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August 01, 2019
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Biologic therapy for psoriasis reduces coronary inflammation

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Biologic therapy for moderate to severe psoriasis reduced in coronary inflammation, as assessed by perivascular fat attenuation index via coronary CTA, a measurement that may be able to track response to CAD interventions, researchers reported in JAMA Cardiology.

Fat attenuation index (FAI) using coronary CTA (CCTA) is a novel imaging biomarker that evaluates coronary inflammation by mapping spatial changes of perivascular fat composition. Previous research has revealed favorable associations between various biologic agents for psoriasis and luminal coronary plaque.

“FAI is a new method of analyzing CT scans that can predict a patient’s risk of fatal heart attacks and other cardiac events years in advance, and independent of other traditional risk factors for heart disease,” Charalambos Antoniades, MD, professor of cardiovascular medicine at Oxford University, said in a press release. “In fact, our research has found that an abnormal perivascular FAI was linked to a six- to nine fold increased risk of major adverse cardiovascular events.”

Cardiology Today spoke with Nehal N. Mehta, MD, MSCE, FAHA, chief of the section of inflammation and cardiometabolic diseases at the NHLBI, about the implications of these findings.

“Fat attenuation index [is] going to allow us the ability to understand, before we see actual blood vessel disease, whether the area of coronary artery inflammation has reduced,” Mehta said. “[Usually] when plaques form, they don't reverse. [This] is a technology that is not dependent on the presence or absence of atherosclerotic plaque. It's actually using physiology; an inflamed blood vessel secretes inflammatory cytokines, and then the fat around there actually lysis and it changes the attenuation we see on CT.”

In the new prospective cohort study, conducted from January 2013 through March 2019, researchers analyzed FAI changes in 134 patients (mean [SD] age, 51.1 [12.1] years; 84 [62.5%] men) with moderate to severe psoriasis. None of the patients were receiving biologic psoriasis therapy at baseline.

During the study, 82 patients received biologic psoriasis therapy for 1 year, including anti-tumor necrosis factor , anti-interleukin 12/23 or anti-IL-17 and 52 patients received topical or light therapy but no biologic therapy. Patients underwent CCTA at baseline and 1 year. All patients presented with low CV risk (median 10-year Framingham Risk Score, 3% [interquartile range, 1%-7%]). Focal coronary atherosclerotic plaque was present in 46 patients at baseline.

Researchers found that biologic therapy was associated with a significant decrease in FAI at 1 year (median FAI, 71.22 HU [interquartile range (IQR), 75.85 to 68.11 HU] at baseline vs. 76.09 HU [IQR, 80.08 to 70.37 HU] at 1 year; P < .001). In comparison, there was no change in FAI of the patients with psoriasis not receiving biologic therapy (median FAI, 71.98 [IQR, 77.36 to 65.64] at baseline vs. 72.66 [IQR, 78.21 to 67.44] at 1 year; P = .39).

Moreover, the researchers noted that the associations with FAI were “independent of the presence of coronary plaque and were consistent among patients receiving different biologic agents.”

“Treating the source of inflammation is very important. Cardiologists should keep an open mind that there are emerging risk factors, like psoriasis, that, when properly accounted for and treated, may mitigate vascular disease risks,” Mehta said.

Additionally, FAI improvement coincided with significant improvement of psoriasis (median PASI, 7.7 [IQR, 3.2-12.5] at baseline vs 3.2 [IQR, 1.8-5.7] at 1 year; P < .001).

“Treating remote areas of inflammation in the body matters,” Mehta said. “Cardiologists need to understand, it's not always just going to be manipulation of cardiovascular risk factors that we know of. It's got to be keeping an open mind that there are emerging risk factors that when properly accounted for and treated they may mitigate vascular disease risks.” – by Scott Buzby

Disclosures: Antoniades reported receiving personal fees from Caristo Diagnostics during the conduct of the study and having a pending, issued, licensed, and with royalties paid patent to PCT/GB2015/05235 and PCT/GB2016/1620494.3 and pending patents to GB2018/1818049.9,GR2018/0100490, and GR2018/0100510. Mehta reported being a full-time US government employee and serving as a consultant to and receiving grants or other payments from Amgen, EliLilly and LeoPharma; serving as a principal investigator and/or investigator to and receiving grants and/or research funding from AbbVie, Celgene, Janssen Pharmaceuticals, Inc. and Novartis; and serving as a principal investigator and receiving grants and/or research funding from the National Institutes of Health(NIH). Please see the study for all other authors’ relevant financial disclosures.