A 42 year-old male with minimal previous medical history is hospitalized with newly diagnosed decompensated heart failure. He is short of breath at rest [New York Heart Association (NYHA) class IV heart failure]. His exam demonstrates evidence of congestion and volume overload, and he appears to be well-perfused with normal cardiac output. His primary symptoms include fatigue and dyspnea. In addition, he endorses chest discomfort at night. His BMI is 32 and his left ventricular ejection fraction (LVEF) on transthoracic echocardiogram (TTE) is 22%. Electrocardiogram (ECG) and cardiac telemetry demonstrate frequent premature ventricular contractions and several runs of non-sustained ventricular tachycardia. Left- and right-heart catheterization reveals no obstructive coronary artery disease, elevated left- and right-sided filling pressures consistent with congestion/volume overload, normal pulmonary pressures, and normal cardiac output and cardiac index. He has never been evaluated for sleep-disordered breathing and he denies excessive daytime sleepiness. He is treated with intravenous diuretics, and appropriate goal-directed medical therapy for non-ischemic cardiomyopathy is initiated. The patient receives heart failure education regarding nutrition and lifestyle modifications.
During his seven-day hospitalization, he is screened for sleep-disordered breathing on the second night of his stay. A bedside sleep study reveals an apnea hypopnea index of 21 (signifying 21 episodes of apnea, hypopnea, or respiratory-effort related arousals per hour of sleep) consistent with a diagnosis of obstructive sleep-disordered breathing. Treatment with continuous positive airway pressure (CPAP) is initiated on the third night of his stay.
At the time of hospital discharge, the patient is given prescriptions for his standard heart failure medications which were begun during the hospitalization as well as a prescription for home CPAP therapy. Outpatient validation polysomnography (PSG) confirms a diagnosis of obstructive sleep apnea. Over the next six months, the patient follows up regularly with his heart failure and sleep medicine clinics. He is not re-hospitalized for heart failure, and he reports excellent compliance with his medications and nocturnal CPAP use. His BMI does not change.
At six months, his symptoms are improved to New York Heart Association (NYHA) class II heart failure (mild limitation of activity). ECG and 24-hour Holter monitor reveal no evidence of ventricular dysrhythmias. TTE at six months shows and LVEF of 41%, an improvement from 22% at the time of initial presentation.
Figure 1
Figure 1, from overnight polysomnography, shows four 30-second epochs of sleep from an adult sleep study. Shown are two complete obstructive apneas with associated events as below.
#1: obstructive apneas
#2: paradoxical movement of the thorax and abdomen in the effort channels
#3: oxyhemoglobin desaturation
#4: arousal
#5: leg movement
Abbreviations: LOC: left oculogram; ROC: right oculogram; CHIN: chin EMG; C3A2, C4A1: central EEG leads; O1A2, O2A1: occipital EEG leads; LLEG: left leg EMG; RLEG: right leg EMG; PSNR: snoring channel; CPAP: CPAP flow channel; FLOW: nasal pressure flow channel; THOR: thorax effort channel; ABDM: abdominal effort channel; EKG: electrocardiogram; SAO2: oxygen saturation channel.
Which of the following is FALSE in regards to the association between obstructive sleep apnea and heart failure?
Show Answer
The correct answer is: G. Unlike ambulatory patients with HF, it is difficult to evaluate patients hospitalized for decompensated HF for OSA and SDB, and so the hospitalized patient does not receive the benefit of SDB treatment (i.e. improvement in LVEF).
Discussion:
A-Sleep-disordered breathing occurred in 76% of patients in an observational study of 700 patients with heart failure. 36% of patients had obstructive sleep apnea and 40% of patients had central sleep apnea. The frequency of obstructive sleep apnea was not related to more severe sleep apnea, although central sleep apnea was.1
B-A prospective cohort study of 108 patients in a heart failure clinic on maximal medical therapy who were without hospitalization or medication changes within the previous 30 days found that 61% had sleep-disordered breathing. This diagnosis was independently associated with atrial fibrillation and a worse NYHA class.2
C-155 patients with heart failure and obstructive sleep apnea were compared to a random community sample of obstructive sleep apnea patients. Based on the Epworth Sleepiness Scale (a standard tool used in sleep medicine clinics to help quantitate symptoms of sleepiness), heart failure patients had a lower score compared to non-heart failure patients, indicating less daytime sleepiness, even though the heart failure patients slept less overall. These findings were regardless of severity of obstructive sleep apnea.3
D-Sleep apnea occurred in 90% of patients with nocturnal angina in one study, and treatment with CPAP improved symptoms.4 In a prospective study of patients with heart failure and obstructive sleep apnea, 55% of those treated with CPAP showed an improvement in ventricular irritability.5
E-Two randomized trials showed an improvement in LVEF after treatment with CPAP in heart failure patients with obstructive sleep apnea,6, 7 while a randomized trial showed a greater intermediate-term improvement in LVEF in those heart failure patients treated with BiPAP compared to those patients treated with CPAP.8
F-A prospective study of 395 patients showed that similar to stable chronic heart failure, decompensated heart failure requiring hospitalization is associated with a high prevalence of sleep-disordered breathing.9 The prevalence of predominantly obstructive sleep-disordered breathing was greater than that of central sleep-disordered breathing in this population. The presence of obstructive sleep-disordered breathing during hospitalization predicted a diagnosis of obstructive sleep apnea on validation, outpatient polysomnography.
G-A pilot randomized control trial examined hospitalized patients with decompensated heart failure and a diagnosis (via inpatient sleep study) of sleep-disordered breathing.10 Those patients treated with positive airway pressure demonstrated a greater improvement in LVEF compared to those patients who did not receive treatment.
References
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Franklin KA, Nilsson JB, Sahlin C, Näslund U. Sleep apnoea and nocturnal angina. Lancet 1995; 345:1085.
Javaheri S. Effects of continuous positive airway pressure on sleep apnea and ventricular irritability in patients with heart failure. Circulation 2000; 101:392.
Mansfield DR, Gollogly NC, Kaye DM, et al. Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure. Am J Respir Crit Care Med 2004; 169:361.
Kaneko Y, Floras JS, Usui K, et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med 2003; 348:1233.
Khayat RN, Abraham WT, Patt B, et al. Cardiac effects of continuous and bilevel positive airway pressure for patients with heart failure and obstructive sleep apnea: a pilot study. Chest 2008; 134:1162.
Khayat RN, Jarjoura D, Patt B, et al. In-hospital testing for sleep-disordered breathing in hospitalized patients with decompensated heart failure: report of prevalence and patient characteristics. J Card Fail 2009; 15:739.
Khayat RN, Abraham WT, Patt B, et al. In-hospital treatment of obstructive sleep apnea during decompensation of heart failure. Chest 2009; 136:991.