Rapid Fire Abstracts
Shuo Wang, MD, PhD
Research Associate
University of Virginia Health System
Shuo Wang, MD, PhD
Research Associate
University of Virginia Health System
Jamey Cutts, MD
Cardiology Fellow
University of Virginia Medical center
John T. Echols
PhD Candidate
University of Virginia
Julia Bresticker, MS
MD/PhD Student
University of Virginia
.jpg "Patricia Rodriguez-Lozano, MD,MS photo")
Patricia Rodriguez-Lozano, MD,MS
Director Women's Heart Program
University of Virginia
Patrick Norton, MD
Associate Professor
University of Virginia
Christopher M. Kramer, MD
Chief, Cardiovascular Division
University of Virginia Health
University of Virginia
Amit R. Patel, MD
Professor of Medicine
Division of Cardiology, University of Virginia Health System, Charlottesville, Virginia, USA.
Epicardial adipose tissue (EAT) is an organ of ever-increasing interest due to its close proximity to the heart, shared blood supply with the myocardium, variable metabolic activity, and recent data suggesting a pro-inflammatory and restraining effect on the myocardium. While EAT volume correlates with adverse cardiac outcomes, EAT quality is less well studied. We hypothesized that pro-inflammatory EAT, as determined using Cardiac Magnetic Resonance (CMR) EAT T1 relaxation time, may better correlate with severity of heart failure with preserved ejection fraction (HFpEF) than EAT volume.
Methods:
We enrolled 30 patients with prior echo demonstrating HFpEF who were scheduled to undergo CMR at UVA Health. CMR was performed on a 1.5T Siemens Aera scanner. EAT volume (EATV) was manually quantified at end systole on short axis (SA) SSFP cine images. EAT T1-mapping was acquired using a modified Look-Locker Imaging (MOLLI) sequence with a 5(3)3 scheme before gadolinium contrast injection (Figure 1). EAT T1 values were obtained by averaging regions of interest within the EAT on basal and mid ventricular SA images. A subgroup of 13 patients underwent stress CMR using the saturation preparation pulse dual sequence technique for quantification of stress myocardial blood flow (MBF). All subjects were stratified by echocardiographic degree of left ventricle diastolic dysfunction (LVDD) into three groups: controls (no LVDD), Grade I DD, or Grade II and III DD. Subjects were also stratified into low (0-1), intermediate (2-5), and high (6-9) probability of HFpEF by H2FPEF score. ANOVA was used to compare EAT T1 and EATV between different DD categories or probability of HFpEF. The relation of EAT T1 or EATV and stress MBF were tested using linear regression analysis.
Results:
Baseline characteristics and groupings are showed in Table 1. EAT T1 was significantly lower in the Grade II and III DD group compared to controls (239 (221, 273) vs 266 (260, 277) ms, p=0.03) (Fig.2a). Similarly, the high risk H2FPEF group had lower EAT T1 values compared to the low (p=0.02) and intermediate (p=0.01) risk groups (Fig 1, Fig.2b). However, there was no significant difference in EATV between LVDD groups (p=0.296) (Fig.2d) or H2FPEF risk category (p=0.124) (Fig.2e). On subgroup analysis, stress MBF showed good correlation with EAT T1 (r=0.60, p=0.035) (Fig. 2c), but no correlation with EATV (r=0.10, p=0.811) (Fig. 2f).
Conclusion:
In this study, we demonstrate that EAT quality (as defined by EAT T1 measurements) associate more strongly with severity of diastolic dysfunction and features of HFpEF than EAT volume. Additionally, we show a correlation between EAT T1 and stress MBF suggesting pro-inflammatory EAT may trigger coronary microvascular dysfunction as a mechanism for the development of HFpEF.
