Cardiac function and hypertension in patients with obstructive sleep apnea

Abstract

Cardiovascular disease is one of the major causes of death worldwide. Among its risk factors, obstructive sleep apnea (OSA) is a common but still underestimated condition. OSA often coexists and interacts with obesity, sharing multiple pathophysiological mechanisms and subsequent cardiovascular risk factors, such as type 2 diabetes, dyslipidemia, systemic inflammation, and in particular hypertension. There is also evidence suggesting an increased risk of arrhythmia, heart failure, renal failure, acute myocardial infarction, stroke, and death. OSA is characterized by recurrent episodes of partial (hypopnea) or complete interruption (apnea) of breathing during sleep due to airway collapse in the pharyngeal region. The main mechanisms linking OSA to impaired cardiovascular function are secondary to hypoxemia and reoxygenation, arousals, and negative intrathoracic pressure. Consequently, the sympathetic nervous and the renin-angiotensin-aldosterone systems may be overestimulated, and blood pressure increased. Resistance to treatment for hypertension represents a growing issue, and given that OSA has been recognized as the major secondary cause of resistant hypertension, clinical investigation for apnea is mandatory in this population. Standard diagnosis includes polysomnography, and treatment for OSA should include control of risk factors for cardiovascular disease, including obesity. So far, continuous positive airway pressure is the treatment of choice for OSA, impacting positively on blood pressure goals; however, the impact on long-term follow-up and on cardiovascular disease should be better assessed.