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.