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.