Arrhythmia Risk Associated with Sleep Disordered Breathing in Chronic Heart Failure
Abstract The intersecting relationships of sleep disordered breathing (SDB), arrhythmogenic risk and chronic heart failure (HF) are complex and most likely multi-directional and synergistic. Autonomic dysfunction is a common pathophysiological feature of each of these entities. Intermittent hypoxia, hypercapnia, mechanical cardiac influences due to upper airway obstruction and rostral fluid shifts are SDB-specific mechanisms which may trigger, perpetuate and exacerbate HF and arrhythmogenesis. Specific pathophysiological mechanisms will vary according to the predominance of central as compared to obstructive sleep apnea. The risk of cardiac arrhythmias and HF attributable to SDB may be considerable given the high prevalence of SDB and its likely physiologic burden. The current review focuses on the data, which have accrued elucidating the specific contributory mechanisms of SDB in cardiac arrhythmias and HF, highlighting the clinical relevance and effects of standard SDB treatment on these outcomes, and describing the role of novel therapeutics..
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2013 |
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Erschienen: |
2013 |
Enthalten in: |
Zur Gesamtaufnahme - volume:11 |
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Enthalten in: |
Current heart failure reports - 11(2013), 1 vom: 15. Nov., Seite 88-97 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Mehra, Reena [VerfasserIn] |
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Links: |
Volltext [lizenzpflichtig] |
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Anmerkungen: |
© Springer Science+Business Media New York 2013 |
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doi: |
10.1007/s11897-013-0171-7 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
OLC2102945227 |
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520 | |a Abstract The intersecting relationships of sleep disordered breathing (SDB), arrhythmogenic risk and chronic heart failure (HF) are complex and most likely multi-directional and synergistic. Autonomic dysfunction is a common pathophysiological feature of each of these entities. Intermittent hypoxia, hypercapnia, mechanical cardiac influences due to upper airway obstruction and rostral fluid shifts are SDB-specific mechanisms which may trigger, perpetuate and exacerbate HF and arrhythmogenesis. Specific pathophysiological mechanisms will vary according to the predominance of central as compared to obstructive sleep apnea. The risk of cardiac arrhythmias and HF attributable to SDB may be considerable given the high prevalence of SDB and its likely physiologic burden. The current review focuses on the data, which have accrued elucidating the specific contributory mechanisms of SDB in cardiac arrhythmias and HF, highlighting the clinical relevance and effects of standard SDB treatment on these outcomes, and describing the role of novel therapeutics. | ||
650 | 4 | |a Acetazolamide | |
650 | 4 | |a Adaptive servoventilation | |
650 | 4 | |a Apnea hypopnea index | |
650 | 4 | |a Arrhythmia | |
650 | 4 | |a Atrial fibrillation | |
650 | 4 | |a Autonomic dysfunction | |
650 | 4 | |a Cardiac resynchonization therapy | |
650 | 4 | |a Central sleep apnea | |
650 | 4 | |a Cheyne stokes respirations | |
650 | 4 | |a Continuous positive airway pressure | |
650 | 4 | |a Hypoxia | |
650 | 4 | |a Heart failure | |
650 | 4 | |a Hypercapnia | |
650 | 4 | |a Oxygen | |
650 | 4 | |a Obstructive sleep apnea | |
650 | 4 | |a Phrenic nerve stimulation | |
650 | 4 | |a Polysomnography | |
650 | 4 | |a Renal sympathetic denervation | |
650 | 4 | |a Sleep disordered breathing | |
650 | 4 | |a Sudden cardiac death | |
650 | 4 | |a Theophylline | |
650 | 4 | |a Ventricular arrhythmia | |
700 | 1 | |a Redline, Susan |4 aut | |
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