Síndrome de apneas-hipopneas del sueño, hipertensión y riesgo cardiovascular

Abstract

Obstructive sleep apnea/hypopnea (OSAH) syndrome is a condition characterized by recurrent episodes of restricted airflow through the upper airway that causes oxygen desaturation, microarousals and destructed sleep with negative repercussions for quality of life and cardiovascular risk. This condition has been attracting special interest as it has been shown to be a cause of arterial hypertension as well as its concurrence with other risk factors. OSAH also produces other modifications in the circadian rhythm of arterial pressure, resulting in a tendency for patients to exhibit a less favorable nondipper pattern. In the present review, we examine the pathophysiological mechanisms involved in the relationship between OSAH and systemic arterial hypertension. We also consider other parallel processes through which OSAH may produce vascular lesions, including an increase in oxidative stress, and its negative impact on both the lipid profile and plaque adhesion. All of this contributes to the appearance of atheromatosis lesions in patients with OSAH and their repercussions in terms of related events. Furthermore, the article examines evidence provided by clinical trials that associates OSAH with a higher risk of left ventricular hypertrophy, systolic and diastolic cardiac failure, ischemic heart disease, cardiac arrhythmias, cerebrovascular disease, and a greater incidence of cardiovascular morbidity-mortality.The usual treatment recommended for this syndrome is continuous positive airway pressure (CPAP). CPAP has been shown to be effective in reducing arterial pressure in hypertensive patients with OSAH. Although this effect is apparently moderate, its results are clearly as the cases become more severe or when the level of arterial hypertension is greater. CPAP has also been shown in observational studies to be effective in reducing cardiovascular morbidity-mortality associated with the syndrome.