| PURPOSE OF REVIEW: High blood pressure and obstructive sleep apnea
are closely related, and the latter is considered to induce hypertension.
The primary underlying mechanism is sympathetic activation triggered
by apneic episodes. This type of hypertension is difficult to treat.
The purpose of this review is (1) to evaluate the epidemiological data
in view of the current focus on preclinical sleep apnea and prehypertension,
(2) to examine additional factors that might contribute to high blood
pressure, and (3) to indicate the best therapeutic strategy for treatment
of hypertension in these patients. RECENT FINDINGS: Cardiovascular
effects of sleep apnea can be detected early in the course of the disease,
and young subjects are particularly susceptible to its deleterious
effect. Blood pressure profiles in these patients show higher diastolic
blood pressure and no nocturnal dipping. The renin-angiotensin axis
in conjunction with other vasoactive hormones add to the sympathetic
activation in elevating blood pressure in sleep apnea. Pro-inflammatory
cytokines further contribute to the atherosclerotic consequences that
primarily affect the heart and brain, and spare the kidneys. Mounting
evidence indicates that treatment of sleep apnea using positive airway
pressure, palato-nasal surgery and weight reduction correct the associated
hypertension. Conversely, antihypertensive therapy is less effective.
SUMMARY: Even the early stages of sleep apnea are associated with high
blood pressure and cardiovascular consequences. Despite our knowledge
of the role of the sympathetic activation and vasoactive hormones,
no specific antihypertensive therapy is superior, and the optimal way
of controlling hypertension is to treat sleep apnea and associated
obesity. |
