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 493 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.My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Wednesday, February 28, 2018

Inflammation and CVD: Recent data heighten interest in effects, new strategies

Once again 12 years out of date(WHO - 2006) in not knowing that strokes are no longer cardiovascular they are neurological diseases.  Symptomatic in stroke, no one knows anything. I've been suggesting inflammation was the real problem for years. 
https://www.healio.com/cardiology/vascular-medicine/news/print/cardiology-today/%7B3136e8e8-66d7-4745-b5a1-ebcaa434ae4f%7D/inflammation-and-cvd-recent-data-heighten-interest-in-effects-new-strategies?utm_source=selligent&utm_medium=email&utm_campaign=cardiology%20news&m_bt=59283581626




For many years, cardiologists and basic science researchers suspected that inflammation plays a role in CVD, but definitive evidence proved elusive. That changed in August 2017 when findings from the CANTOS trial, presented at the European Society of Cardiology Congress and published in The New England Journal of Medicine, proved the inflammation hypothesis.
CANTOS evaluated whether canakinumab (Novartis), a fully human monoclonal antibody that targets interleukin-1 beta, would prevent CV events in MI survivors who were at increased risk for recurrent events due to persistent inflammation. Canakinumab has known anti-inflammatory effects and has approval for clinical use in rheumatologic disorders.

Paul M. Ridker, MD, MPH, from Brigham and Women’s Hospital and Harvard Medical School, said cardiologists now better understand the inflammation-CVD relationship.
Source: CaughtintheMoment.com

In CANTOS, 10,061 patients who randomly received one of three doses of canakinumab experienced a marked reduction of C-reactive protein over a median of 3.7 years of follow-up. The 150-mg dose conferred a 15% reduction in the primary endpoint of first occurrence of nonfatal stroke, nonfatal MI or CV death (see Table) and a 17% reduction in the key secondary endpoint of any component of the primary endpoint in addition to hospitalization for unstable angina resulting in urgent revascularization. Further analyses showed that canakinumab was also associated with reduced risk for lung cancer and cancer mortality, compared with placebo.
Cardiology Today assembled a panel of experts to discuss inflammation and CVD, the inflammation hypothesis, significance of the CANTOS results, the promise of new research, financial implications and how a focus on patients who show robust response to a therapy may be a cornerstone of CV medicine in the future.
Read on for insight from some of the leading experts in this area.

Biological plausibility

Carl J. Pepine, MD, MACC: When and where did the notion of inflammation relating to CVD begin?
Paul M. Ridker, MD, MPH, FACC, FAHA: The idea that inflammation was part of a broad disease process goes back a very long way, to Greek medicine. In fact, prior to the lipid hypothesis, there was a fair amount of interest in this and a group of vascular biologists and translational biologists who were thinking about this. During the explosion of the lipid hypothesis, those biologists kept at it, and it is a good thing that they did. I came in during the clinical/translational period about 20 years ago, but my colleague, Dr. Libby, was involved before that.

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