Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sydney, Australia.
Faculty of Medicine and Health, University of Sydney, Sydney, Australia.
J Clin Sleep Med. 2022 Apr 1;18(4):1063-1071. doi: 10.5664/jcsm.9804.
The main cause of death in patients with obesity hypoventilation syndrome (OHS) is cardiac rather than respiratory failure. Here, we investigated autonomic-respiratory coupling and serum cardiac biomarkers in patients with OHS and obstructive sleep apnea (OSA) with comparable body mass index and apnea-hypopnea index.
Cardiopulmonary coupling (CPC) and cyclic variation of heart rate analysis was performed on the electrocardiogram signal from the overnight polysomnogram. Cardiac serum biomarkers were obtained in patients with OHS and OSA with a body mass index > 40 kg/m. Samples were obtained at baseline and after 3 months of positive airway pressure (PAP) therapy in both groups.
Patients with OHS (n = 15) and OSA (n = 36) were recruited. No group differences in CPC, cyclic variation of heart rate, and serum biomarkers were observed at baseline and after 3 months of PAP therapy. An improvement in several CPC metrics, including the sleep apnea index, unstable sleep (low-frequency coupling and elevated low-frequency coupling narrow band), and cyclic variation of heart rate were observed in both groups with PAP use. However, distinct differences in response characteristics were noted. Elevated low-frequency coupling narrow band coupling correlated with highly sensitive troponin-T ( < .05) in the combined cohort. Baseline highly sensitive troponin-T inversely correlated with awake oxygen saturation in the OHS group ( < .05).
PAP therapy can significantly improve CPC stability in patients with obesity with OSA or OHS, with key differences. Elevated low-frequency coupling narrow band may function as a surrogate biomarker for early subclinical cardiac disease. Low awake oxygen saturation could also increase this biomarker in OHS.
Registry: Australian New Zealand Clinical Trials Registry; Name: Obesity Hypoventilation Syndrome and Neurocognitive Dysfunction; URL: https://anzctr.org.au/Trial/Registration/TrialReview.aspx?id=367492; Identifier: ACTRN12615000122550.
Sivam S, Wang D, Wong KKH, et al. Cardiopulmonary coupling and serum cardiac biomarkers in obesity hypoventilation syndrome and obstructive sleep apnea with morbid obesity. . 2022;18(4):1063-1071.
肥胖低通气综合征（OHS）患者的主要死亡原因是心脏而不是呼吸衰竭。在这里，我们研究了在体质量指数（BMI）和呼吸暂停低通气指数（AHI）相似的肥胖合并阻塞性睡眠呼吸暂停（OSA）患者中，自主呼吸耦合和血清心脏生物标志物的变化。
对整夜多导睡眠图的心电图信号进行心肺耦合（CPC）和心率周期性变化分析。对 BMI＞40 kg/m2 的 OHS 和 OSA 患者进行血清心脏生物标志物检测。两组患者均在基线和接受正压通气（PAP）治疗 3 个月后留取标本。
共纳入 OHS 患者（n=15）和 OSA 患者（n=36）。两组患者在基线和 PAP 治疗 3 个月时 CPC、心率周期性变化和血清生物标志物均无差异。两组患者在使用 PAP 后，多项 CPC 指标均有改善，包括睡眠呼吸暂停指数、不稳定睡眠（低频耦合和升高的低频耦合窄带）和心率周期性变化。然而，两组患者的反应特征存在明显差异。在联合队列中，升高的低频耦合窄带与高敏肌钙蛋白 T（<0.05）呈显著相关。在 OHS 组中，基线高敏肌钙蛋白 T 与清醒时氧饱和度呈负相关（<0.05）。
PAP 治疗可显著改善肥胖合并 OSA 或 OHS 患者的 CPC 稳定性，但存在关键差异。升高的低频耦合窄带可能是早期亚临床心脏疾病的替代生物标志物。OSH 患者的低清醒时氧饱和度也会增加这种生物标志物。
注册机构：澳大利亚和新西兰临床试验注册中心；名称：肥胖低通气综合征和神经认知功能障碍；网址：https://anzctr.org.au/Trial/Registration/TrialReview.aspx?id=367492；标识符：ACTRN12615000122550。
Sivam S, Wang D, Wong KKH, et al. Cardiopulmonary coupling and serum cardiac biomarkers in obesity hypoventilation syndrome and obstructive sleep apnea with morbid obesity.. 2022;18(4):1063-1071.
