Laaban J P, Cassuto D, Orvoën-Frija E, Iliou M C, Mundler O, Léger D, Oppert J M
Dept of Pneumology and Intensive Care, Hôtel-Dieu Hospital, Paris, France.
Eur Respir J. 1998 Jan;11(1):20-7. doi: 10.1183/09031936.98.11010020.
Assessment of cardiorespiratory consequences of sleep apnoea syndrome (SAS) is difficult owing to confounding factors, especially obesity, that are strongly associated with SAS. This study was designed to assess the cardiorespiratory consequences of SAS by comparing the results of a comprehensive cardiorespiratory evaluation in apnoeic and nonapnoeic patients with massive obesity. In a retrospective chart-review study, we studied 60 patients with massive obesity defined by a body mass index (BMI) >40 kg.m(-2), presenting no chronic respiratory disease, who underwent an extensive assessment of cardiorespiratory consequences of obesity, including overnight polysomnography, lung function tests, arterial blood gas analysis, evaluation of vascular risk factors, myocardial scintigraphy with dipyridamole stress-test, isotopic ventriculography, Doppler echocardiography and Holter electrocardiogram recording. SAS defined by an apnoea + hypopnoea index (AHI) > or = 10 was diagnosed in 42% of patients (25 out of 60). Mean+/-SD AHI of SAS-positive (SAS+) patients was 38+/-24. Age, BMI, ventilatory function parameters, prevalence of smoking history and diabetes mellitus did not differ significantly in SAS+ versus SAS-negative (SAS-) groups. The following complications were observed more frequently in SAS+ than in SAS- patients: daytime hypoxaemia (35 vs 9%, p<0.02), pulmonary arterial hypertension (36 vs 7%, p<0.05) and increased interventricular septal thickness (50 vs 15%, p<0.03). No association was found between SAS on the one hand and systemic arterial hypertension, coronary artery disease, left ventricular dysfunction and nocturnal cardiac arrhythmias on the other. Nocturnal apnoeas in massive obesity may thus be associated with moderate daytime hypoxaemia, mild pulmonary arterial hypertension and moderate left ventricular hypertrophy, but not with severe cardiorespiratory complications.
由于存在混杂因素,尤其是与睡眠呼吸暂停综合征(SAS)密切相关的肥胖,对SAS的心肺后果进行评估很困难。本研究旨在通过比较重度肥胖的呼吸暂停患者和非呼吸暂停患者全面心肺评估的结果,来评估SAS的心肺后果。在一项回顾性病历审查研究中,我们研究了60例体重指数(BMI)>40 kg·m⁻²、无慢性呼吸系统疾病的重度肥胖患者,他们接受了肥胖心肺后果的广泛评估,包括整夜多导睡眠图、肺功能测试、动脉血气分析、血管危险因素评估、双嘧达莫负荷试验心肌闪烁显像、同位素心室造影、多普勒超声心动图和动态心电图记录。42%(60例中的25例)的患者被诊断为呼吸暂停低通气指数(AHI)≥10的SAS。SAS阳性(SAS+)患者的平均±标准差AHI为38±24。SAS+组和SAS阴性(SAS-)组在年龄、BMI、通气功能参数、吸烟史和糖尿病患病率方面无显著差异。与SAS-患者相比,SAS+患者更频繁地出现以下并发症:白天低氧血症(35%对9%,p<0.02)、肺动脉高压(36%对7%,p<0.05)和室间隔厚度增加(五十%对15%,p<0.03)。一方面,未发现SAS与另一方面的系统性动脉高血压、冠状动脉疾病、左心室功能障碍和夜间心律失常之间存在关联。因此,重度肥胖患者的夜间呼吸暂停可能与中度白天低氧血症、轻度肺动脉高压和中度左心室肥厚有关,但与严重的心肺并发症无关。