Didn't your competent? stroke doctor start using colchicine and canakinumab years ago? Or don't you have functioning stroke doctor? I'd run away from such incompetence!
AHA: Colchicine Prevents Postop Afib December 2011
Could Old Gout Drug Offer New CV Benefits? November 2015
Anti-inflammatory therapy for preventing stroke and other vascular events after ischaemic stroke or transient ischaemic attack November 2017
canakinumab (5 posts to August 2012)
The latest here:
Inflammatory Biomarkers and Stroke Subtype
Abstract
Inflammation
is an established pathway in the formation, growth, and rupture of
atherosclerotic plaques. Inflammation is thus essential to the
pathogenesis of coronary heart disease and some types of ischemic
stroke.1 The benefit of anti-inflammatory therapies, such as colchicine2 and the anti-IL1β canakinumab,3
is proven in patients with coronary heart disease, yet it remains
unproven for patients with ischemic stroke. Compared with coronary heart
disease, the etiology of stroke is more heterogeneous. Besides
arterio-arterial atherogenic embolism, possible etiologies are
penetrator artery occlusion, cardioembolism, and other mechanisms.
Finding a stroke etiology remains elusive in up to 30%–40% of patients
despite a full evaluation. Understanding whether the stroke etiology
modifies the association between inflammatory markers and recurrence
risk is an important step to improve selection of patients for
randomized trials on anti-inflammatory agents. IL-6 and high-sensitive
CRP (hs-CRP) have been implicated in a higher recurrence risk after
ischemic stroke by both an individual participant data meta-analysis4 and a Mendelian randomization study,5 but granular, in vivo results stratified by stroke etiology are lacking.
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