Sleep-disordered breathing and cardiovascular disease

Abstract

Sleep-disordered breathing (SDB) is a common comorbidity in a number of cardiovascular diseases, and mounting clinical evidence demonstrates that it has important implications in the long-term outcomes of patients with cardiovascular disease (CVD). While recognition among clinicians of the role of SDB in CVD is increasing, it too often remains neglected in the routine care of patients with CVD, and therefore remains widely undiagnosed and untreated. In this article, we provide an overview of SDB and its relationship to CVD, with the goal of helping cardiovascular clinicians better recognize and treat this important comorbidity in their patients. We will describe the two major types of SDB and discuss the pathophysiologic, diagnostic, and therapeutic considerations of SDB in patients with CVD.

Keywords: Central sleep apnea; Obstructive sleep apnea; Review; Sleep-disordered breathing.

Fig. 1

The pathophysiologic consequences of sleep-disordered breathing. Despite differing mechanisms underlying the development of obstructive sleep apnea and central sleep apnea, both disorders are characterized by repeated, prolonged apneas that result in hypoxia and partial neurological arousals that significantly disrupt sleep. These repeated episodes of apnea, hypoxia, and arousal trigger various neurohormonal, hemodynamic, metabolic, thrombotic, and inflammatory mechanisms that place patients with sleep-disordered breathing at significantly greater risk for hypertension, myocardial ischemia, arrhythmias, and ventricular dysfunction. Abbreviations: CSA, central sleep apnea; LDL, low density lipoprotein; NE, norepinephrine; OSA: obstructive sleep apnea; RAAS, renin-angiotensin-aldosterone system; SDB: sleep-disordered breathing; SNS, sympathetic nervous system.