When Snoring Has More Ominous Consequences Than a Sleepless Spouse

December 31, 2006

Q:How frequently does hypertension occur in association withobstructive sleep apnea (OSA), and how is OSA best treated?

Q:How frequently does hypertension occur in association withobstructive sleep apnea (OSA), and how is OSA best treated?A:Thousands of Americans have OSA, the most common form of sleepdisordered breathing. Affected persons experience repeated partial or complete closure of the upper airway during sleep. In the course of the resulting episodes of asphyxia, acute physiologic changes are induced; these include arterial oxygen desaturation, surges in sympathetic activity, and acute hypertension.In persons with moderate to severe OSA, these cycles may occurhundreds of times each night.As many as half of persons with hypertension may have some degree of OSA. OSA may also be found in as many as 25% of patients with congestive heart failure (CHF), 30% of patients with acute coronary syndromes, and 60% of patients with a history of a cerebrovascular accident. Unfortunately, many clinicians are unaware of the association between OSA and vascular disease. A recent state-of-the-art report provides a comprehensive review of OSA and its relation tocardiovascular disease.1Making the diagnosis. Table 1 lists symptoms andclinical signs that may suggest OSA, such as loud snoring(particularly if the patient is obese), episodes of chokingor gasping, and daytime drowsiness despite an adequateamount of sleep. However, atypical presentations are common.Patients with OSA who are not obese or who haveno symptoms from their apneic episodes may consult avariety of specialists because of such conditions as angina,an acute coronary syndrome, arrhythmia, hypertension,or CHF.The apnea hypopnea index (AHI)--the number ofobstructive events per hour--is the measure most commonlyused to quantify OSA. Patients with mild OSA experience5 to 15 events per hour; those with severe OSAexperience more than 30 events per hour. Echocardiographicstudies have revealed both systolic and diastolicdysfunction in patients with an elevated AHI. A prospectivestudy showed the AHI to be a significant independentpredictor of hypertension in patients with OSA.2 Anotherstudy showed a linear relationship between hypertensionand the severity of OSA: each extra apneic episode perhour increased the odds of hypertension by 1%.3Refractory hypertension is common in patients withOSA. Ambulatory blood pressure monitoring studies havedemonstrated that some patients experience a loss of thenocturnal "dipper" effect. The results of these studies areimportant; they suggest that OSA represents a significantsecondary cause of hypertension.Ask all patients with hypertension,obesity, or heart failure aboutOSA. Simple screening questions,such as "Do you snore?" "Are youtired on awakening?" or "Do you fallasleep during the day?" can usuallyidentify patients with significant OSA.The Epworth Sleepiness Scale, a validatedscreening method with standardizedquestions, can be used inclinical practice and research settings(Table 2). If you strongly suspectOSA, refer the patient for polysomnography,which requires an overnightstay in a sleep laboratory.Treatment. For obese persons--including those with the metabolicsyndrome (hypertension, hyperlipidemia,obesity, and insulin resistance)--weight loss represents a criticalcomponent of treatment. Significantweight reduction reduces thefrequency of apneic episodes andmay improve hypertension, lipid metabolism,and insulin resistance.Many obese patients, as well asthose with a normal body mass indexwho have severe OSA, require continuouspositive airway pressure(CPAP), the mainstay of OSA therapyfor the past several decades. CPAP,which helps maintain a patent airwaywith positive pressure applied through a nasal mask, is designed to eliminate apneic episodes and the resulting hemodynamic changes that may contribute to hypertension and other cardiovascular sequelae.Alternative treatments--such as mandibular advancement splints andsurgical interventions--are available for patients who cannot tolerate CPAP;however, these interventions are rarely as beneficial. A number of small studies have shown that effective CPAP therapy lowers blood pressure, but it is not a cure-all for the hypertension associated with OSA. The skillful use of antihypertensive therapies, often in combination, is required to achieve optimal blood pressure control for many patients.

References:

REFERENCES:


1

. Lattimore JD, Celermajer DS, Wilcox I. Obstructive sleep apnea and cardiovascular disease. J Am CollCardiol. 2003;41:1429-1437.

2.

Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disorderedbreathing and hypertension. N Engl J Med. 2000;342:1378-1384.

3.

Lavie P, Herer P, Hoffstein V. Obstructive sleep apnoea syndrome as a risk factor for hypertension: populationstudy. BMJ. 2000;320:479-482.

FOR MORE INFORMATION:

  • The Report of an American Academy of Sleep Medicine Task Force. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. Sleep.1999;22:667-689.