Heart failure (HF) is a chronic, progressive condition in which the heart muscle is weakened and cannot pump enough blood to meet the body’s needs for blood and oxygen. A better understanding of HF’s pathogenesis and comorbidities is essential for improvement of risk stratification and prevention.
Among multiple comorbidities, sleep-disordered breathing (SDB), and obstructive sleep apnea (OSA), in particular, are the most common. Almost 50% of patients with HF have alterations of ventilation during sleep that can disrupt the positive effects of physiological sleep on the cardiovascular system. In two studies of patients with HF undergoing polysomnography, OSA was detected in 37% and 11% of patients. The Sleep Heart Health Study, a prospective study of 6,424 men and women, indicated that the presence of OSA (defined as an apnea-hypopnea index [AHI] ≥10 per hour) favored the appearance of HF independently of other known risk factors, with a 2.20 relative risk.
The complex interaction between HF and OSA seems to be bi-directional. Some factors of HF can lead to the collapse of the upper airways, increasing the risk of OSA. For example, HF is characterized by fluid shifts from the legs to central structures (peripheral edema), especially in the supine position, which can lead to upper airways narrowing.
Conversely, OSA increases the risk of HF by multiple mechanisms. Obstructive apneas during sleep induce a series of systemic hemodynamic, autonomic, and humoral changes with adverse consequences on the cardiovascular system in individuals with normal ventricular function. The repeated occurrence of apneas and hypopneas has been associated with reduced endothelial function, an increase in the plasma concentration of inflammatory markers, increased platelet aggregation, and increased variability in blood pressure and heart rate.
Moreover, the negative intrathoracic pressure during OSA results in increased venous return to the right ventricle and increased left ventricular (LV) transmural pressure, both damaging LV function. These recurrent events that accompany repeated obstructive apnea determine a further increase of the already elevated sympathetic activity in patients with HF, documented by increased plasma catecholamine. Obstructive events during sleep can also have long-term effects by the induction of genes involved in ventricular remodeling caused by the repetitive increases in wall stress, and by inducing myocyte slippage and contractile dysfunction. Accordingly, there’s a growing understanding that the OSA-HF interaction has causal aspects and does not reflect mere co-morbidity.
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