The link between obstructive sleep apnea and heart failure: Underappreciated opportunity for treatment

Abstract

Obstructive sleep apnea (OSA) is a newly recognized risk factor for the development of systemic hypertension, ischemic heart disease, and congestive heart failure. Mechanisms responsible for these links include OSA-related hypoxemia and arousal from sleep-induced increased sympathetic activity, large negative intrathoracic pressure-induced increased left ventricular transmural pressure gradient and impaired vagal activity, plus formation of oxygen radicals. Secondary phenomena include increased platelet aggregability, insulin resistance, and endothelial dysfunction with reduced endogenous nitric oxide production. Safe, nonpharmacologic, nonsurgical therapy, namely continuous positive airway pressure, can attenuate OSA and improve cardiac function and quality of life. Searching for signs or symptoms of OSA from the patient (or bed partner), namely loud habitual snoring, apneas, nocturnal choking, orthopnea, paroxysmal nocturnal dyspnea, excessive daytime sleepiness, or cardiovascular disease which is difficult to control, may reward the curious physician with another treatment avenue.

Enhancement of sleep stability with Tai Chi exercise in chronic heart failure: Preliminary findings using an ECG-based spectrogram method

“…Recurrent arousals can severely fragment sleep, contributing to impaired cognitive function and quality of life [2]. In addition, repeated episodes of apnea and hypopnea can have deleterious effects on cardiac physiology and function, causing arterial oxyhemoglobin desaturations, nocturnal hypertensive surges amplified by arousals, triggering of arrhythmias, and an amplification of neurohumoral activation [3,4]. Improving sleep and sleep-breathing, therefore, is considered an important therapeutic target in the heart failure population.…”

The Right Heart Diaries in Sleep Disordered Breathing

“…Following the initial vasoconstrictive response, the restorative reperfusion generates shear stresses inhibiting complete recovery and eventually leads to persistent vasoconstriction (61). This combined with the reduced production of Nitric Oxide (NO) a potent vasodilator and increasing vascular sensitivity to endothelin-1 in SDB may result in the hemodynamic changes preceding the development of PH (54,62,63). In fact the vascular and endothelial dysfunction markers ( endotelin-1 ,Thrombomodulin and ICAM) have recently been described to have a linear relationship with the severity of SDB (64).…”

A novel therapeutic approach for central sleep apnea: Phrenic nerve stimulation by the remedē® System

“…Despite major advances, HF continues to be associated with high mortality rates and symptom burden [1]. Accordingly, there has been increasing focus on targeting treatment toward not only HF itself but also common co-morbid conditions [2]. Among the most frequent in this patient population is sleep disordered breathing (SDB), which includes obstructive sleep apnea (OSA) and central sleep apnea (CSA).…”