Obstructive sleep apnea is common in patients with heart failure. This case illustrates that treatment with PAP therapy can improve cardiac function in patients with both conditions. CPAP-emergent central apnea, as seen in this patient, has multiple etiologies. It is commonly seen in patients with severe sleep apnea, usually resolves over time, and does not need treatment with adaptive servoventilation. keywords: Heart failure, obstructive sleep apnea, PAP therapy, CPAP-emergent central sleep apnea Citation: Grewal RG. 2 Despite its association with cardiovascular diseases, sleep apnea remains underdiagnosed in patients with heart disease.3,4 Meanwhile, there has been increased development and promotion of new, advanced, and more expensive devices by industry to treat sleep apnea despite the lack of any evidence that these devices have superior clinical outcomes. 5 Following is a case which highlights both these issues.
repOrt Of CaSeTC, a 44-year-old obese African American male with a BMI of 41, longstanding history of hypertension, non-smoker, with no history of alcohol use, and a 2-3 year history of progressively increasing shortness of breath and cough, was diagnosed with New York Heart Association (NYHA) class III heart failure (HF) in July 2008. Electrocardiogram (ECG) fi ndings were notable for biatrial abnormality and borderline left ventricular (LV) hypertrophy, with no evidence of heart block. Echocardiogram showed severe dilation and global hypokinesis of LV with a LV ejection fraction (LVEF) of 10% and moderately reduced right ventricular (RV) function. Left heart catheterization did not show any occlusive coronary artery disease. Right heart catheterization showed elevated right atrial (RA) pressure at 17 mm Hg, pulmonary capillary wedge pressure (PCWP) of 30 mm Hg, pulmonary artery (PA) pressure of 74/30 mm Hg, and severely reduced right ventricular (RV) function. Cardiopulmonary exercise test showed maximum oxygen consumption (VO 2 ) of 12 cc/kg/minute. His clinical presentation was consistent with idiopathic dilated cardiomyopathy of unknown etiology. An endomyocardial biopsy was not performed to rule out any treatable causes of heart failure, in keeping with current recommendations by the American Heart Association/American college of Cardiology (AHA/ACC).6 He was treated with aspirin and maximal tolerated doses of ACE receptor inhibitor, β-blocker, and a diuretic. An ICD (implantable cardioverterdefi brillator) was placed, and he was evaluated and placed on the cardiac transplant list. Due to his longstanding history of snoring, witnessed apneas, and excessive daytime sleepiness (Epworth Sleepiness Scale [ESS] score of 17), he was evaluated for OSA in December 2008. Polysomnography, performed with a split-night protocol revealed an apnea-hypopnea index (AHI) of 68 with a SaO 2 nadir of 58%. Respiratory events were all obstructive in nature with no central apneas. Continuous positive airway pressure (CPAP) titration to a maximum pressure of 20 cm H 2 O was unsuccessful in controlling the obstruc...