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.
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.
Original language | English |
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Journal | Chest Journal |
DOIs | |
Publication status | Published - 28 Nov 2024 |
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