Epicardial adipose tissue is associated with increased systolic pulmonary artery pressure in patients with chronic obstructive pulmonary disease

Objectives Pulmonary hypertension (PHT) is one of the essential predictors of mortality in chronic obstructive pulmonary disease (COPD). It is thought that PHT is due to vasoconstriction secondary to hypoxia caused by airway obstruction in COPD patients; however, loss of capillary bed with emphysema, inflammation, and endothelial dysfunction may also play a role in the development of PHT. Epicardial adipose tissue (EAT) has a role as a metabolically active endocrine organ and secretes various proinflammatory cytokines. We hypothesized that EAT thickness in COPD patients might be associated with the systolic pulmonary arterial pressure (PAPs) level, and we aimed to test it. Methods The present study included 129 consecutive patients with the diagnosis of COPD. All patients underwent transthoracic echocardiographic evaluation. The relationship between PAPs and EAT thickness was evaluated. Results Positive correlations with PAPs were reported with age, EAT, white blood cell (WBC) and GOLD grade score (range 0.197-0.275, P values 0.026 to 0.002), negative correlations with body-mass index (BMI), hyperlipidemia, FEV1 (% predicted) and pO2 (range -0.216 to -0.340, P values .014 to <.001). In stepwise linear regression analysis, BMI (P = .003), EAT (P = .002), WBC (P = .001), and FEV1 (% predicted) (P = .010), were independently associated with PAPs. Conclusion EAT thickness in COPD patients with preserved left ventricular systolic function is associated with increased PAPs, and this association is independent of the parameters indicating the severity of COPD.

Automated summary

This study found that EAT thickness in COPD patients is positively correlated with systolic pulmonary arterial pressure (PAPs) levels, and is independently associated with factors such as BMI, WBC, and FEV1 in linear regression analysis. This suggests that EAT may play a role in the development of PHT in COPD patients, regardless of the severity of COPD.