One of the most clinically important aspects of recent advances in our understanding of
psoriasis has been the detection of an association between this disease and an increased prevalence of cardiovascular risk factors. This increase in prevalence is, in turn, linked to a greater risk of morbidity and mortality related to acute
myocardial infarction,
cerebrovascular accident, and
peripheral arterial disease. The chronic systemic
inflammation present in
psoriasis could explain why moderate to severe
psoriasis is an independent risk factor for
cardiovascular disease. The introduction of
biologic therapies has greatly improved the expectations of treatment as well as the long-term control of
psoriasis, and there is epidemiological evidence that these
therapies may lower cardiovascular risk in
psoriasis as they do in
rheumatoid arthritis. Caution should, however, be exercised when prescribing
biologic drugs in this setting, because adverse effects have been reported in association with the use of
tumor necrosis factor inhibitors in patients with advanced
congestive heart failure. Furthermore, a numerical imbalance (without statistical significance) between the groups receiving the
biologic drug and the placebo groups was recently observed in the incidence of major cardiovascular events (nonfatal
myocardial infarction and
cerebrovascular accident and cardiovascular death) during the controlled periods of clinical trials of
briakinumab and
ustekinumab, 2
monoclonal antibodies that target the p40 subunit shared by
IL-12 and
IL-23. We review the current scientific evidence on this topic.