Association between obesity and obstructive sleep apnoea

Miguel A. Arias

Servicio de Cardiología
Complejo Hospitalario de Jaén
Pza del Zodiaco No. 8, 5B
23009 Jaén
Spain
Tel: +34 637 463857
Fax: +34 953 270692
E-mail address: maapalomares{at}secardiologia.es

Alberto Alonso-Fernández

Servicio de Neumología
Hospital Universitario La Paz
Madrid
Spain

Francisco García-Río

Servicio de Neumología
Hospital Universitario La Paz
Madrid
Spain

Carlos Pagola

Servicio de Cardiología
Complejo Hospitalario de Jaén
Jaén
Spain

We read with interest the article by Murphy et al.1 who report a significant association between obesity and fatal and non-fatal cardiovascular events in a large, population-based cohort of middle-aged obese patients compared with normal weight subjects followed for 20 years.

These comments are focused on the role of obstructive sleep apnoea (OSA) as another possible factor contributing to the described high rates of cardiovascular events and mortality in obese patients, an aspect not evaluated in this study. OSA is characterized by periodic reduction or cessation of breathing due to narrowing of the upper airways during sleep. Prevalence surveys estimate that 2% of women and 4% of men of middle age are affected by this syndrome.2 In patients with untreated severe OSA, a higher incidence of fatal and non-fatal cardiovascular events has been reported in comparison with that observed in untreated patients with mild–moderate OSA, patients treated with continuous positive airway pressure, and healthy subjects.3 Importantly, it has been estimated that OSA is present in 40%4 to 90%5 of obese subjects. Prevalence of OSA is probably rising as a consequence of increasing obesity, obesity being the most important risk factor for OSA. It may be related to changes in upper airway muscle tone, effects of fat deposition on upper airway anatomic structures, and changes in central mechanisms of breathing control. Obesity and OSA share multiple pathophysiological mechanisms such as endothelial dysfunction, insulin resistance, hyperleptinaemia, systemic inflammation, impaired baroreflex, or sympathetic hyperactivity.6 As a result, OSA may contribute to the presence of cardiovascular events observed in many obese patients.

In contrast, weight loss in OSA patients is associated to reductions in apnoea index,7 and chronic application of continuous positive airway pressure, the treatment of choice for OSA, reduces body fat and visceral fat accumulation in OSA patients.8 Therefore, clinicians must be aware to diagnose and treat obese patients for previously undiagnosed OSA, probably helping to reduce the high rates of cardiovascular events related to both conditions.

References

  1. Murphy NF, Maclntyre K, Stewart S, Hart CL, Hole D, McMurray JJV. Long-term cardiovascular consequences of obesity: 20-year follow-up of more than 15 000 middle-aged men and women (the Renfrew-Paisley study). Eur Heart J. Published online ahead of print September 23, 2005.
  2. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230–1235.[Abstract/Free Full Text]
  3. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea–hypoapnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005;365:1046–1053.[ISI][Medline]
  4. Vgontzas AN, Tan TL, Bixler EO, Martin LF, Shubert D, Kales A. Sleep apnea and sleep disruption in obese patients. Arch Intern Med 1994;154:1705–1711.[Abstract]
  5. Frey WC, Pilcher J. Obstructive sleep-related breathing disorders in patients evaluated for bariatric surgery. Obes Surg 2003;13:676–683.[CrossRef][ISI][Medline]
  6. Gami AS, Caples SM, Somers VK. Obesity and obstructive sleep apnea. Endocrinol Metab Clin North Am 2003;32:869–894.[CrossRef][ISI][Medline]
  7. Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA 2000;284:3015–3021.[Abstract/Free Full Text]
  8. Chin K, Shimizu K, Nakamura T, Narai N, Masuzaki H, Ogawa Y, Mishima M, Nakamura T, Nakao K, Ohi M. Changes in intra-abdominal visceral fat and serum leptin levels in patients with obstructive sleep apnea syndrome following nasal continuous positive airway pressure therapy. Circulation 1999;100:706–712.[Abstract/Free Full Text]




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