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.
Case Report
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.
The correct answer is: B. Treatment with CPAP.
CPAP is the most effective of all therapeutic options. There are no long-term studies on oxygen in patients with heart failure and OSA. Adaptive servo-ventilation has been used for the treatment of CSA. Hypoglossal nerve stimulation has been used in patients with OSA without heart failure and may be considered for patients who are intolerant or refuse to be treated with CPAP. Mandibular advancement device is also a second option. Therapy with mandibular advancement devices have been shown to reduce snoring and improve hypertension and, in one study, to improve sleep-disordered breathing in patients with heart failure.9
The patient returns to the laboratory for CPAP titration. In an overnight laboratory stay, the air pressure is progressively increased from about 5 cm water to eliminate obstructive apneas, hypopneas, and eventually snoring. In this patient, a CPAP titration study is performed and at a pressure of 11 cm water, the apnea hypopnea index is reduced to 4 per hour, and minimal oxygen saturation is improved to 90%. The patient is instructed to use the device every night, all night while sleeping in bed.
What Next?
The most important issue is CPAP adherence. The first 2 weeks of adherence to CPAP is an important predictor of long-term adherence. For this reason, we recommend the patients to return within 2 weeks or earlier, in case of a problem, for follow-up consultation. During these 2 weeks, a number of issues may arise that could impede the long-term use of the device. These include mask discomfort, claustrophobia, nasal congestion, excess inspiratory pressure, or difficulty to exhale against pressure. Fortunately, these issues can normally be taken care of easily. There are multiple interface choices, including nasal pillows, nasal masks, and full-face masks that cover the nose and the mouth. In regard to claustrophobia, we recommend the smallest mask, or nasal pillows and a desensitization process. Desensitization involves the patient wears the mask with CPAP running during the daytime while watching television, reading, etc. With the mind off the mask and device, the patient gradually gets used to the mask, pressure, and the device. The more and the longer the patient practices during the daytime, the faster one gets used to the mask and pressure. If the nasal congestion is an issue, it can also be treated with the nasal steroids. However, a number of patients with heart failure who have elevated right atrial pressure might complain of nasal congestion/clogging particularly in supine position. In this case a topical vasoconstrictor may be used. Sometimes, the patient wakes up with either dry mouth or noise. If the pressure is too high, it can be lowered, or the humidity level of inspired air can be increased. Much information is downloaded from the smart card of the device or via a cloud server, including home AHI, hours of use, and the amount of excess leak.
Follow-Up Visit
The patient returns to the sleep laboratory 2 weeks later. He is accompanied by his wife. She indicates that when he uses the device, his snoring has been eliminated. In addition, when asked, the patient says his nocturia has also been eliminated. However, he is using the device only 4 hours a night and takes the mask off at about 5 a.m. or so and sleeps without it until 7 a.m. He says he does not feel any better with the use of the device. As noted in the history, this patient does not feel sleepy to begin with and has seen no benefits in the short-term. However, his wife is sleeping peacefully throughout the night. And his wife could be an important source of encouragement for her husband to use the device. In this regard, the reason for initial consultation was snoring causing the wife to leave the bedroom.
References:
- Javaheri S. Basics of Sleep Apnea. http://www.acc.org/. February 19, 2013. Accessed January, 4, 2016. http://www.acc.org/latest-in-cardiology/articles/2014/07/22/08/25/basics-of-sleep-apnea-and-heart-failure.
- Javaheri S. Heart failure. In: Kushida CA, ed. The Encyclopedia of Sleep. Waltham: Academic Press; 2013:374-86.
- Javaheri S. Cardiovascular Diseases. In: Kryger MH, Avidan AY, Berry RB, eds. Atlas of Clinical Sleep Medicine. 2nd Edition. Philadelphia: WB Saunders; 2014:316-28.
- Javaheri S, Caref B, Chen E, Tong KB, Abraham WT. Sleep apnea testing and outcomes in a large cohort of Medicare beneficiaries with newly diagnosed heart failure. Am J Respir Crit Care Med 2011;183:539-46.
- Javaheri S, Parker TJ, Wexler L, et al. Occult sleep-disordered breathing in stable congestive heart failure. Ann Intern Med 1995;122:487-92.
- Javaheri S, Parker TJ, Liming JD, et al. Sleep apnea in 81 ambulatory male patients with stable heart failure: Types and their prevalences, consequences and presentations. Circulation 1998;97:2154-9.
- Javaheri S. Sleep disorders in systolic heart failure: a prospective study of 100 male patients. The final report. Int J Cardiol 2006;106:21-8.
- Javaheri S, Brown L, Randerath W. Positive airway pressure therapy with adaptive servo-ventilation: part II: clinical applications. Chest 2014;146:855-68.
- Eskafi M. Sleep apnea in patients with congestive heart failure: an intervention with a mandibular advancement device. Swedish Dent J Suppl 2004;168:1-107.
- Mokhlesi B, Finn LA, Hagen EW, et al. Obstructive sleep apnea during REM sleep and hypertension. results of the Wisconsin Sleep Cohort. Am J Respir Crit Care Med 2014;190:1158-67.
- Grimaldi D, Beccuti G, Touma C, Van Cauter E, Mokhlesi B. Association of obstructive sleep apnea in rapid eye movement sleep with reduced glycemic control in type 2 diabetes: therapeutic implications. Diabetes Care 2014;37:355-63.
- Pamidi S, Wroblewski K, Stepien M, et al. Eight hours of nightly continuous positive airway pressure treatment of obstructive sleep apnea improves glucose metabolism in patients with prediabetes: a randomized controlled trial. Am J Respir Crit Care Med 2015;192:96-105.
Log in to MyACC
