Heart Failure Comorbid With Obstructive Sleep Apnea
There is a high prevalence of obstructive sleep apnea in patients with heart failure, both with reduced and preserved ejection fraction.1,2,3 Despite maximal medical therapy, approximately 50% of patients with heart failure have moderate-to-severe sleep apnea, defined as an apnea hypopnea index of 15 or more per hour of sleep. An apnea is defined as cessation of breathing for at least 10 seconds or more and hypopnea is reduction in breathing also for at least 10 seconds or more. The pathogenesis of obstructive apnea involves the falling backwards of the relaxed genioglossus muscle, causing collapse of the upper airway while the patient is attempting to breathe.1 The resulting physiology is similar to Müller’s maneuver, performed when the individual is trying to breathe against closed upper airway. An obstructive apnea is, therefore, polygraphically characterized by absence of airflow with continued thoracoabdominal excursions.1 These events are associated with repetitive, large, negative changes in intrathoracic pressure, hypoxia/reoxygenation, cycles of hypercapnia and hypocapnia, arousals, and increased sympathetic activity during sleep. The acute consequences of obstructive sleep apnea incite oxidative stress and upregulate the inflammatory cascade underlying endothelial dysfunction, with adverse long-term sequelae of increased hospitalization and mortality.4 In heart failure patients, even severe obstructive sleep apnea is underdiagnosed,4 because patients may not complain of symptoms such as excessive daytime sleepiness.5-7 While a history of snoring, the presence of obesity, or hypertension should alert the cardiologist that obstructive sleep apnea is highly likely to be present, the absence of these symptoms does not exclude a diagnosis of sleep apnea in heart failure patients.4-6
A few comments about the rapid eye movement (REM) phase of sleep are warranted. In this state of sleep, the burden of sleep apnea may increase because during REM sleep, there is skeletal muscle atonia that also involves the genioglossus muscle. Consequently, the tongue falls backward and obstructive sleep apneas occur frequently and can be prolonged. Desaturation and excessive sympathetic activity ensue. In this regard, two recent studies have shown that REM-phase apnea hypopnea index predicts incident hypertension10 and a rise in hemoglobin A1c.11
Importantly, obstructive sleep apnea is treatable with the use of continuous positive airway pressure (CPAP) devices. One large study of Medicare beneficiaries showed that those heart failure patients who were tested, diagnosed and treated for sleep apnea, had improved survival and decreased hospitalizations and health care cost when compared to the rest of undiagnosed patients.4,8 However, there are a number of hiccups along the road that affect long-term adherence to the use of CPAP. The following case illustrates some of these issues.
A 55-year-old male patient is referred for evaluation of snoring that has been keeping his wife awake at night. He is now sleeping by himself. He gets about 7.5 hours of sleep each night, wakes up a couple of times for nocturia and falls back to sleep quickly. He does not feel sleepy during the daytime and does not nap. He scored 6 on the Epworth sleepiness scale, which is within normal range (up to 10 is considered normal). He smokes a pack of cigarettes a day and does not drink caffeinated products or alcoholic beverages.
His past medical history is relevant for a history of hypertension, type 2 diabetes, and myocardial infarction. His medical regimen has been stable and includes a beta-blocker, angiotensin-converting enzyme inhibitor, a loop diuretic, and aspirin. A recent echocardiogram showed a left ventricular ejection fraction of 34%.
His blood pressure is 110/70 mm Hg, pulse rate is 60 and regular, oxygen saturation is 94%, neck size is 17.2 inches in circumference, and body mass index is 35 kg/m2. Cardiopulmonary examination is normal. There is no pretibial edema.
Although patients with heart failure are at risk for both central sleep apnea (CSA) and obstructive sleep apnea (OSA), this patient has features more consistent with OSA, including habitual snoring, obesity, and a large neck circumference. In fact, severe OSA was confirmed by polysomnography, showing an obstructive apnea-hypopnea index (AHI) of 33/hour of sleep, and a minimal saturation of 75%. An AHI of less than 5 is considered normal, 5-15 mild, 15-30 moderate, and > 30/hour of sleep is severe OSA.
Despite severe sleep disruption, note that this patient does not endorse daytime sleepiness. This is not an uncommon observation, as there are multiple studies showing that patients with heart failure and sleep apnea do not necessarily feel sleepy,4-6 a mechanism that may be mediated by increased sympathetic tone in this population.
Which of the following statements describes the next treatment option for this patient?