持续气道正压通气对阻塞性睡眠呼吸暂停与肥胖低通气综合征患者肺血流动力学及左心室功能的影响：系统综述与荟萃分析。
完整摘要 · 中文译文
背景：阻塞性睡眠呼吸暂停（OSA）和肥胖低通气综合征（OHS）与肺动脉高压和左心室异常密切相关，可导致心血管问题。伴有日间高碳酸血症的OHS影响10%-20%的OSA患者。持续气道正压通气（CPAP）是一线治疗，但其心脏效应不一致。 方法：我们按照PRISMA 2020声明进行了系统综述和荟萃分析。偏倚风险分别使用RoB 2（随机对照试验）和纽卡斯尔-渥太华量表（NOS；队列研究）进行评估。连续结局使用随机效应模型（限制性最大似然法）并采用Hartung-Knapp校正，以均数差（MD）及95%CI进行合并。 结果：共纳入8项研究（574名参与者；2项随机对照试验，6项队列研究），显示与对照组相比，CPAP显著降低肺动脉压（MD = -2.32 mmHg，95% CI：-3.88至-0.76，p = 0.004）。二次分析表明左心室舒张功能改善（二尖瓣流入舒张早期与晚期速度比值[E/A]：MD = 0.29，95% CI：0.09至0.48，p = 0.004）。未发现对左心室质量指数（LVMi）（MD = -2.31个百分点，95% CI：-6.38至1.77，p = 0.27）或左心室射血分数（LVEF）（MD = 0.53个百分点，95% CI：-1.49至2.55，p = 0.61）有显著影响。敏感性分析证实了稳健性。漏斗图分析提示肺动脉收缩压（PASP）/平均肺动脉压（mPAP）、E/A比值和LVEF可能存在发表偏倚，而LVMi显示lo w偏倚。 结论：在患有OSA或OHS的成人中，CPAP可降低肺动脉压并改善左心室舒张功能，但不会显著改变左心室质量指数或射血分数。这些发现支持将CPAP作为减轻该高危人群肺血流动力学负担和舒张功能障碍的关键干预措施，而其逆转心脏结构重塑的潜力仍需进一步研究。
完整摘要 · 英文原文
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.