Rheumatoid arthritis (RA) is an autoimmune inflammatory arthritis. Inflammation, however,
can spread beyond the joints to involve other organs. During the past few years, it has been well recognized
that RA associates with increased risk for cardiovascular (CV) disease (CVD) compared with the
general population. This seems to be due not only to the increased occurrence in RA of classical CVD
risk factors and comorbidities like smoking, obesity, hypertension, diabetes, metabolic syndrome, and
others but also to the inflammatory burden that RA itself carries. This is not unexpected given the strong
links between inflammation and atherosclerosis and CVD. It has been shown that inflammatory cytokines
which are present in abundance in RA play a significant role in every step of plaque formation and
rupture. Most of the therapeutic regimes used in RA treatment seem to offer significant benefits to that
end. However, more studies are needed to clarify the effect of these drugs on various parameters, including
the lipid profile. Of note, although pharmacological intervention significantly helps reduce the
inflammatory burden and therefore the CVD risk, control of the so-called classical risk factors is equally
important. Herein, we review the current evidence for the underlying pathogenic mechanisms linking
inflammation with CVD in the context of RA and reflect on the possible impact of treatments used in
RA.
Maslinic acid in the treatment of heart damage in obesity hypertension through activating Nrf2 pathway
