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Mechanisms and Treatment of Obstructive Sleep ApneaMechanisms and Treatment of Obstructive Sleep Apnea

JAMA. 2004;291(5):557-557. doi:10.1001/jama.291.5.557-a
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AUTHOR INFORMATION

Letters Section Editor: Stephen J. Lurie, MD, PhD, Senior Editor.

MECHANISMS AND TREATMENT OF OBSTRUCTIVE SLEEP APNEA

To the Editor: Dr Shamsuzzaman and colleagues1 concluded that obstructive sleep apnea (OSA), which is often undiagnosed, can worsen cardiac and vascular disease. They also suggested that untreated OSA may decrease the effectiveness of conventional therapeutic strategies. Although the authors discussed several possible mechanisms that may occur during sleep, they did not address the effects of OSA on pulmonary hypertension and the right ventricle during wakefulness. Sanner et al,2 for instance, concluded that OSA can cause mild pulmonary hypertension even in the absence of pulmonary disease, which, in patients with normal left ventricular function, is strongly related to severity of OSA. In another study, Sanner et al3 reported that 18% of patients with OSA had impaired right ventricular ejection fraction, and that 95% of these patients had clinical signs or symptoms of mild right ventricular failure. Marrone and Bonsignore4 found that mild pulmonary hypertension may be present at rest in fewer than 50% of patients with OSA. Patients with OSA and pulmonary hypertension are more likely to have daytime hypoxemia and hypercapnia than are patients without pulmonary hypertension.5

The etiology of OSA-related daytime pulmonary hypertension is probably multifactorial, and may include nocturnal and diurnal hypoxia, pulmonary vascular remodeling, increased sympathetic tone, and humoral factors. It has been estimated that 20% of patients with OSA who attend sleep clinics have stable pulmonary hypertension.4 It is not clear, however, what percentage of such patients have pulmonary hypertension due to isolated OSA because obesity, left ventricular dysfunction, and chronic lung disease are important contributing factors. Even more severe impairment of pulmonary hemodynamics can occur in patients with concomitant lung disease.

References
Shamsuzzaman ASM, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease.  JAMA.2003;290:1906-1914.
PubMed
Sanner BM, Doberauer C, Konermann M, Sturm A, Zidek W. Pulmonary hypertension in patients with obstructive sleep apnea syndrome.  Arch Intern Med.1997;157:2483-2487.
PubMed
Sanner BM, Konermann M, Sturm A, Muller HJ, Zidek W. Right ventricular dysfunction in patients with obstructive sleep apnoea syndrome.  Eur Respir J.1997;10:2079-2083.
PubMed
Marrone O, Bonsignore MR. Pulmonary haemodynamics in obstructive sleep apnoea.  Sleep Med Rev.2002;6:175-193.
PubMed
Chaouat A, Weitzenblum E, Krieger J, Oswald M, Kessler R. Pulmonary hemodynamics in obstructive sleep apnea syndrome: results in 220 consecutive patients.  Chest.1996;109:380-386.
PubMed

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Shamsuzzaman ASM, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease.  JAMA.2003;290:1906-1914.
PubMed
Sanner BM, Doberauer C, Konermann M, Sturm A, Zidek W. Pulmonary hypertension in patients with obstructive sleep apnea syndrome.  Arch Intern Med.1997;157:2483-2487.
PubMed
Sanner BM, Konermann M, Sturm A, Muller HJ, Zidek W. Right ventricular dysfunction in patients with obstructive sleep apnoea syndrome.  Eur Respir J.1997;10:2079-2083.
PubMed
Marrone O, Bonsignore MR. Pulmonary haemodynamics in obstructive sleep apnoea.  Sleep Med Rev.2002;6:175-193.
PubMed
Chaouat A, Weitzenblum E, Krieger J, Oswald M, Kessler R. Pulmonary hemodynamics in obstructive sleep apnea syndrome: results in 220 consecutive patients.  Chest.1996;109:380-386.
PubMed
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