Epicardial adipose tissue is the pad of fat that sits directly on the surface of the heart, wrapped around the coronary arteries that supply the heart muscle itself. Unlike the subcutaneous fat under the skin or the visceral fat deeper in the abdomen, this depot shares the same blood supply as the coronary vessels and is separated from the arterial wall by only a thin barrier. That anatomical intimacy matters, because epicardial fat is not merely inert storage. It is metabolically active, secreting inflammatory signaling molecules such as interleukin-6 and other cytokines, and growing evidence links an expanded or inflamed epicardial depot to coronary atherosclerosis and adverse cardiac events.

The study, led by Ruilin Wang, Meichen Liu, Ming Yang, and Xiaomei Chen of West China Hospital, Sichuan University, took a cross-sectional design with a methodological safeguard. The researchers enrolled 157 adults with psoriasis and matched each one to two controls by age, sex, and body mass index, yielding 314 comparison subjects. Propensity score matching is a statistical technique that pairs participants who have similar likelihoods of belonging to one group based on measured characteristics, which helps ensure that any differences observed between groups are not simply artifacts of age, sex, or overall body size. Because obesity itself drives epicardial fat expansion, this matching step is critical to isolating any effect specific to psoriasis.

The measurement itself was elegantly simple. On non-contrast CT scans, the team drew a region of interest on a single axial slice at the level of the left main coronary artery, one of the first branches off the aorta, and quantified two things: the cross-sectional area of the fat and its mean density in Hounsfield units, the standard radiological scale on which water measures zero and fat typically reads well below that. Prior work has shown that a single-slice measurement at this anatomical level serves as a reasonable proxy for total epicardial fat burden, making it a practical tool when CT is already being performed for other reasons.

The results were unambiguous. Patients with psoriasis had an average epicardial fat area of 13.4 square centimeters, compared with 9.5 square centimeters in matched controls, a difference of nearly 40 percent. The density finding was subtler but arguably more intriguing: psoriasis patients’ epicardial fat averaged -70.3 Hounsfield units, while controls averaged -75.3 Hounsfield units. Both differences were highly statistically significant, with P values below 0.001. Because fat is less dense than water, a higher, less negative Hounsfield value means the tissue is denser than ordinary fat, a pattern that in other contexts has been interpreted as a signature of inflammation, increased water content, and greater metabolic activity within the fat depot.

The inverse relationship between the two measurements adds another layer. Across participants, larger epicardial fat area went hand in hand with higher density, and this inverse correlation was stronger in the psoriasis group than in the controls. In other words, the psoriasis-associated fat depot was not just bigger; it appeared to be compositionally altered in a way consistent with the idea that chronic inflammatory signaling reshapes this tissue. Previous systematic reviews and meta-analyses of CT-derived epicardial fat density have reported that denser epicardial fat tracks with subclinical atherosclerosis, inflammation, and major adverse cardiac events in asymptomatic people, which makes the present finding potentially meaningful for cardiovascular risk stratification.

Within the psoriasis group, the correlates of epicardial fat area were telling. The depot expanded with body mass index, age, and disease duration, but notably not with the Psoriasis Area and Severity Index, the standard clinical measure of current skin involvement. That dissociation suggests that the cumulative lifetime exposure to psoriatic inflammation, rather than the severity of the current skin flare, may be what leaves its mark on the fat surrounding the heart. It aligns with earlier observations that the duration of psoriasis relates to vascular inflammation and cardiovascular events independently of current disease activity scores.

The clinical implications extend beyond dermatology. Greater epicardial fat area in the psoriasis patients was also associated with a higher burden of cardiovascular risk factors even after accounting for age and body mass index. Psoriasis is already known to confer elevated risk of cardiovascular disease through mechanisms that include shared inflammatory pathways, particularly the interleukin-23 and T helper 17 axis that drives both the skin lesions and systemic inflammation. If epicardial fat serves as a local amplifier of coronary inflammation, then a CT-derived phenotype of enlarged, denser epicardial fat could help identify which patients with psoriasis warrant closer cardiovascular surveillance, without requiring any additional imaging beyond what may already exist in their medical records.

The authors are careful about what the study can and cannot show. As a cross-sectional, propensity score-matched analysis, it demonstrates association rather than causation; it cannot prove that psoriatic inflammation causes epicardial fat expansion, only that the two co-occur after matching for major confounders. The single-slice approach, while validated as an indirect measure of total fat burden, captures one plane of anatomy rather than a full volumetric assessment. And because the scans were non-contrast and retrospective, the study reflects routine clinical imaging rather than a dedicated research protocol. Still, the combination of area and density measurements on a single slice is an appealingly low-cost way to extract cardiometabolic information from scans that are ordered for entirely unrelated reasons.

What emerges is a picture of psoriasis as a disease whose consequences reach well beyond the skin, inscribed in the very tissue that hugs the coronary arteries. The finding that this fat is both larger and denser in psoriasis, independent of age, sex, and body size, strengthens the case that chronic skin inflammation reshapes the cardiac fat depot in ways that may matter for the heart. As imaging biomarkers of fat inflammation, such as fat attenuation indices around the coronaries, gain traction in cardiology, dermatologists and cardiologists may find themselves reading the same scans for different reasons, and the humble chest CT could become an unexpected bridge between the two specialties in the care of patients with psoriasis.

Subject of Research: CT-measured epicardial adipose tissue area and density in patients with psoriasis compared with matched controls

Article Title: CT-derived epicardial adipose tissue area and density in psoriasis: a propensity score–matched cross-sectional study

Article References: Wang, R., Liu, M., Yang, M., & Chen, X. (2026). CT-derived epicardial adipose tissue area and density in psoriasis: a propensity score–matched cross-sectional study. Archives of Dermatological Research, 318(1), Article 414. https://doi.org/10.1007/s00403-026-04884-1

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04884-1

Keywords: psoriasis, epicardial adipose tissue, computed tomography, cardiovascular risk, inflammation, cardiometabolic burden, propensity score matching, visceral fat, Hounsfield units, dermatology, atherosclerosis, CT-derived