Obstructive sleep apnea (OSA) is a common clinical condition in the general population, especially among patients with cardiovascular diseases. More than just a local phenomenon of upper respiratory tract obstruction, OSA leads to systemic consequences that may include intermittent hypoxia, sudden reduction of the intrathoracic pressure, and the occurrence of micro-awakenings with sleep fragmentation. In the past decades, innumerous evidences have consistently pointed to OSA as an important factor related to the presence of cardiovascular diseases. In particular, the relationship between OSA and systemic hypertension (SH) is the one supported by the largest body of evidence. Currently, there are data suggesting that OSA is an important secondary cause of SH. More importantly, OSA is independently associated with poorer blood pressure control, changes in sleep dip, and presence of target-organ damage such as left ventricular hypertrophy and microalbuminuria. Randomized studies suggest that the management of OSA, especially with continuous positive airway pressure (CPAP) - which is considered the standard treatment for OSA - promotes a significant 24-hour blood pressure reduction, and this effect is more significant in the subgroup of patients with uncontrolled SH and drug-resistant SH. Despite all those evidences, OSA has still been underdiagnosed. The objective of this review is to discuss the recent advances in the pathophysiological mechanisms, clinical presentation, and treatment of OSA, as well as the benefits this treatment can bring on blood pressure.
Sleep apnea, obstructive; hypertension; cardiovascular diseases
