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.

Wednesday, October 28, 2015

Anti-Inflammatory Flops in Acute MI

If this reduces inflammation immediately post heart attack in arteries, this sounds like a very important possibility for poststroke interventions for arteries in the brain. But this won't occur because we have no strategy for following up any interesting research. Our stroke associations are completely fucking worthless.
http://www.medpagetoday.com/Cardiology/MyocardialInfarction/54340?
The novel anti-inflammatory agent losmapimod failed to improve heart attack outcomes, GlaxoSmithKline announced in top-line results for the LATITUDE-TIMI 60 trial.
The p38 MAP kinase inhibitor did not reduce the primary composite endpoint of cardiovascular death, myocardial infarction, or severe recurrent ischemia requiring urgent coronary artery revascularization at an interim analysis.


The findings came from part A of the phase III trial, with 3,503 ST-segment or non-ST-segment elevation myocardial infarction (STEMI or NSTEMI) patients, designed to support a larger part B with more than 20,000 additional patients.
While the part A results will be presented in full at an upcoming scientific meeting, the second portion of the trial will be scrapped, GlaxoSmithKline said.
The subset of STEMI patients did show reductions of 30% to 50% in prespecified endpoints of cardiovascular death, heart failure hospitalization, and the composite of the two, but these did not reach statistical significance because of small numbers of events. GSK said it would consider that option for future development, although some industry observers such as FierceBiotech were skeptical.
Losmapimod's p38 MAP kinase target is "associated with the acute inflammation and cellular injury that occurs in the blood vessels and in the heart during and immediately after an acute coronary syndrome," the company noted in a press release.
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