presence of microbleeds was linked to a greater risk for both future ischemic stroke and intracranial hemorrhage (ICH) in the analysis. Although the number of microbleeds was associated with a greater relative risk for subsequent ICH than for ischemic stroke, the absolute risk for ischemic stroke was consistently higher than the absolute risk for ICH regardless of microbleed burden or anatomic distribution.
The analysis was presented today at the 5th European Stroke Organisation Conference (ESOC) 2019 and was simultaneously published online May 23 in the Lancet Neurology.
"We found that the relative risk of ICH goes up more dramatically with increasing microbleed burden than the relative risk for ischemic stroke," senior author David J. Werring, PhD, UCL Queen Square Institute of Neurology, London, United Kingdom, told Medscape Medical News.
"But — and this is the really key finding — it doesn't matter how many microbleeds there were. The absolute risk of ischemic stroke is always higher than the absolute risk of ICH," Werring said.
"This evidence therefore does not support withholding antithrombotic treatment in patients with a history of stroke/TIA in patients with a high microbleed burden," he said.
Werring explained that new, sophisticated scanning methods that are often used in assessing stroke patients can detect the presence of microbleeds in the cerebral circulation. In radiologic examinations, these microbleeds appear as small, hypointense, ovoid or rounded regions.
"The question we are addressing in this analysis is whether the presence of microbleeds in patients who have had an ischemic stroke or TIA is a signal of an increased risk of ICH, which could have implications for the use of antithrombotic medications," he said. "This is something that has been challenging stroke doctors for several years now and generating considerable anxiety about whether to continue antithrombotic medication.
"Our results show that regardless of the type of antithrombotics/anticoagulants/antiplatelets used and however many microbleeds were present, the risk of ischemic stroke is always higher than the risk of ICH," he added. "This provides reassurance for clinicians and patients that in patients with a previous ischemic stroke or TIA, we do not need to worry too much about the presence of microbleeds on the scan — they should be treated with antithrombotic regardless."
In the Lancet Neurology article, Werring and colleagues note that in previous studies of this issue, the sample sizes were small and there were few ICH outcome events. Thus, these studies could not reliably answer the important clinical question of whether many cerebral microbleeds or patterns of cerebral microbleeds indicate a higher risk for ICH than for recurrent ischemic stroke.
The authors therefore conducted the current pooled analysis. The analysis included data regarding individual patients with ischemic stroke or TIA from 38 cohort studies in which microbleeds and future stroke/ICH events were documented. The analysis included a total of 20,322 patients; the median follow-up was 1.34 years.
During follow-up, 189 ICH events and 1113 ischemic strokes occurred.
Results showed that patients with cerebral microbleeds were at increased risk for ischemic stroke (hazard ratio [HR], 1.23) and ICH (HR, 2.45) in comparison with patients who did not have microbleeds.
Although the HR for ICH increased more with increasing microbleed burden than the HR for ischemic stroke, the rate of ischemic stroke always exceeded that of ICH.
Table. Rate of ICH and Ischemic Stroke With Increasing Microbleed Burden
Number of Microbleeds Symptomatic ICH (Rate/1000 Patient-Years) Symptomatic Ischemic Stroke (Rate/1000 Patient-Years)
0 4 30
1 8 37
2 – 4 9 48
≥5 23 64
≥10 27 64
≥20 39 73
"These microbleeds appear to be a marker of small vessel disease," Werring commented. "The vessels can either get blocked or bleed. The dots on the scan might not all be actual bleeds — they could be red cells that have not been cleared properly or previous ischemic lesions than have transformed into hemorrhage."
Commenting on the study for Medscape Medical News, Alistair Webb, BMBCh, MRCP(Neurol), DPhil FESO, University of Oxford, United Kingdom, said the results were "very interesting."
"This is observational data, so it is not the most reliable data we can have, but it does provide reassurance," Webb said. "It has been a concern that these imaging changes are a risk of future bleeding which we haven't quantified, but this new information shows patients with numerous microbleeds are still much more likely to have an ischemic stroke than an ICH, so antithrombotic treatment is still likely to have more benefit than harm."

Complements RESTART

Webb noted that this study fits in well with the RESTART study, which was also presented at ESOC 2019. That study showed that restarting antithrombotic therapy for patients after an ICH was safe.
"With these two new studies, we have a lot more security that in a patient who has an increased risk of ischemic stroke, we can give antithrombotic therapy and not be deterred by whether they've had an ICH (as in RESTART) or their scan shows the presence of these microbleeds (as in this study)," Webb said.
Werring agreed. "There is a common theme in these two studies — that antithrombotics appear to be safer than we thought."
In a comment that accompanied the article in the Lancet Neurology, Georgios Tsivgoulis, MD, and Aristeidis Katsanos, MD, University of Athens, Greece, point out that the main strengths of the new microbleed analysis are the large sample size, the prospective study design with strict inclusion and exclusion criteria, and the comprehensive, prespecified, robust statistical analysis. They add that the observational study design is prone to confounding and selection and indication biases.
They agree that the findings "suggest that cerebral microbleed presence, burden, and pattern on neuroimaging should not influence the decision to select appropriate antithrombotic therapy for secondary stroke prevention."
But they add that additional research is required to establish whether cerebral microbleeds should be incorporated as a neuroimaging marker in clinical risk prediction scores of recurrent ischemic stroke or ICH in patients with recent cerebral ischemia treated with oral anticoagulants or antiplatelet drugs.
The study was supported by the British Heart Foundation and UK Stroke Association. Werring has received personal fees from Bayer outside the submitted work. Disclosures of relevant financial relationships of the study's coauthors appear in the original article. The editorialists have disclosed no relevant financial relationships.
Lancet Neurol. Published online May 23, 2019. Full text, Comment
5th European Stroke Organisation Conference (ESOC) 2019: Presented May 23, 2019.

Tuesday, July 26, 2016

Prior antithrombotic use is associated with favorable mortality and functional outcomes in acute ischemic stroke

This really is useless, nothing on the amount of the intervention(aspirin size) and nothing on the length of time used. So you will have to do it by the by guess and by golly method just like everything else in stroke.
http://www.mdlinx.com/internal-medicine/medical-news-article/2016/07/26/antiplatelet-agents-antithrombotic-agents-mortality-prognosis/6769817/?
This research was designed to explore the association between prior antithrombotic use with favorable mortality and clinical outcomes in acute ischemic stroke. Findings imply previous antithrombotic therapy was independently associated with improved clinical outcomes after acute ischemic stroke. Guaranteeing the use of antithrombotics in suitable patient populations might be associated with benefits beyond stroke prevention.

Methods

  • The authors examined the unadjusted and adjusted associations between previous antithrombotic use and clinical outcomes, using data from Get With The Guidelines–Stroke with over half a million acute ischemic strokes recorded between October 2011 and March 2014 (n=540993) from 1661 hospitals across the United States.

Results

  • As per this study, there were 250104 (46%) stroke patients not receiving any antithrombotic before stroke; of whom approximately 1/3rd had a documented previous vascular indication.
  • Patients who were receiving antithrombotics before stroke had better outcomes than those who did not, after controlling for clinical and hospital factors, regardless of whether a previous vascular indication was present or not: adjusted odds ratio (95% confidence intervals) were 0.82 (0.80–0.84) for in–hospital mortality, 1.18 (1.16–1.19) for home as the discharge destination, 1.15 (1.13–1.16) for independent ambulatory status at discharge, and 1.15 (1.12–1.17) for discharge modified Rankin Scale score of 0 or 1.
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

Thursday, May 26, 2016

The Novel Oral Syk Inhibitor, Bl1002494, Protects Mice From Arterial Thrombosis and Thromboinflammatory Brain Infarction

More research needed. Don't know who to tell you to call to accomplish more human research because stroke has NO leadership or strategy.
http://atvb.ahajournals.org/content/36/6/1247.abstract?etoc
  1. Bernhard Nieswandt
+ Author Affiliations
  1. From the Department of Experimental Biomedicine (J.M.M.v.E., D.S., S.B., I.T., B.N.) and Department of Neurology (P.K., G.S.), University Hospital Würzburg and Rudolf Virchow Center for Experimental Biomedicine (J.M.M.v.E., D.S., S.B., I.T., B.N.), University of Würzburg, Würzburg, Germany; Respiratory Diseases Research, Boehringer Ingelheim Pharma GmbH & Co KG, Biberach an der Riß, Germany (D.J.L.); Mammalian Cell Signaling Laboratory, Department of Vascular Cell Biology, Max Planck Institute for Molecular Biomedicine, Münster, Germany (F.K.); and Walter Brendel Centre of Experimental Medicine, Department of Cardiovascular Physiology and Pathophysiology, Ludwig Maximilian University of Munich, Munich, Germany (B.W.).
  1. Correspondence to Bernhard Nieswandt, PhD, Department of Experimental Biomedicine, University Hospital, University of Würzburg, Josef-Schneider-Str. 2/D15, Würzburg 97078, Germany. E-mail bernhard.nieswandt@virchow.uni-wuerzburg.de
  1. * These authors contributed equally to this article.

Abstract

Objective—Ischemic stroke, which is mainly caused by thromboembolic occlusion of brain arteries, is the second leading cause of death and disability worldwide with limited treatment options. The platelet collagen receptor glycoprotein VI (GPVI) is a key player in arterial thrombosis and a critical determinant of stroke outcome, making its signaling pathway an attractive target for pharmacological intervention. The spleen tyrosine kinase (Syk) is an essential signaling mediator downstream of not only GPVI but also other platelet and immune cell receptors. We sought to assess whether Syk might be an effective antithrombotic target.
Approach and Results—We demonstrate that mice lacking Syk in platelets specifically are protected from arterial thrombus formation and ischemic stroke but display unaltered hemostasis. Furthermore, we show that mice treated with the novel, selective, and orally bioavailable Syk inhibitor BI1002494 were protected in a model of arterial thrombosis and had smaller infarct sizes and a significantly better neurological outcome 24 hours after transient middle cerebral artery occlusion, also when BI1002494 was administered therapeutically, that is, after ischemia.
Conclusions—These results provide direct evidence that pharmacological Syk inhibition might provide a safe therapeutic strategy to prevent arterial thrombosis and to limit infarct progression in acute stroke.

Tuesday, June 18, 2013

Earlier Treatment of Seniors After Stroke Reduces Risk of Death, Increases Chance to Go Home

The authors congratulations of themselves is wrong. They are completely missing the huge cause of dead and dying neurons. The neuronal cascade of death. Doesn't anyone read stroke research??
http://www.seniorjournal.com/NEWS/Health/2013/20130618-Earlier_Treatment_of_Seniors.htm
With all the promotion by the American Heart Association and others about the critical need for quick treatment after a stroke, it is not surprising that a large new study of senior citizens hit with acute ischemic stroke finds that thrombolytic treatment (to help dissolve a blood clot) that was started more rapidly after symptom onset was associated with reduced in-hospital deaths and intracranial hemorrhage and higher rates of independent walking ability at discharge and discharge to home.
The study, which included nearly 60,000 patients with acute ischemic stroke, appears in the June 19 issue of the Journal of the American Medical Association (JAMA).
The researchers found that for every 15-minute-faster interval of tPA therapy -
   ● mortality was less likely to occur,
   ● symptomatic intracranial hemorrhage was less likely to occur,
   ● independence in ambulation at discharge was more likely to occur, and
   ● discharge to home was more likely to occur.
For patients treated in the first 90 minutes, compared with 181-270 minutes after onset -
   ● mortality was 26 percent less likely to occur,
   ● symptomatic intracranial hemorrhage was 28 percent less likely to occur,
   ● independence in ambulation at discharge was 51 percent more likely to occur, and
   ● discharge to home was 33 percent more likely to occur.
�These findings support intensive efforts to accelerate patient presentation and to streamline regional and hospital systems of acute stroke care to compress OTT times,� the authors conclude.









Jeffrey L. Saver, M.D., of the David Geffen School of Medicine at UCLA, Los Angeles, and colleagues conducted a study to determine the association between time to treatment with intravenous thrombolysis and outcomes among patients with acute ischemic stroke.
The study included data from 58,353 patients with acute ischemic stroke treated with tPA within 4.5 hours of symptom onset in 1,395 hospitals participating in the Get With The Guidelines-Stroke Program, April 2003 to March 2012. The median (midpoint) age of the patients was 72 years.
The median OTT time was 144 minutes, 9.3 percent had OTT time of 0 to 90 minutes, 77.2 percent had OTT time of 91 to 180 minutes, and 13.6 percent had OTT time of 181 to 270 minutes.

Patient factors most strongly associated with shorter OTT included greater stroke severity, arrival by ambulance and arrival during regular hours. Overall, there were 5,142 (8.8 percent) in-hospital deaths, 2,873 (4.9 percent) patients had intracranial hemorrhage, 19,491 (33.4 percent) patients achieved independent ambulation (walking ability) at hospital discharge, and 22,541 (38.6 percent) patients were discharged to home.
�Intravenous (IV) tissue-type plasminogen activator (tPA) is a treatment of proven benefit for select patients with acute ischemic stroke as long as 4.5 hours after onset. Available evidence suggests a strong influence of time to therapy on the magnitude of treatment benefit,� according to background information in the article.
Imaging studies show the volume of irreversibly injured tissue in acute cerebral ischemia expands rapidly over time. �However, modest sample sizes have limited characterization of the extent to which onset to treatment (OTT) time influences outcome; and the generalizability of findings to clinical practice is uncertain.

Wednesday, December 19, 2012

Tissue Window in Stroke Thrombolysis Study (TWIST): A Safety Study

Follow up with your ER doctors to see if this study changes their procedures for stroke intervention. You may need this, so do it now!
If the Joint Commission is pushing this out it is impossible to tell, so do it yourself.
http://cjns.metapress.com/content/h50558454080g083/?id=H50558454080G083

Abstract

Background: Stroke thrombolysis is limited by the "last-seen well" principle, which defines stroke onset time. A significant minority of stroke patients (~15%) awake with their symptoms and are by definition ineligible for thrombolysis because they were "last-seen well" at the time they went to bed implying an interval that is most often greater than three hours. Methods: A single-centre prospective, safety study was designed to thrombolyse 20 subjects with stroke-on-awakening. Patients were eligible for inclusion if they were last seen well less than 12 hours previously, specifically including those who awoke from sleep with their stroke deficits. They had a baseline computed tomogram (CT) scan with an ASPECTS score greater than 5, no evidence of well-evolved infarction and a CT angiogram / Trans-cranial Doppler ultrasound study demonstrating an intracranial arterial occlusion. Patients fulfilled all other standard criteria for stroke thrombolysis. The primary outcome was safety defined by symptomatic ICH or death. Results: Among 89 screened patients, 20 were treated with thrombolysis. Two patients (10%) died due to massive carotid territory stroke and two patients (10%) died of stroke complications. Two patients (10%) showed asymptomatic intracerebral hemorrhage (ICH) (petechial hemorrhage) and none symptomatic ICH. Reasons for exclusion were: (a) ASPECTS ≤ 5 (29); (b) well-evolved infarcts on CT (19); (c) historical mRS > 2 (17); (d) no demonstrable arterial occlusion or were too mild to warrant treatment (10). Conclusions: Patients who awake with their deficits can be safely treated with thrombolysis based upon a tissue window defined by NCCT and CTA/TCD.

Wednesday, May 2, 2012

Thrombosis Breakthrough May Lead To New Treatment Options

Maybe eventually a better treatment than warfarin or pradaxa.
http://www.doctortipster.com/9500-thrombosis-breakthrough-may-lead-to-new-treatment-options.html
Researchers at the Institute for Cardiovascular and Metabolic Research (ICMR) at the University of Reading, have discovered the mechanism by which platelets bind together to form blood clots. This discovery, they say, can lay the foundation for new treatments to prevent stroke or heart attacks.
In healthy people, blood is always in a physiological fluid-coagulant equilibrium. In other words, when the endothelium is damaged, platelets and fibrinogen  form a network plug that repair the defect and the bleeding stops. Then the network of fibrin is lysed and the blood vessel is recanalized. This process occurs continuously in the body. In certain diseases or conditions such hypercoagulability or atrial fibrillation, platelets aggregate together to form a thrombus that may obstruct imporant blood vessels. What researchers found is how platelets communicate with each other. It seems that platelets are interconnected by gap junctions, some pore-like structures. ‘Gap junction’ is a common type of connection to other cells, such as myocardial cells or neurons. Gap junctions are a special type of connection that  interconnects the cytoplasm of two cells.
Thrombus
Professor Jonathan Gibbins and Dr. Sakthivel Vaiyapuri, said: “This appears to be a very important communication mechanism for blood clotting and thrombosis”. He added that by blocking those channels involved in the formation of junctions thrombosis can be reduced. The new discovery may be a target  in antithrombotic therapy.
Currently, stroke is prevented by oral anticoagulant medication (warfarin) which inhibits the synthesis of coagulation factors dependent on vitamin K. This medication has several drawbacks. On the one hand, and patient dose should be adjusted by measuring the INR (International Normalised Ratio), on the other hand, there are plenty of side effects. Oral anticoagulants can cause bleeding and give drug interactions. It is important to note that the risk of bleeding is significantly increased when combined with anticoagulants such as clopidogrel antiplatelet or aspirin. In addition to this, anticoagulants are prohibited during pregnancy.
Anticoagulant medication is commonly prescribed in patients with cardiovascular disorders. Oral anticoagulants are prescribed long-term in patients with atrial fibrillation to prevent thromboembolic accidents. Because atria no longer contract, blood tends to clot and the formed thrombi can migrate into circulation and stroke can occur. Also, patients with metal valves need to follow long-term treatment with oral anticoagulants to prevent thrombosis.
Understanding the mechanisms underlying thrombosis may be a target for discovery of new anticoagulants. Dr. Vaiyapuri notes that this discovery is exciting even if their work is still not complete.