Obstructive Sleep Apnea as a Cardiovascular Risk Factor-Beyond CPAP

Abstract

Patients with obstructive sleep apnea (OSA) experience repetitive partial or complete airway collapse during sleep resulting in nocturnal hypoxia-normoxia cycling, and are at increased cardiovascular risk. The number of apneas and hypopneas indexed per hour of sleep (apnea-hypopnea index) along with the associated intermittent hypoxia predict the increased cardiovascular risk; thus, their attenuation or prevention are objectives of OSA therapy. Continuous positive airway pressure (CPAP) is the gold standard treatment for OSA and, when effective, mitigates the apnea-hypopnea index and hypoxemia. As such, it is reasonable to expect CPAP would decrease cardiovascular risk. However, 3 recent randomized clinical trials of CPAP vs usual care did not show any significant effects of CPAP in attenuating incident cardiovascular events in patients with OSA. In this review, we discuss these studies in addition to potential complementary therapeutic options to CPAP (eg, neurostimulation) and conclude with suggested therapeutic targets for future interventional studies (eg, the autonomic nervous system). Although these areas of research are exciting, they have yet to be tested to any similar degree of rigour as CPAP.

Figure 1.

Overview of pathophysiologies and epiphenomema associated with obstructive sleep apnea which increase cardiovascular (CV) risk (dark text) along with potential adjunct treatments and therapeutic targets to reduce CV risk (red text). OB, obesity; HTN, hypertension; T2DM, type 2 diabetes mellitus; HNS; hypoglossal nerve stimulators; MAD, mandibular advancement devices.