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aaSleep apnoea syndrome (SAS) has been reported to be associated with excess mortality [1,2] and a wide range of cardiac and respiratory sequelae [3][4][5]: daytime alveolar hypoventilation, pulmonary arterial hypertension, systemic arterial hypertension, left ventricular hypertrophy and dysfunction, cardiac arrhythmias and ischaemic heart disease. However, conflicting data have been published on the cardiorespiratory consequences of SAS. This might be due to the fact that most studies did not take sufficient account of the potential effects of confounding variables, such as age, smoking, and obesity [6]. Obesity is a major confounding factor as it is strongly associated with SAS [7,8], and may yield the same cardiorespiratory complications as SAS. Therefore, observing cardiac and respiratory abnormalities in an obese patient with SAS does not necessarily imply a causal association between nocturnal apnoeas and cardiorespiratory morbidity.Another confounding factor is the association of chronic obstructive pulmonary disease (COPD), which may explain certain conflicting results on the role of SAS in the development of daytime alveolar hypoventilation and pulmonary arterial hypertension [9][10][11].The aim of the present study was to assess the cardiorespiratory consequences of SAS by comparing the results of a comprehensive cardiorespiratory evaluation in apnoeic and nonapnoeic patients with a similar degree of obesity, i.e. massive obesity and without COPD. This study investigated the role of SAS in the development of daytime alveolar hypoventilation, pulmonary arterial hypertension, systemic arterial hypertension, left ventricular dysfunction, left ventricular hypertrophy and dilatation, cardiac arrhythmias and coronary artery disease. Patients and methods Study populationThe study population included morbidly obese patients admitted consecutively over a 3 yr period to the Nutrition department of Hôtel-Dieu Hospital for an extensive 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.

Biological or morphological parameters of medullary thyroid carcinoma are not significantly improved in a large series of patients treated by octreotide.

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