Systemic inflammation in psoriasis accelerates CVD risk
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LOUISVILLE, Ky. — Persistent, chronic inflammation seen in moderate to severe psoriasis is associated with plaque destabilization and rupture that drives MI, and biologic treatment can reduce CV risk, according to a speaker.
Data have long shown that inflammation drives cardiometabolic disease in humans; however, systemic inflammatory diseases such as rheumatoid arthritis, lupus and psoriasis are associated with a spectrum of CV and cardiometabolic diseases and further accelerate risk, Nehal N. Mehta, MD, MSCE, FAHA, chief of the lab of inflammation and cardiometabolic diseases and the Lasker senior investigator at the NHLBI, said during a presentation at the American Society for Preventive Cardiology Congress on CVD Prevention. For psoriasis in particular, studies show adults with the condition have more CV factors and experience events like MI about a decade sooner than those without psoriasis, Mehta said. Psoriasis and other inflammatory disease are also individually associated with plaque destabilization and plaque rupture, Mehta said.
“There are over 1 billion immune cells activated within the body during severe psoriatic flare,” Mehta said during his presentation. “Because of that, there is important overlap with CV and atherosclerotic diseases.”
Role of inflammation
CVD in psoriasis is highly prevalent; data show people with severe psoriasis lose on average 5 years of life due to infection, cancer and CVD, compared with those without psoriasis. A patient with severe psoriasis aged 40 to 50 years has a twofold risk for experiencing a first MI compared with an adult without psoriasis, Mehta said.
Immune factors seen in psoriasis overlap with those seen in atherosclerosis, Mehta said. Keratinocytes and T cells activate myeloid dendritic cells, which then drive a Th1 and Th17 cell response onto the keratinocytes.
“In the skin itself, all of these perpetuating molecules become very important for driving not only psoriatic skin disease but also atherosclerotic CVD,” Mehta said.
To better understand atherogenesis and atherosclerosis, as well as cardiometabolic diseases, researchers at the NIH have used psoriasis as a human model, Mehta said. In ongoing atheroprogression studies at the NIH, participants with moderate to severe psoriasis provide blood and tissue samples and agree to deep phenotyping via imaging, including coronary CT angiography. Researchers compared those patients with adults with diabetes, coronary disease or no disease.
Researchers have found that psoriasis itself, compared with age-, gender- and BMI-matched healthy volunteers, is associated with a 20% increase in total plaque burden, Mehta said.
“Most of this is noncalcified, so when one looks at fully adjusted models, there is an independent increase in the amount of noncalcified burden by the amount of psoriasis,” Mehta said.
Impact of biologic treatment
In a study published in Cardiovascular Research in 2019, Mehta and colleagues compared coronary CT angiography scans at baseline and 1 year for changes in total plaque among 89 patients with moderate to severe psoriasis who chose to begin biologic therapy and 32 patients with psoriasis who opted for no biologic treatment. Those who opted to initiate biologic therapy experienced a 33% decrease in systemic inflammation as well as an improvement in coronary plaque compared with the patients who did not choose biologic therapy, Mehta said.
“This is showing 1 year of untreated inflammation is dangerous for the vasculature,” Mehta said.
Additionally, higher resolution imaging via VascuCAP, which allows researchers to quantify atherosclerotic plaque stability, showed an improvement in lipid-rich necrotic core after biologic treatment, Mehta said.
“The conclusion here is that chronic inflammation is driving these findings, and when we treat the inflammation we reduce it,” Mehta said.
References:
- Elnabawi YA, et al. Cardiovasc Res. 2019;doi:10.1093/cvr/cvz009.
- Lerman JB, et al. Circulation. 2017;doi:10.1161/CIRCULATIONAHA.116.026859.
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Mehta N. Chronic inflammation in humans drives ASCVD risk and cardiometabolic disease. Presented at: American Society for Preventive Cardiology Congress on CVD Prevention; July 29-31, 2022; Louisville, Kentucky.
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