Continuous Positive Airway Pressure Effects on Pulmonary Hemodynamics and Left Ventricular Function in Obstructive Sleep Apnea and Obesity Hypoventilation Syndrome: A Systematic Review and Meta-Analysis.
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.
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.
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.
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.
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.
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.
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.