BACKGROUND: The clinical significance of obstructive sleep apnea (OSA) in pulmonary hypertension (PH) patients remains unclear. We investigated the hemodynamics and serum troponin T concentrations associated with OSA in PH patients. METHODS: Cross-sectional study was performed on data from 97 clinically stable PH patients. Using overnight sleep study, we evaluated apnea-hypopnea index (AHI) and divided patients into two groups: none-to-mild OSA (AHI < 15/h, N = 81) and moderate-to-severe OSA (AHI ≥ 15/h, N = 16). Clinical, hemodynamic, and laboratory data were compared with OSA severity. RESULTS: Moderate-to-severe OSA patients had higher pulmonary vascular resistance (PVR; 6.5 [5.7-12.9] vs 4.4 [2.9-6.4] Wood units, p = 0.001) and mean pulmonary artery pressure (mPAP; 37 [30-49] vs 30 [22-37] mmHg, p = 0.045), and a lower cardiac index (2.2 [1.6-2.6] vs 2.8 [2.3-3.5] L/min/m2, p = 0.001) than those without. There was no association between plasma B-type natriuretic peptide (BNP) or serum C-reactive protein levels and OSA. However, high-sensitivity troponin T (hs-TnT) level was significantly higher in moderate-to-severe OSA patients (13 [8-18] vs 6 [4-10] ng/L, p <0.001). The hs-TnT level positively correlated with the plasma BNP level, mPAP, PVR, AHI, obstructive apnea index, and 6-min walking distance. After adjustment for age, estimated glomerular filtration rate, hypertension, smoking, and plasma BNP level, moderate-to-severe OSA was an independent factor for determining the plasma level of log hs-TnT level (β = 0.419, 95% confidence interval 0.119-0.718, p = 0.007). CONCLUSIONS: Moderate-to-severe OSA is associated with impaired hemodynamics and subclinical myocardial damage in PH patients. Thus, OSA-related myocardial injury may play a role in hemodynamic destabilization with its associated poor prognosis.
BACKGROUND: The clinical significance of obstructive sleep apnea (OSA) in pulmonary hypertension (PH) patients remains unclear. We investigated the hemodynamics and serum troponin T concentrations associated with OSA in PH patients. METHODS: Cross-sectional study was performed on data from 97 clinically stable PH patients. Using overnight sleep study, we evaluated apnea-hypopnea index (AHI) and divided patients into two groups: none-to-mild OSA (AHI < 15/h, N = 81) and moderate-to-severe OSA (AHI ≥ 15/h, N = 16). Clinical, hemodynamic, and laboratory data were compared with OSA severity. RESULTS: Moderate-to-severe OSA patients had higher pulmonary vascular resistance (PVR; 6.5 [5.7-12.9] vs 4.4 [2.9-6.4] Wood units, p = 0.001) and mean pulmonary artery pressure (mPAP; 37 [30-49] vs 30 [22-37] mmHg, p = 0.045), and a lower cardiac index (2.2 [1.6-2.6] vs 2.8 [2.3-3.5] L/min/m2, p = 0.001) than those without. There was no association between plasma B-type natriuretic peptide (BNP) or serum C-reactive protein levels and OSA. However, high-sensitivity troponin T (hs-TnT) level was significantly higher in moderate-to-severe OSA patients (13 [8-18] vs 6 [4-10] ng/L, p <0.001). The hs-TnT level positively correlated with the plasma BNP level, mPAP, PVR, AHI, obstructive apnea index, and 6-min walking distance. After adjustment for age, estimated glomerular filtration rate, hypertension, smoking, and plasma BNP level, moderate-to-severe OSA was an independent factor for determining the plasma level of log hs-TnT level (β = 0.419, 95% confidence interval 0.119-0.718, p = 0.007). CONCLUSIONS: Moderate-to-severe OSA is associated with impaired hemodynamics and subclinical myocardial damage in PH patients. Thus, OSA-related myocardial injury may play a role in hemodynamic destabilization with its associated poor prognosis.