The Importance and Management of Chronic Sleep Apnea in Cardiology

Editor's Note: Based on Jaffe LM, Kjekshus J, Gottlieb SS. Importance and management of chronic sleep apnoea in cardiology. Eur Heart J 2013;34:809-815.

Sleep apnea is a chronic and common condition that has a major impact on morbidity and mortality.1 Many conditions treated by clinical cardiologists, electrophysiologists, interventionalists as well as experts in advanced heart failure and pulmonary hypertension are impacted by sleep-disordered breathing. The review by Jaffe and colleagues is an excellent resource for cardiologists interested in an up-to-date review of the literature analyzing the complex link between sleep and cardiovascular disease along with comments on diagnosis and management.2 Jaffe’s clinical update includes sections on coronary artery disease, acute coronary syndromes and pulmonary hypertension; however, this summarizes the associations between sleep apnea and hypertension, heart failure and arrhythmias.


The classification and pathophysiology connecting sleep apnea to multiple chronic cardiovascular diseases are nicely covered and summarized in two figures.2 The prevalence of sleep apnea in the general population is estimated to range from one in five adults having at least mild sleep apnea to as many as one in 15 affected with moderate or more sleep apnea.3 More interesting is the estimated prevalence over the past two decades has increased substantially.4 This estimate is based on the largest ongoing community-based study of more than 5000 men and women (ages 30-60) part of the Wisconsin Sleep Cohort Study, which was established in 1988, randomly selecting state employees to undergo polysomnography to assess the presence of sleep disordered breathing.

The gold standard for diagnosing and outlining a treatment program is based on the polysomnogram. Sleep apnea represents the vast majority of sleep breathing disorders diagnosed by polysomnography. The two forms of sleep apnea are obstructive sleep apnea (OSA) and central sleep apnea (CSA). Both include disruptions of nocturnal breathing, desaturations and sleep fragmentation, mostly unrecognized by the patient.The more common, OSA is characterized by a collapse of the upper airway during sleep despite preservation of respiratory and abdominal muscle movements associated with breathing. Central Sleep Apnea is characterized by a cessation of breathing and an absence of respiratory muscle movements. Although CSA is typically described in patients with heart failure, it is not uncommon to observe both obstructive and central events during sleep studies conducted in patients with congestive heart failure.


Significant overlap of cofounding risk factors for high blood pressure and sleep apnea help explain the association between OSA and hypertension. OSA has been linked to the development of hypertension. Acute improvement in blood pressure readings have been demonstrated in randomized controlled studies using CPAP to treat OSA in hypertensive patients.5 In a large single-centered sleep center study, participants without OSA were associated with lower incident hypertension (median follow-up 12 years) compared to the presence of OSA. Continuous positive airway pressure (CPAP) therapy was associated with a lower risk of hypertension as well.6  One of the leading causes of resistant hypertension is OSA.7 Emerging data suggests that blocking aldosterone in patients with resistant hypertension can improve not only blood pressure readings but also OSA severity.8 

Heart Failure

The relationship between sleep and systolic heart failure is complex. The prevalence of OSA among patients with heart failure is as high as 47-76%.9 Sleep apnea causes increased sympathetic tone and heart rate, which are especially detrimental in congestive heart failure. However, apnea is not the sole culprit for cardiovascular disruption in OSA, hypoxia also contributes to hemodynamic consequences in chronic heart failure.10 Cheyne-Stokes respirations are common in chronic congestive heart failure, resulting in hyperventilation and decreased CO2, which in turn results in a strong inhibitory reflex. This reflex results in cessation of breathing and worsening hypoxia, leading to arousals and hyperventilation that further exacerbates the breathing disorder.11

An association also exists between heart failure with preserved ejection fraction and sleep apnea. It is likely linked to the overlap of hypertension, obesity and other factors. The prevalence of sleep apnea in patients with heart failure and preserved ejection fraction ranges between 38-62%, the majority of cases having predominantly OSA.12,13

The high prevalence of sleep apnea in patients with reduced and preserved ejection fractions, suggests that heart failure experts will be forced to focus more time on screening and diagnosing sleep disorders in this population. Although therapies aimed at treating the symptoms of sleep apnea have had modest benefit, evidence from long term morbidity and mortality studies are lacking. The most recent trial using auto-servoventilation (ASV) to reduce breathing disturbances in heart failure did reduce CSA events more effectively compared with standard positive airway therapy, but there were no improvements in exercise performance or echocardiographic parameters.14 Future clinical trials aimed at reducing CSA events in this population of heart failure may help reduce 30-day hospital readmissions.15


Patients suffering from OSA commonly experience arrhythmias during sleep.16 But the strongest association is with atrial fibrillation.17 Hypoxia causes imbalances on the sympathetic-parasympathetic effects, diastolic dysfunction leading to remodeling in left atrial electrical conduction, thereby promoting atrial fibrillation. The reported prevalence of OSA among patients with atrial fibrillation ranges from 43-73%, independent of age, sex, weight, hypertension or heart failure.18 The presence of OSA increases recurrence rate after ablation of atrial fibrillation and treatment with CPAP significantly lowered arrhythmia recurrence of atrial fibrillation in a recently published study.22 Not only is CPAP therapy associated with lower recurrence of atrial fibrillation after cardioversion, it also will decrease nocturnal rates of bradycardia and sinus pauses commonly recorded on home monitors.19,20

In summary, sleep apnea is fast becoming recognized as a risk for developing cardiovascular disease. In fact, the relationship is bi-directional.21 However the diagnosis and treatments are awkward and cumbersome, which lead to wide-spread poor compliance, see Table I.2 Cardiologists are accustomed to discussion of how therapies will improve their patients’ quality of life, including a host of proven therapies aimed at improving mortality. As more studies explore the critical connection between OSA and cardiovascular disease, sleep will be added to discussion regarding quality of life. 

Sleep is good for one’s health and cardiologists should begin to explain its benefits, similar to diet and exercise. Since poor sleep can increase the severity of many cardiovascular conditions, cardiologists are finding themselves learning more about their patients’ sleep patterns. An enlarging body of evidence is available to the cardiologist interested in screening subsets of patients for evaluation and treatment. Since the gold standard for diagnosis and treatment of sleep apnea have their drawbacks, future studies should focus on uncovering improved options for evaluation and management of sleep apnea.


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Keywords: Acute Coronary Syndrome, Arrhythmias, Cardiac, Anti-Arrhythmia Agents, Coronary Artery Disease, Coronary Disease, Heart Failure, Hypertension, Hypertension, Pulmonary, Sleep Apnea Syndromes

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