Abstract / Summary
Background: Obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS) are strongly linked to pulmonary hypertension and left ventricular abnormalities, driving cardiovascular issues. OHS, with daytime hypercapnia, affects 10%-20% of OSA patients. Continuous positive airway pressure (CPAP) is the first-line therapy, but its cardiac effects are inconsistent.
Methods: We conducted a systematic review and meta-analysis adhering to the PRISMA 2020 statement. Risk of bias was assessed using RoB 2 (RCTs) and the Newcastle-Ottawa Scale (NOS; cohort studies). Continuous outcomes were pooled as mean differences (MDs) with 95% CIs using random-effects models (restricted maximum likelihood) with Hartung-Knapp adjustment.
Results: Eight studies (574 participants; 2 RCTs, 6 cohorts) were included, showing that CPAP significantly reduced pulmonary arterial pressure (MD = -2.32 mmHg, 95% CI: -3.88 to -0.76, p = 0.004) versus controls. Secondary analyses indicated improved left ventricular diastolic function (early-to-late diastolic mitral inflow velocity [E/A] ratio: MD = 0.29, 95% CI: 0.09 to 0.48, p = 0.004). No significant effects on left ventricular mass index (LVMi) (MD = -2.31 percentage points, 95% CI: -6.38 to 1.77, p = 0.27) or left ventricular ejection fraction (LVEF) (MD = 0.53 percentage points, 95% CI: -1.49 to 2.55, p = 0.61) were found. Sensitivity analyses confirmed robustness. Funnel plot analysis suggested potential publication bias for pulmonary artery systolic pressure (PASP)/mean pulmonary artery pressure (mPAP), E/A ratio, and LVEF, while LVMi showed low bias.
Conclusions: In adults with OSA or OHS, CPAP reduces pulmonary arterial pressure and improves LV diastolic function, but it does not significantly alter LVMi or ejection fraction. These findings support CPAP as a key intervention to mitigate pulmonary hemodynamic burden and diastolic dysfunction in this high-risk population, while its potential to reverse structural cardiac remodeling requires further study.