1324 Recognizing Central Sleep Apnea in the Setting of Heart Failure with Bioprosthetic Aortic Valve

Abstract Introduction Central sleep apnea (CSA) and Cheyne–Stokes respiration (CSR) frequently occur in patients with heart failure, atrial fibrillation, and low cardiac output states. However, severe CSA associated with progressive dysfunction of a bioprosthetic aortic valve is less commonly recognized. We present a case of profound CSA in the setting of worsening central aortic regurgitation and heart failure physiology. Report of case(s) A 72-year-old man with ischemic cardiomyopathy (prior EF 40%), bioprosthetic aortic and mitral valves, redo aortic valve replacement for endocarditis, atrial fibrillation on anticoagulation, multiple prior strokes, vascular dementia, coronary artery disease, hypertension, diabetes, and extensive comorbidities presented with one month of worsening fatigue, fluctuating alertness, and erratic breathing patterns. His Epworth Sleepiness Scale was 13. Family and inpatient teams reported episodes consistent with CSR, though none were directly observed during examination. He denied habitual snoring. Laboratory studies showed hemoglobin 11 g/dL, creatinine 1.5 mg/dL, proBNP >18,000 pg/mL, and serum bicarbonate 20–21 mmol/L. Infectious and metabolic evaluations were negative. Brain MRI demonstrated chronic infarcts. CT chest showed a dilated pulmonary artery, small effusions, and contrast reflux into the IVC and hepatic veins, suggesting elevated right-sided pressures. Echocardiography in August 2025 revealed EF 55% with wall motion abnormalities and moderate to severe aortic regurgitation across a bioprosthetic valve. Repeat echocardiography in October demonstrated mild systolic dysfunction, severe apical hypokinesis, moderate-to-severe central aortic regurgitation, mild paravalvular leak, diastolic flow reversal in the descending aorta, mild mitral regurgitation, moderate tricuspid regurgitation, and a moderately dilated left atrium. Due to concern for CSA, a diagnostic polysomnogram was performed on 10/8/2025, revealing severe central sleep apnea with total sleep time 85.7 minutes, AHI 82.6/hr, central apnea index 74.2/hr, oxygen nadir 78%, and persistent atrial fibrillation. No significant periodic limb movements were seen. A PAP titration study was scheduled. Conclusion This case highlights severe CSA occurring concurrently with worsening bioprosthetic aortic regurgitation and heart failure physiology. Elevated filling pressures, atrial fibrillation, impaired forward flow, and increased loop gain likely contributed to ventilatory instability. Recognition of CSA in valvular deterioration is important, as optimization of cardiac function may significantly improve respiratory patterns and clinical outcomes. Support (if any)

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SLEEP
Published
2026-05-01
DOI
https://doi.org/10.1093/sleep/zsag091.1323
Primary Topic
Obstructive Sleep Apnea Research
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article
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article

1324 Recognizing Central Sleep Apnea in the Setting of Heart Failure with Bioprosthetic Aortic Valve

H. Bakhtiar, Peter Huh
SLEEP
Obstructive Sleep Apnea Research
article

1324 Recognizing Central Sleep Apnea in the Setting of Heart Failure with Bioprosthetic Aortic Valve

H. Bakhtiar, Peter Huh
article en

Abstract

Abstract Introduction Central sleep apnea (CSA) and Cheyne–Stokes respiration (CSR) frequently occur in patients with heart failure, atrial fibrillation, and low cardiac output states. However, severe CSA associated with progressive dysfunction of a bioprosthetic aortic valve is less commonly recognized. We present a case of profound CSA in the setting of worsening central aortic regurgitation and heart failure physiology. Report of case(s) A 72-year-old man with ischemic cardiomyopathy (prior EF 40%), bioprosthetic aortic and mitral valves, redo aortic valve replacement for endocarditis, atrial fibrillation on anticoagulation, multiple prior strokes, vascular dementia, coronary artery disease, hypertension, diabetes, and extensive comorbidities presented with one month of worsening fatigue, fluctuating alertness, and erratic breathing patterns. His Epworth Sleepiness Scale was 13. Family and inpatient teams reported episodes consistent with CSR, though none were directly observed during examination. He denied habitual snoring. Laboratory studies showed hemoglobin 11 g/dL, creatinine 1.5 mg/dL, proBNP >18,000 pg/mL, and serum bicarbonate 20–21 mmol/L. Infectious and metabolic evaluations were negative. Brain MRI demonstrated chronic infarcts. CT chest showed a dilated pulmonary artery, small effusions, and contrast reflux into the IVC and hepatic veins, suggesting elevated right-sided pressures. Echocardiography in August 2025 revealed EF 55% with wall motion abnormalities and moderate to severe aortic regurgitation across a bioprosthetic valve. Repeat echocardiography in October demonstrated mild systolic dysfunction, severe apical hypokinesis, moderate-to-severe central aortic regurgitation, mild paravalvular leak, diastolic flow reversal in the descending aorta, mild mitral regurgitation, moderate tricuspid regurgitation, and a moderately dilated left atrium. Due to concern for CSA, a diagnostic polysomnogram was performed on 10/8/2025, revealing severe central sleep apnea with total sleep time 85.7 minutes, AHI 82.6/hr, central apnea index 74.2/hr, oxygen nadir 78%, and persistent atrial fibrillation. No significant periodic limb movements were seen. A PAP titration study was scheduled. Conclusion This case highlights severe CSA occurring concurrently with worsening bioprosthetic aortic regurgitation and heart failure physiology. Elevated filling pressures, atrial fibrillation, impaired forward flow, and increased loop gain likely contributed to ventilatory instability. Recognition of CSA in valvular deterioration is important, as optimization of cardiac function may significantly improve respiratory patterns and clinical outcomes. Support (if any)

SLEEPVol. 49(Supplement_1)
Norwalk Hospital (US)
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Openalex Percentile: Top 7%
Obstructive Sleep Apnea Research
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