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SLEEP AND BREATHING: Jean-Pierre Laaban, Sophie Pascal-Sebaoun, Evelyne Bloch, Elizabeth Orvoën-Frija, Jean-Michel Oppert, and Gérard Huchon Left Ventricular Systolic Dysfunction in Patients With Obstructive Sleep Apnea Syndrome Chest 2002; 122: 1133-1138 [Abstract] [Full text] [PDF]

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Left ventricular dysfunction and sleep apnea syndrome: cause or consequence?

Karim Bendjelid, Surgical Intensive Care   (7 November 2002)

Left ventricular dysfunction and sleep apnea syndrome: cause or consequence? 7 November 2002
Karim Bendjelid, Chef de Clinique Geneva University Hospitals, Surgical Intensive Care Send letter to journal: Re: Left ventricular dysfunction and sleep apnea syndrome: cause or consequence? karim.bendjelid{at}hcuge.ch Karim Bendjelid, et al.	Left ventricular dysfunction and sleep apnea syndrome: cause or consequence? Karim BENDJELID, MD Surgical Intensive Care Division, Department APSIC, Geneva University Hospitals, Switzerland. word count : 254 Correspondence and requests for reprints should be addressed to : Dr Karim Bendjelid Chef de Clinique Hôpitaux universitaires de Genève Soins Intensifs Chirurgicaux CH-1211 Genève 14 Switzerland : 41/22/382 74 52 Fax: 41/22/382 74 55 E-mail: Karim.Bendjelid@hcuge.ch To the Editor Sir: In an article published recently in Chest, Dr Laaban and colleagues1 conclude that obstructive sleep apnea syndrome (OSAS) may be a direct cause of daytime left ventricular systolic dysfunction (LVSD) that can resolve following reversal of nocturnal apneas by nasal continuous positive airway pressure (CPAP). We would like to take this opportunity to address the authors some suggestions: First, this finding can not definitely ruled out the hypothesis that LVSD and/or congestive heart failure may be the cause of OSAS and not the opposite. Indeed, a high prevalence and persistence of sleep apnea are observed in patients with chronic left ventricular failure2,3. Rather, as CPAP improve cardiac output in patients with LVSD4, the useful effect of nasal CPAP observed in Laaban et al study could a direct effect of positive pressure ventilation on heart5. Thus, we are not sure about the validity of these results and we may expect that after a time of optimal medical treatment (angiotensin converting enzyme inhibitors (23% patients treated in the study), diuretics, …) the episodes of OSAS may be treated. Second, the authors have stated that associated cardiac disease had been excluded in the present study. We may expect that this statement may be erroneous as to our knowledge the onset of an idiopathic dilated cardiomyopathy in patient with LVSD could not be excluded. Finally, we believe that more research is required to better understand the pathophysiological association between OSAS and LVSD and to define the potential role of CPAP in the treatment of chronic heart failure. REFERENCES: 1 Laaban JP, Pascal-Sebaoun S, Bloch E, et al. Left ventricular systolic dysfunction in patients with obstructive sleep apnea syndrome. Chest 2002; 122:1133-1138 2 Tremel F, Pepin JL, Veale D, et al. High prevalence and persistence of sleep apnoea in patients referred for acute left ventricular failure and medically treated over 2 months. Eur Heart J 1999; 20:1201-1209 3 Andreas S. Nocturnal insights in chronic heart failure. Eur Heart J 1999; 20:1140-1141 4 Pinsky MR, Summer WR, Wise RA, et al. Augmentation of cardiac function by elevation of intrathoracic pressure. J Appl Physiol 1983; 54:950-955 5 Yan AT, Bradley TD, Liu PP. The role of continuous positive airway pressure in the treatment of congestive heart failure. Chest 2001; 120:1675-1685