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Published on: April 24, 2018
Epicardial Adipose Tissue as an Independent Risk Factor for Mortality in Pulmonary Arterial Hypertension
Breanne E McCarthy1, Rui Feng2, Drew A Torigian3
1Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA.
Background:
Increased epicardial adipose tissue (EAT) has adverse effects in cardiovascular diseases, independent of BMI. Estrogen levels may affect EAT accumulation. Little is known about the predictors and potential impact of EAT in pulmonary arterial hypertension (PAH).
Research Question:
Is EAT associated with estrogen levels, disease severity, and mortality in PAH?
Study Design And Methods:
We conducted a retrospective cohort study of patients with PAH enrolled in the Penn Pulmonary Hypertension registry and used chest CT scans to quantify EAT. Serum estrone and estradiol levels were also measured.
Results:
A total of 221 patients were included in the analysis, with median follow-up of 88 months. Mean age was 55.1 years, 74.7% were female, mean BMI was 27.20 kg/m2, and the most common PAH etiology was connective tissue disease-associated PAH (43.0%) followed by idiopathic or heritable PAH (35.3%). Median EAT volume was 52.1 mL/m2. Of the 102 patients with a follow-up chest CT scan, EAT increased over time in 74 (71.8%). High EAT volume (hazard ratio, 2.62; 95% CI, 1.62-4.24; P < .001) and greater accumulation of EAT over time (hazard ratio, 1.09; 95% CI, 1.01-1.17; P = .03) were both independently associated with worse survival. Patients with high EAT volume had lower serum estrone (13.70 vs 30.60 pg/mL; P = .009) and estradiol (6.05 vs 19.40 pg/mL; P = .002) levels compared with those with low EAT volume.
Interpretation:
In patients with PAH, high EAT and a greater rate of accumulation of EAT volume were independently associated with worse survival. Higher EAT volume was also associated with lower estrogen levels. The association of EAT volume with survival was independent of BMI and disease severity, suggesting that EAT may be a marker for a unique PAH phenotype. Future research should investigate the role of EAT-modifying therapies in PAH and consider incorporating EAT into PAH risk models.
