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 edoxaban. Show all posts
Showing posts with label edoxaban. Show all posts

Thursday, July 28, 2016

Improving Patient Outcomes in Preventing Atrial Fibrillation-related Stroke with Non-Vitamin K Antagonist Oral Anticoagulants

You might want to read if you have atrial fibrillation, unless you think your doctor will tell you this in the next two weeks.
http://www.touchneurology.com/articles/improving-patient-outcomes-preventing-atrial-fibrillation-related-stroke-non-vitamin-k
European Neurological Review, 2016;11(1):27–35 DOI: http://doi.org/10.17925/ENR.2016.11.01.1a

Abstract:

The rising incidence of atrial fibrillation (AF) is increasingly resulting in a substantial worldwide increase in AF-related stroke, particularly in elderly patients and this is creating an increasingly serious healthcare burden. Guidelines recommend the use of AF-related stroke prophylaxis but adherence to these remains poor. Studies conducted in the 1990s showed that warfarin reduced the risk of AF-related stroke by an overall 64% compared with placebo. Subsequently, prophylactic treatment was further improved with the development of non-vitamin K antagonist oral anticoagulants (NOACs). More recently, a meta-analysis of four large clinical trials on NOACs (dabigatran, rivaroxaban, apixaban, and edoxaban) showed there was a relative risk reduction of 0.81 (p<0.0001) favouring NOAC treatment over warfarin for stroke or systemic embolic events in patients with AF. The largest trial of NOACs in AF-related stroke, to date, was the ENGAGE AF-TIMI 48 study (n=21,105) which showed that edoxaban was non-inferior to warfarin for ischaemic stroke reduction but significantly reduced bleeding and cardiovascular mortality. A recent subgroup analysis of this study showed that with edoxaban the incidences of intracranial haemorrhage (ICH) subtypes (all ICH, fatal ICH, fatal, subdural and epidural bleed) were significantly lower with 60 mg of edoxaban (p=0.013–<0.001). Edoxaban was also shown to be an effective option in patients with prior stroke. In addition edoxaban was shown to reduce deaths due to fatal bleeds compared with warfarin. The results of current studies, especially the ENGAGE AF-TIMI 48 subgroup analysis therefore, show that the benefits of anticoagulation therapy in patients with AF substantially outweigh the risks
Keywords: Atrial fibrillation-related stroke, outcomes, non-vitamin K oral anticoagulants (NOACs)
Disclosure: Peter Kelly has served on advisory boards or received speakers fees or benefits from the American Stroke Association, Bayer and Daiichi Sankyo, and has received research unit grants from the Health Research Board of Ireland, Irish Heart Foundation and Bayer. Carlos Molina has nothing to declare in relation to this article. Christian T. Ruff has received research support from GlaxoSmithKline, Daiichi Sankyo, Intarcia and AstraZeneca, and serves as a consultant and on the advisory boards for Boehringer Ingelheim, Bayer, Daiichi Sankyo, Portola and DrugDev. Roland Veltkamp has received speaker fees, consulting honoraria and research support from Bayer, Boehringer Ingelheim, BMS, Pfizer, Daiichi Sankyo, CSL Behring, Apoplex Medical Technologies, Morphosys, Biogen, Medtronic.
Acknowledgments: Editorial assistance was provided by James Gilbart at Touch Medical Media, London, this was supported by an unrestricted grant from Daiichi Sankyo Europe GmbH. This article reports the proceedings of a sponsored satellite symposium and as such has not been subject to the journal’s usual peer-review process
Received: October 16, 2015 Accepted February 19, 2016
Correspondence: Peter Kelly, Stroke Service and NeuroVascular Unit for Translational and Therapeutics Research, University College Dublin, Ireland E: pjkelly@mater.ie.
Support: The publication of this article was supported by Daiichi Sankyo Europe GmbH. The views and opinions expressed are those of the authors and not necessarily those of Daiichi Sankyo Europe GmbH.
Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit
In atrial fibrillation (AF), considerable harm can result from the lack of appropriate preventive therapy, and optimal prevention is critical, especially in vulnerable elderly or frail patients. AF markedly increases the risk of stroke and this condition must be monitored and potentially treated wherever it is detected.1–4 AF is an increasing concern for physicians worldwide as populations age and more people are at risk.5–7 Although guidelines for stroke prevention in AF that recommend anticoagulation have been established for many years, many at-risk patients receive inadequate anticoagulation or none at all.8–11 This ‘reluctance to treat’ stems largely from a fear of inducing intracranial haemorrhage (ICH) and other serious bleeding types that are associated with warfarin and the non–vitamin K antagonist oral anticoagulants (NOACs). This risk, however, is often over-stated and substantially less than the risks that are associated with the lack of stroke prevention treatment in AF. This review discusses the burden of AF-related stroke and evidence that supports current treatments, and considers novel insights on the use of edoxaban as provided by recent subgroup analyses of the ENGAGE AF-TIMI 48 trial results (see end of article for trial name definitions). These topics were presented at a satellite symposium convened at the European Stroke Organisation Annual Meeting in Glasgow, UK, in April 2015.
Preventing the Rise of AF-related Stroke– A Call to Action
Large-scale population-based observational studies have shown AF to be a serious factor increasing the likelihood of strokes and substantially worsening mortality and morbidity after a stroke.12 Various studies have predicted increasing incidence and prevalence of AF-related stroke and the associated heavy burden this will place on healthcare authorities worldwide. Professor Peter Kelly assessed the history and rising incidence of AF-related stroke. His message constitutes a call to action, encouraging physicians to treat all patients with AF to help stem the burgeoning number of ischaemic strokes and reduce the burden strokes impose on healthcare services.

7 more pages at link.

Sunday, December 13, 2015

Abstract 17392: Gastrointestinal Bleeding With Edoxaban versus Warfarin: Results From the ENGAGE AF-TIMI 48 Trial

Be careful out there.
http://circ.ahajournals.org/content/132/Suppl_3/A17392.short
  1. Eugene Braunwald3
+ Author Affiliations
  1. 1Internal Medicine, Icahn Sch of Medicine, Mount Sinai Med Cntr, New York, NY
  2. 2Internal Medicine, McMaster Univ and Thrombosis and Atherosclerosis Rsch Institute, Hamilton, Canada
  3. 3TIMI Study Group, Div of Cardiovascular Medicine, Brigham and Women’s Hosp and Harvard Med Sch, Boston, MA
  4. 4Pharma Development, Daiichi Sankyo, Edison, NJ
  5. 5Pharma Development, Daiichi Sankyo, New York, NY

Abstract

Background: There is more major gastrointestinal bleeding (M-GIB) with most NOACs than with warfarin. The clinical impact of this finding is poorly understood.
Methods: The ENGAGE AF-TIMI 48 trial compared the efficacy and safety of higher-dose (HD-E: 60 mg/ 30mg) or lower-dose (LD-E: 30 mg/15 mg) edoxaban regimens with dose-adjusted warfarin for prevention of stroke and systemic embolism in non-valvular atrial fibrillation. ISTH definitions for major and life-threatening (LT) bleeding events were utilized. In this pre-specified analysis, we investigated the adjudicated M-GIB events utilizing pre-defined severity and outcome endpoints.
Results: Although the risk of M-GIB was higher with HD-E than with warfarin, the risk of LT or fatal GIB was similar (figure), and surgery for GIB was required less frequently with HD-E than warfarin (HR 0.37; 95%CI, 0.16-0.88; p=0.03). The risk for M-GIB-related permanent drug discontinuation was similar with HD-E and warfarin (HR 0.96; 95% CI, 0.67-1.37, p=0.8), as were the risks of hospitalization (HR 1.14; 95%CI, 0.92-1.40, p=0.2) and Hgb decrease > 5 g/dL (HR 1.01; 95%CI, 0.74-1.38; p=0.9). The risks of M-GIB and of LT or fatal GIB were lower with LD-E than with warfarin (Figure), as were the risks of M-GIB-related permanent drug discontinuation (HR 0.51; 95% CI, 0.33-0.78, p=0.002), hospitalization (HR 0.67; 95%CI, 0.53-0.85; p=0.001), Hgb decrease > 5 g/dL (HR 0.58; 95%CI, 0.40-0.84; p=0.003), and M-GIB requiring transfusion of > 2 units of red cells (HR 0.66; 95%CI, 0.50-0.89; p=0.006). Fatal GIB occurred in 2, 3 and 7 patients treated with HD-E, LD-E and warfarin, respectively.
Conclusions: M-GIB and LT-GIB with edoxaban are dose-dependent. Although the risk of M-GIB is higher with HD-E than warfarin, the risk of LT-GIB or fatal GIB is similar and the severity and outcomes are no worse than with warfarin. The risks of M-GIB, and of LT-GIB or fatal GIB, are lower with LD-E than warfarin.

Saturday, August 8, 2015

Edoxaban versus placebo, aspirin, or aspirin plus clopidogrel for stroke prevention in atrial fibrillation. An indirect comparison analysis

So when you talk to your doctor about this you can make some intelligent observations. 

Edoxaban versus placebo, aspirin, or aspirin plus clopidogrel for stroke prevention in atrial fibrillation. An indirect comparison analysis



Abstract

As non-valvular atrial fibrillation (AF) brings a risk of stroke, oral anticoagulants (OAC) are recommended. In 'real world' clinical practice, many patients (who may be, or perceived to be, intolerant of OACs) are either untreated or are treated with anti-platelet agents. We hypothesised that edoxaban has a better net clinical benefit (NCB, balancing the reduction in stroke risk vs increased risk of haemorrhage) than no treatment or anti-platelet agents. We performed a network meta-analysis of published data from 24 studies of 203,394 AF patients to indirectly compare?? edoxaban with aspirin alone, aspirin plus clopidogrel, and placebo. Edoxaban 30 mg once daily significantly reduced the risk of all stroke, ischaemic stroke and mortality compared to placebo and aspirin. Compared to aspirin plus clopidogrel, there was a lower risk of intra-cranial haemorrhage (ICH). Edoxaban 60 mg once-daily had a reduced risk of any stroke and systemic embolism compared to placebo, aspirin, and aspirin plus clopidogrel. Mortality rates for both edoxaban doses were estimated to be lower compared to any anti-platelet, and significantly lower compared to placebo. With overall reduced risk of ischemic stroke and ICH, both edoxaban doses bring a NCB of mean (SD) 1.68 (0.15) saved events per 100 patients per year compared to anti-platelet drugs in a clinical trial population. The NCB was demonstrated to be lower, at 0.77 (0.12) events saved (p< 0.01) when modeled to data from a 'real world' cohort of AF patients. In conclusion, edoxaban is likely to provide even better protection from stroke and ICH than placebo, aspirin alone, or aspirin plus in  both clinical trial populations and unselected community populations. Both edoxaban doses would also bring a positive NCB compared to anti-platelet drugs or placebo/non-treatment based on 'real world' data.