The effect of Obstructive Sleep Apnea on the Heart and Cardiovascular System

Introduction

Obstructive Sleep Apnea in Patients With Heart Failure

Epidemiology

In the Sleep Heart Health Study, comprising 6424 men and women, the presence of OSA (defined as an apnea-hypopnea index >=11/h) conferred a 2.38 relative increase in the likelihood of having HF, independent of other known risk factors.60 In the 2 largest case series of patients with HF undergoing polysomnography, OSA was detected in 37% of 45014 and 11% of 8115 subjects studied, with the prevalence of OSA greater in men (38%) than in women (31%).14 Risk factors for OSA differ between men and women; the main risk factor in men is obesity, whereas in women it is older age.

There are 2 major forms of sleep apnea: obstructive sleep apnea (OSA) and central sleep apnea (CSA). Because their pathophysiologies and clinical implications in the setting of HF are quite different, OSA and CSA will be dealt with separately in the 2 parts of this review. In Part I, we will provide a general overview of the effects of normal sleep on the cardiovascular system and then discuss the impact of OSA and its therapy on HF. In Part II, will focus on the pathophysiology and treatment of CSA.

Sleep Apnea: Classification and Diagnosis

Obstructive apneas and hypopneas result from complete or partial collapse of a narrowed pharynx,27 respectively, whereas central apneas and hypopneas arise from reductions in central respiratory drive28 (Table 1). During obstructive apnea, the effort generated to produce airflow increases, causing the rib cage and abdomen to distort and move out of phase. In contrast, in central events respiratory movements are absent or attenuated, but in phase. The reported prevalence of OSA in otherwise healthy adults is approximately 4% in women and 9% in men. Of these, less than half report symptoms of a sleep apnea syndrome.29 The prevalence of CSA in otherwise healthy adults has not been determined, but appears to be far less common than OSA.29,30

Obstructive Sleep Apnea

Pathophysiology

Obstructive apneas are caused by collapse of the pharynx during sleep. In subjects with normal pharyngeal anatomy, the partial withdrawal of pharyngeal dilator muscle tone that accompanies the onset of sleep is insufficient to cause pharyngeal collapse. However, the pharynx of patients with OSA is anatomically narrowed and highly compliant. In this setting, the superimposition of the normal withdrawal of pharyngeal dilator muscle tone at sleep onset causes the pharynx to occlude, triggering apnea.32 Obesity is the chief risk factor of OSA, partly because layering of fat adjacent to the pharynx narrows its lumen.33 In addition to this mechanism, other factors may come in to play in HF. For example, periodic oscillations in ventilatory drive related to Cheyne-Stokes respiration may cause withdrawal of pharyngeal dilator muscle tone during the waning of ventilation, predisposing to upper airway narrowing or collapse.34 In the recumbent position, fluid from the legs shifts to more central structures. If some of this fluid should accumulate in the upper airway, the pharynx could become narrowed and more susceptible to ...