Background-Atrial fibrillation (AF) has been linked to inflammatory factors and obesity. Epicardial fat is a source of several inflammatory mediators related to the development of coronary artery disease. We hypothesized that periatrial fat may have a similar role in the development of AF. Methods and Results-Left atrium (LA) epicardial fat pad thickness was measured in consecutive cardiac CT angiograms performed for coronary artery disease or AF. Patients were grouped by AF burden: no (nϭ73), paroxysmal (nϭ60), or persistent (nϭ36) AF. In a short-axis view at the mid LA, periatrial epicardial fat thickness was measured at the esophagus (LA-ESO), main pulmonary artery, and thoracic aorta; retrosternal fat was measured in axial view (right coronary ostium level). LA area was determined in the 4-chamber view. LA-ESO fat was thicker in patients with persistent AF versus paroxysmal AF (Pϭ0.011) or no AF (Pϭ0.003). LA area was larger in patients with persistent AF than paroxysmal AF (Pϭ0.004) or without AF (PϽ0.001). LA-ESO was a significant predictor of AF burden even after adjusting for age, body mass index, and LA area (odds ratio, 5.30; 95% confidence interval, 1.39 to 20.24; Pϭ0.015).A propensity score-adjusted multivariable logistic regression that included age, body mass index, LA area, and comorbidities was also performed and the relationship remained statistically significant (Pϭ0.008). Conclusions-Increased

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Pulmonary hypertension is a disabling disease characterized by progressive functional worsening, right heart failure, and death. Although pulmonary hypertension has been associated with poor quality of life, sleep quality has not been investigated in pulmonary hypertension patients. This was a cross-sectional study in which patients (N = 40) were asked to complete standardized questionnaires to assess sleep quality [using Pittsburgh Sleep Quality Index (PSQI)], insomnia, sleepiness, dyspnea, depression, restless leg syndrome, and quality of life [using Cambridge Pulmonary Hypertension Outcome Review (CAMPHOR)] during routine office visits. Baseline hemodynamics, pulmonary function tests, exercise capacity, and transthoracic echocardiogram were analyzed. Pulmonary hypertension functional class was World Health Organization class II [20 (50%)], III [18 (45%)], and IV [2 (5%)], and 29 (72.5%) had poor sleep quality. PSQI score was associated with CAMPHOR symptoms score (R = 0.61, P < 0.001), CAMPHOR activities score (R = 0.38, P = 0.016), CAMPHOR quality-of-life score (R = 0.45, P = 0.004), depression (R = 0.42, P = 0.007), and dyspnea (R = 0.36, P = 0.02). Sleep quality was not associated with age, gender, other comorbidities, pulmonary hypertension etiology, baseline hemodynamics, pulmonary function testing, echocardiographic parameters, or exercise capacity. Poor sleep quality is common in patients with pulmonary hypertension and correlates with depression, dyspnea, and poor quality of life. Improving sleep quality in patients with pulmonary hypertension may improve quality of life.

Lower serum albumin concentrations in patients with PAH are associated with higher mortality and can serve as a marker of disease severity in this patient population.