†These authors contributed equally.
Academic Editor: Brian Tomlinson
Inflammation plays an important role in all stages of atherosclerosis — from
endothelial dysfunction, to formation of fatty streaks and atherosclerotic
plaque, and its progression to serious complications, such as atherosclerotic
plaque rupture. Although dyslipidemia is a key driver of atherosclerosis,
pathogenesis of atherosclerosis is now considered interplay between cholesterol
and inflammation, with the significant role of the immune system and immune
cells. Despite modern therapeutic approaches in primary and secondary
cardiovascular prevention, cardiovascular diseases remain the leading cause of
mortality worldwide. In order to reduce residual cardiovascular risk, despite the
guidelines-guided optimal medical therapy, novel therapeutic strategies are
needed for prevention and management of coronary artery disease. One of the
innovative and promising approaches in atherosclerotic cardiovascular disease
might be inflammation-targeted therapy. Numerous experimental and clinical
studies are seeking into metabolic pathways underlying atherosclerosis, in order
to find the most suitable pathway and inflammatory marker/s that should be the
target for anti-inflammatory therapy. Many anti-inflammatory drugs have been
tested, from the well-known broad range anti-inflammatory agents, such as
colchicine, allopurinol and methotrexate, to targeted monoclonal antibodies
specifically inhibiting a molecule included in inflammatory pathway, such as
canakinumab and tocilizumab. To date, there are no approved anti-inflammatory
agents specifically indicated for silencing inflammation in patients with
coronary artery disease. The most promising results came from the studies which
tested colchicine, and studies where the inflammatory-target was NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3)
inflammasome/interleukin-1 beta (IL-1