Sleep-Disordered Breathing and Diastolic Heart Disease

Abstract

Sleep-disordered breathing (SDB) is highly prevalent in heart failure (HF), and the coexistence of these two disease conditions increases mortality. The purpose of this review is to examine the mechanistic interactions and associations between SBD, specifically obstructive sleep apnea (OSA), obesity hypoventilation (OHS), left ventricular (LV) diastolic heart function, and pulmonary hypertension (PH), as factors that directly contribute to the development of HF. The mechanistic interactions may be thought of as direct and indirect effects. The direct effects are related to abnormalities caused by sleep-disordered breathing that induce LV remodeling. Recent studies support the notion that the severity of OSA and recurrent hypoxia enhance LV remodeling even after accounting for age, weight, and underlying cardiorespiratory comorbid conditions. Indirect effects are due to the mechanical alterations intrathoracic organs during sleep due to negative intrathoracic pressure, obesity, as well as multiple derangements causing activation of the sympathetic nervous system and endothelium. The review also delineates multiple mechanisms that eventually lead to pulmonary vascular remodeling and PH. The severity of daytime arterial oxygen levels and/or duration of nocturnal hypoxia, rather than the severity of SDB, seems to be the major determinants of PH in SBD, after adjusting for other cardiorespiratory diseases. Mechanisms by which hypercapnia contributes to PH and diastolic dysfunction need to be explored. Moreover, interactions between central sleep apnea and diastolic heart function are not well delineated. Further investigations are needed to elucidate any direct effect of hypercapnia on pulmonary pressures and potential cardiovascular consequences. There is limited evidence on the impact of PAP or oxygen therapy on these intermediary mechanisms of HF in SDB populations. The collection of evidence indicates that PAP may enhance diastolic function and reduce pulmonary artery pressure in OSA whereas studies in OHS populations are sparse and inconclusive. Thus, future research should delineate whether pathophysiology-based therapies can alleviate HF and HF related mortality in these SDB populations.