Epicardial adipose tissue is an independent risk factor for mortality in pulmonary arterial hypertension

McCarthy, Breanne E. and Feng, Rui and Torigian, Drew A. and Tong, Yubing and Fritz, Jason S. and Minhas, Jasleen K. and Mazurek, Jeremy A. and Smith, K. Akaya and Palevsky, Harold I. and Pugliese, Steven C. and Homer, Natalie Z. and MacLean, Margaret R. and Udupa, Jayaram K. and Nadine Al-Naamani, Nadine (2024) Epicardial adipose tissue is an independent risk factor for mortality in pulmonary arterial hypertension. CHEST. ISSN 0012-3692 (In Press)

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Abstract

Background: Increased epicardial adipose tissue (EAT) has adverse effects in cardiovascular diseases, independent of body mass index (BMI). Estrogen levels may impact EAT accumulation. Little is known about the predictors and potential impact of EAT in 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 computed tomography (CT) scans to quantify EAT. We also measured serum estrone and estradiol levels. Results: 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 PAH (35.3%). Median EAT volume was 52.1 mL/m2. Of the 102 patients with a follow-up chest CT, EAT increased over time in 74 (71.8%). High EAT volume (HR 2.62, 95% CI 1.62-4.24, p<0.001) and greater accumulation of EAT over time (HR 1.09, 95% CI 1.01 – 1.17, p=0.03) were both independently associated with worse survival. Patients with high EAT volume had lower serum estrone (13.70 versus 30.60 pg/mL, p=0.009) and estradiol (6.05 versus 19.40 pg/mL, p=0.002) levels compared to 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.

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