Correspondence: Olalla Castro-Añón, Respiratory Division and Sleep Disorders Unit. Hospital Lucus Augusti., San Cibrao S/N, 27003 Lugo, Spain. Email:


See correspondence, page 385


obesity hypoventilation syndrome

Dear Editor:

We thank Dr Esquinas and Dr. Petroianni for their interest in our study.[1] All the patients were included at the time of diagnosis, and therefore none of them had previously received oxygen therapy or positive airway pressure. Given that respiratory failure was a newly diagnosed medical condition, the previous duration of hypoxaemia is merely speculative.

We totally agree that obesity hypoventilation syndrome (OHS) is a heterogeneous entity with a wide range of severities, and that respiratory failure and haemodynamic impairment have a multifactorial nature. Several mechanisms appear able to contribute to respiratory insufficiency in OHS. These include respiratory muscle dysfunction, increased CO2 production, impaired respiratory system mechanics, altered respiratory drive and obstructive apnoeas during sleep. It is likely that the weight of each mechanism may vary from one patient to another. We have found evidence of this heterogeneity in a previous study, which uncovered that OHS patients who could be treated in the long term with single continuous positive airway pressure had higher apnoea–hypopnoea index and less impaired lung function than those who required bi-level positive airway pressure to achieve optimal control.[2] As Dr Esquinas and Dr Petroianni point out, haemodynamic alterations of OHS are also undoubtedly multifactorial, and left heart disease can contribute to secondary pulmonary hypertension in many cases. In our study, left heart abnormalities (left ventricular hypertrophy, mitral valve regurgitation and diastolic dysfunction) were found in the great majority (77%) of patients with right ventricular overload.[1] It should also be noted that left ventricle diameters decreased during follow up without changes in body weight, suggesting that non-invasive ventilation might exert beneficial effects on left ventricle function. However, the possible contribution of other factors like concomitant medication or changes in lifestyle cannot be excluded due to the design of the study.

As Dr. Esquinas and Petroianni mention, improvement on 6-min walk test distance was achieved at 1 month without further significant increases on the 6-month control. This finding is congruent with a previous, larger study in which we found that recovery of gas exchange anomalies in OHS patients were achieved in most cases 1 month after initiation of non-invasive ventilation, without additional significant improvement during a mean follow up of 50 ± 25 months.[3] It was notable that mean SaO2 during 6-min walk test remained below 90% despite the basal arterial blood gas status dramatically improving. This observation suggests that obesity imposes a ventilation–perfusion mismatch during exercise that nocturnal non-invasive ventilation is unable to correct. However, further studies with longer follow up are warranted to clarify whether further improvements in 6-min walk test distance and haemodynamic features might appear in the long term.

Spirometry was not performed at the 6-month visit because we had not found changes in lung function over time in a study that included more patients followed during a longer interval.[3] Thus, we did not expect changes to occur in the shorter interval and smaller study published in Respirology.

We wholly agree that multimodal treatment is essential in OHS and that individual therapeutic strategies must be designed. Clinical experience shows that some patients can be treated with continuous positive airway pressure, while others need bi-level positive pressure devices or volume-cycled ventilators, sometimes with the addition of supplemental oxygen.[3, 4] Also, in some patients who achieve weight reduction either via low-calorie diet or bariatric surgery, non-invasive ventilation can be successfully withdrawn.[3]