Moderate-to-severe obstructive sleep apnea is associated with subclinical myocardial injury and impaired hemodynamics in pulmonary hypertension patients

Abstract

BackgroundThe 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. MethodsCross-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. ResultsModerate-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). ConclusionsModerate-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.