Vascular inflammation contributes to the development and progression of atherosclerosis.
Inflammation is important in both the acute and chronic phases of atherosclerosis.
Increased levels of circulating inflammatory markers are associated with worse prognosis with acute coronary syndromes.
Evidence from randomized trials of aspirin and statin medications, which have anti-inflammatory effects among other anti-atherogenic effects reveal benefits to cardiovascular disease reduction.
Three clinical trials of specific anti-inflammatory agents including canakinuman and colchicine provide evidence of the treatable nature of vascular inflammation.
Anti-inflammatory therapies for cardiovascular disease that reduce cardiovascular events inhibit the interleukin-1 beta, IL-6 and C reactive protein biologic pathways.
IL-1Beta is generated from an inactive precursor by intracellular multimeric inflammasone complex and its activation amplifies the production of key inflammatory promoter IL-6, which in turn induces CRP secretion by the liver.
Both immune mediated systemic inflammatory conditions in certain infections can promote atherosclerosis and cardiovascular events: increased atherosclerotic cardiovascular disease with influenza and HIV infection, rheumatoid arthritis, psoriasis, lupus erythematosus, inflammatory bowel disease, and gout.
Flares of gout are temporary associated with increased near term risk of cardiovascular events.
A gout flare is an indication for colchicine therapy, which targets in the IL beta inflammatory pathway and has been shown to reduce cardiovascular events in patients with chronic coronary artery disease and after acute coronary events.
Colchicine inhibits the actions of neutrophils and the release of inflammatory cytokines including IL-1 and IL-6.
In a trial with colchicine initiated within 30 days after myocardial infarction in patients with stable coronary artery disease, it showed a beneficial effect: however, recent trials did not show reductions in cardiovascular events with colchicine treatment following myocardial infarction.