Congestive heart failure and obstructive sleep apnea
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ACC/AHA Guideline Recommendations
Congestive heart failure and obstructive sleep apnea On the Web
Obstructive sleep apnea is a sleep-related breathing disorder with effects on cardiovascular system by increasing the risk of hypertension, coronary artery disease, cardiac arrhythmias, sudden cardiac death, and heart failure. Obstructive sleep apnea contributes to the development and progression of HF. Hypoxia caused activation of inflammatory pathway leading to endothelial damage, atherogenesis, and heart failure. Activate profibrotic transforming growth factor-β during inflammatory process may cause increased deposition of extracellular matrix and consequent myocardial fibrosis and worsening LV diastolic function.
Sleep apnea in heart failure disease
- Sleep apnea is defined as partial or complete cessation of breathing during night-time sleep, resulting in repeated arousal from sleep, oxyhemoglobin desaturation, and daytime sleepiness.
- Apnea is as complete cessation of airflow for >10 s.
- Hypopnea, or partial cessation of airflow, is defined as a 50% to 90% reduction in airflow for >10 s, and >3% decrease in oxyhemoglobin saturation (SaO2) terminated by arousal.
- The 3 types of apnea include central, obstructive, and mixed.
- Central sleep apnea (CSA) is characterized by a complete withdrawal of central respiratory drive to the inspiratory muscles, including the diaphragm, and results in the simultaneous absence of naso-oral airflow and thoracoabdominal excursions.
- In obstructive sleep apnea (OSA), the thoracic inspiratory muscles, including the diaphragm, are active, so thoracoabdominal excursions are seen.
- Absence of airflow results from upper-airway occlusion caused by lost pharyngeal dilator muscle tone, with consequent pharyngeal collapse.
- Obstructive sleep apnea is classified as mild (apnea-hypopnea index or AHI, 5–14), moderate (AHI, 15–30), or severe (AHI, >30)
- Mixed apnea has an initial central component followed by an obstructive component.
- Two types of hypopnea include obstructive or central.
- Obstructive sleep apnea is characterized by recurrent pharyngeal collapse during sleep.
- Hypopnea or apnea occurs in the presence of pharynx collapse upon normal withdrawal of pharyngeal dilator muscle tone during sleep.
- Obesity and fat deposition around the pharynx are responsible of pharyngeal narrowing.
- During sleeping period, edema of the peripharyngeal area due to leg fluid redistribution, may predispose the patients to OSA.
- Obstructive sleep apnea causes a drop in intrathoracic pressure, hypoxia, and arousal.
- The drop in intrathoracic pressure increases left ventricular (LV) transmural pressure, and afterload.
- This drop in pressure increases venous return, causing right ventricular distention and a leftward shift of the interventricular septum and consequent decreased LV filling.
- Decreased LV filling and increased afterload lead to reduced stroke volume.
- Obstructive sleep apnea leading to elevations in systemic blood pressure (BP) secondary to hypoxia, arousals from sleep, and increased sympathetic nervous system activity (SNA).
- The combination of increased LV afterload and increased heart rate secondary to augmented SNA leads to myocardial oxygen supply/demand mismatch, cardiac ischemia and arrhythmias, LV hypertrophy, LV enlargement, and HF.
- Rapid-eye-movement (REM) sleep constitutes 20% to 25% of sleep and is associated with short surges of sympathetic activity.
- Sleep generally is a period of increased vagal activity and slower heart rates and lower BP. However, arousals after disordered breathing events in OSA leading to increase sympathetic nerve activity and risk of HF disease.
- Hypoxemia caused systolic and diastolic dysfunction may also lessen oxygen delivery to the myocardium.
- Increased free oxygen radicals and inflammation may cause myocardial ischemia, arrhythmias, and sudden cardiac death.
- Plasma nitrite concentrations, and endothelial-mediated vasodilation decrease in patients with OSA.
- Reactive oxygen species selectively activate inflammatory pathways.
- Activation of NFκB leads to increased production of tumor necrosis factor-α, interleukin-6, interleukin-8, and C-reactive protein, as well as adhesion molecules such as intracellular and vascular cell adhesion molecules, E selecting, and CD15, CD32.
- Activate inflammatory pathways can lead to endothelial damage, atherogenesis, and heart failure.
- Activate profibrotic transforming growth factor-β during inflammatory process leads to increased deposition of extracellular matrix and consequent myocardial fibrosis, and to worsening LV diastolic function.
- Common risk factors of OSA in patients with HFrEF include older age, male sex, higher BMI, and habitual snoring.
- In patients with HFrEF and HFpEF, OSA is more prevalent than in the general population.
- Predictors of risk OSA and CSA in HFrEF are atrial fibrillation, ventricular arrhythmias, lower LV ejection fraction (LVEF, and higher levels of serum brain natriuretic peptide (BNP), endothelin-1, and urinary norepinephrine.
- Use of nocturnal continuous positive airway pressure (CPAP) in OSA and HFrEF was associated with reduced central sympathetic vasoconstrictor outflow and improve vagal modulation of the heart by increasing high-frequency heart rate variability.
- Other advantages of use of CPAP in HFrEF include reduction in apnea-hypopnea index, number of arousal per night, and daytime systolic blood pressure and heart rate combined with decrease in left ventricular end-systolic diameter and an 8.8% absolute increase in LVEF.
- Use of CPAP was associated with improvement in quality of life.
- There are no clinical trials regarding the effects of chronic CPAP therapy in patients with OSA and HFpEF. However, CPAP therapy may have beneficial effects on diastolic function as follows:
- Decreased diastolic blood pressure
- Improved systolic and diastolic function (increased E/A ratio, decreased IVRT)
- Regression of LV hypertrophy
- Reduced LV wall thickness (interventricular septum and LV posterior wall)
- Improved diastolic velocities
2022 AHA/ACC/HFSA Heart Failure Guideline (DO NOT EDIT) 
Management of Sleep Disorders
|"1. In patients with HF and suspicion of sleep-disordered breathing, a formal sleep assessment is reasonable to confirm the diagnosis and differentiate between obstructive and central sleep apnea. (Level of Evidence: C-LD) "|
|"2. In patients with HF and obstructive sleeep apnea, continuous positive airway pressure may be reasonable to improve sleep quality and decrease daytime sleepiness. (Level of Evidence: B-R) "|
|Class III (Harm)|
|"3. In patients with NYHA class II to IV HFrEF and central sleep apnea, adaptive servo-ventilation causes harm.  (Level of Evidence: B-R) "|
- 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines
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