Abstract 4366420: Epicardial Adipose Tissue Biomarkers Are Associated with Myocardial Perfusion in Women with Angina and No Obstructive Coronary Artery Disease: A CMR study

S Shuo Wang J John Echols (University of Virginia, Charlottesville, Virginia, United States) B Bishow Paudel (University of Virginia, Charlottesvle, Virginia, United States) N Nisha Hosadurg (University of Virginia, Charlottesville, Virginia, United States) L Lauren Preston (University of Virginia, Charlottesvle, Virginia, United States) G Genevieve Lyons (University of Virginia, Charlottesville, Virginia, United States) K Kelsey M Watts (University of Virginia, Charlottesvle, Virginia, United States) J Jonathan Pan (University of Virginia, Charlottesvle, Virginia, United States) P Peter Kellman (NIH, BETHESDA, Maryland, United States) M Mete Civelek A Amit Patel F Frederick Epstein (UNIVERSITY VIRGINIA, Charlottesvle, Virginia, United States) C Christopher Krämer P Patricia Rodriguez-Lozano (University of Virginia, Charlottesville, Virginia, United States)

Abstract

Background: Angina with no obstructive coronary artery disease (ANOCA) is common in women and often linked to coronary microvascular dysfunction (CMD). Epicardial adipose tissue (EAT), a metabolically active fat depot sharing microcirculation with the myocardium, may promote CMD through inflammatory signaling. T1 relaxation time and saturated fatty acid (SFA) fraction are emerging CMR-derived markers of adipose inflammation and lipid content. We hypothesize that altered EAT composition—characterized by lower T1 and elevated SFA—reflects a pro-inflammatory state and is associated with impaired myocardial perfusion in women with ANOCA. Methods: This was a single-center, prospective study. Subjects underwent CMR scan at 1.5T (Aera), including rest and regadenoson stress perfusion with automated inline global rest and stress myocardial blood flow (MBF), myocardial perfusion reserve (MPR). EAT volume (EATV), Native EAT T1 and EAT SFA were measured using different CMR images. (Figure 1). Pearson correlation coefficients and multivariable linear regression adjusted for age were used to assess associations between EAT biomarkers, MBF, and MPR. CMD was defined as MPR <2.4. Results: Thirty-two women were recruited ( Figure 2) . Ten (32%) of women had CMD. EAT T1 was moderately correlated with stress MBF (r=0.50, p=0.01) and MPR (r=0.4, p=0.05) (Figure). EAT SFA was moderately negatively correlated with stress MBF (r=-0.47, p=0.04), MPR (r=-0.49, p=0.03) (Figure). EATV index (EATVI) showed moderate correlation with stress MBF (r=0.4, p=0.03), but no significant association with MPR (p=0.28) (Figure 3) . After adjusting for age, each 10 ms decrease in EAT T1 was associated with a 0.17 ml/min/g reduction in stress MBF (β = 0.17, 95% CI: 0.05, 0.29, p = 0.01), and a 0.17 reduction in MPR (β = 0.17, 95% CI: 0.02, 0.33, p =0.04). Additionally, each 0.01 increase in SFA was associated with a 0.05 ml/min/g reduction in stress MBF (β = -0.05, 95% CI: -0.10, -0.01, p = 0.05), and a 0.06 reduction in MPR (β = -0.06, 95% CI: -0.12, -0.05, p =0.04). Conclusion: CMR-derived EAT T1 relaxation time and SFA fraction are associated with CMD in women with ANOCA. Elevated SFA and reduced T1, reflective of a pro-inflammatory adipose phenotype, are independently associated with impaired myocardial perfusion. These findings support a potential mechanistic link between EAT metabolic dysfunction and CMD and underscore the value of multiparametric CMR in the phenotyping at-risk women with ANOCA.

Article Details

Journal Circulation
Volume / Issue Vol. 152, Issue Suppl_3
Published November 04, 2025
ISSN 0009-7322
Publisher Lippincott Williams & Wilkins

Journal Info

Circulation

Lippincott Williams & Wilkins

ISSN: 0009-7322 Health Sciences

Authors (14)

S

Shuo Wang

J

John Echols

University of Virginia, Charlottesville, Virginia, United States

B

Bishow Paudel

University of Virginia, Charlottesvle, Virginia, United States

N

Nisha Hosadurg

University of Virginia, Charlottesville, Virginia, United States

L

Lauren Preston

University of Virginia, Charlottesvle, Virginia, United States

G

Genevieve Lyons

University of Virginia, Charlottesville, Virginia, United States

K

Kelsey M Watts

University of Virginia, Charlottesvle, Virginia, United States

J

Jonathan Pan

University of Virginia, Charlottesvle, Virginia, United States

P

Peter Kellman

NIH, BETHESDA, Maryland, United States

M

Mete Civelek

A

Amit Patel

F

Frederick Epstein

UNIVERSITY VIRGINIA, Charlottesvle, Virginia, United States

C

Christopher Krämer

P

Patricia Rodriguez-Lozano

University of Virginia, Charlottesville, Virginia, United States