CARDIORESPIRATORY CONSEQUENCE OF SLEEP-APNEA SYNDROME IN PATIENTS WITH MASSIVE OBESITY

Assessment of cardiorespiratory consequences of sleep apnoea syndrome (SAS) is difficult erring to confounding factors, especially obesity, that are strongly associated with SAS. This study was designed to asse ss the cardiorespiratory consequences of SAS by comparing the results of a comprehensive cardiorespiratory evaluation in apnoeic and nonapno eic patients with massive obesity, In a retrospective chart-review stu dy, 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 consequence s of obesity, including overnight polysomnography, lung function tests , arterial blood gas analysis, evaluation of vascular risk factors, my ocardial scintigraphy with dipyridamole stress-test, isotopic ventricu lography, Doppler echocardiography and Holter electrocardiogram record ing. SAS defined by an apnoea + hypopnoea index (AHI) greater than or equal to 10 was diagnosed in 42% of patients (25 out of 60), Mean+/-SD AHI of SAS-positive (SAS+) patients was 38+/-24. Age, BMI, ventilator y function parameters, prevalence of smoking history and diabetes mell itus did not differ significantly in SAS+ versus SAS-negative (SAS-) g roups. The following complications were observed more frequently in SA S+ than in SAS-patients: daytime hypoxaemia (35 vs 9%, , p<0.02), pulm onary arterial hypertension (36 vs 7%, p<0.05) and increased intervent ricular septal thickness (50 vs 15%, p<0.03). No association was found between SAS on the one hand and systemic arterial hypertension, coron ary artery disease, left ventricular dysfunction and nocturnal cardiac arrhythmias on the other. Nocturnal apnoeas in massive obesity mar th us be associated with moderate daytime hypoxaemia, mild pulmonary arte rial hypertension and moderate left ventricular hypertrophy, but not w ith severe cardiorespiratory complications.