Published online before print April 3, 2006, doi: 10.1161/01.HYP.0000217130.01867.4b
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(Hypertension. 2006;47:818.)
© 2006 American Heart Association, Inc.
Editorial Commentaries |
Sleep Apnea in Hypertension
When, How, and Why Should We Treat?
From the Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, 200 First St, SW, Rochester, Minn.
Correspondence to Virend K. Somers, Mayo Clinic, 200 First St, SW, Rochester, MN 55902. E-mail somers.virend@mayo.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Hypertension is a notoriously complex disease, with a mosaic of potential interactive etiologies. Age, gender, nutrition, environment, stress, obesity, and genetics have been cited as causal factors, as has been dysfunction in renal, endocrine, and neural circulatory control mechanisms. More recently, the epidemic of obesity has prompted recognition of an interaction between obstructive sleep apnea and increased blood pressure. This has, in turn, provided an exciting opportunity for more comprehensive understanding of the pathophysiological mechanisms and potential treatment strategies for hypertensive patients.
Both hypertension and obstructive sleep apnea (OSA) are each increasingly common. Hypertension is present in well over a third of middle-aged subjects, and sleep apnea is reported to be present in 25% of middle-aged men and 10% of middle-aged women.1 Other common characteristics of hypertension and OSA include their association with obesity and male gender. Furthermore, both conditions are often clinically undiagnosed and may be accompanied by increased risk of cardiac and vascular damage.
Although hypertension and OSA are common in the general population, epidemiological studies suggest that their comorbid prevalence exceeds strikingly that which would be anticipated to occur by chance alone. These observations, based on cross-sectional data, have been further strengthened by prospective studies demonstrating that increasing severity of OSA is a risk factor for the development of incident hypertension over 4 years.2 This etiologic interaction is independent of traditional risk factors for hypertension, such as alcohol, body mass index, and gender. Also impressive is that an apnea-hypopnea index of 
15 (indicating that breathing decreases or
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