Arrhythmia Risk Associated with Sleep Disordered Breathing in Chronic Heart Failure

Mehra, Reena; Redline, Susan

doi:10.1007/s11897-013-0171-7

Cited by 20 publications

(8 citation statements)

References 89 publications

(108 reference statements)

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“…Predictors of CA in HFrEF patients identified in different studies were age, male gender, body mass index (BMI), LVEF, atrial fibrillation, awake partial pressure of carbon dioxide and increased natriuretic peptides (5, 11, 12). In HFrEF, CA have been associated with worse symptoms (1, 4, 6), reduced exercise tolerance and peak oxygen consumption (3, 5, 7), increased ventilatory inefficiency on effort, worse left ventricular (LV) systolic and diastolic function (2, 5), increased sympathetic activation and plasma levels of natriuretic peptides (2, 5) as well as increased incidence of atrial and ventricular arrhythmias (13, 14). Moreover, CA have been associated with an increased risk of mortality, both for HF progression and life-threating arrhythmias (2, 4, 6, 7, 9, 10), especially when CA are present also during the daytime (2, 5, 6, 10).…”

Section: Introductionmentioning

confidence: 99%

Central and Obstructive Apneas in Heart Failure With Reduced, Mid-Range and Preserved Ejection Fraction

Borrelli

Gentile

Sciarrone

et al. 2019

Front. Cardiovasc. Med.

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Background: Although central apneas (CA) and obstructive apneas (OA) are highly prevalent in heart failure (HF), a comparison of apnea prevalence, predictors and clinical correlates in the whole HF spectrum, including HF with reduced ejection fraction (HFrEF), mid-range EF (HFmrEF) and preserved EF (HFpEF) has never been carried out so far.Materials and methods: 700 HF patients were prospectively enrolled and then divided according to left ventricular EF (408 HFrEF, 117 HFmrEF, 175 HFpEF). All patients underwent a thorough evaluation including: 2D echocardiography; 24-h Holter-ECG monitoring; cardiopulmonary exercise testing; neuro-hormonal assessment and 24-h cardiorespiratory monitoring.Results: In the whole population, prevalence of normal breathing (NB), CA and OA at daytime was 40, 51, and 9%, respectively, while at nighttime 15, 55, and 30%, respectively. When stratified according to left ventricular EF, CA prevalence decreased (daytime: 57 vs. 43 vs. 42%, p = 0.001; nighttime: 66 vs. 48 vs. 34%, p < 0.0001) from HFrEF to HFmrEF and HFpEF, while OA prevalence increased (daytime: 5 vs. 8 vs. 18%, p < 0.0001; nighttime 20 vs. 29 vs. 53%, p < 0.0001).In HFrEF, male gender and body mass index (BMI) were independent predictors of both CA and OA at nighttime, while age, New York Heart Association functional class and diastolic dysfunction of daytime CA. In HFmrEF and HFpEF male gender and systolic pulmonary artery pressure were independent predictors of CA at daytime, while hypertension predicted nighttime OA in HFpEF patients; no predictor of nighttime CA was identified. When compared to patients with NB, those with CA had higher neuro-hormonal activation in all HF subgroups. Moreover, in the HFrEF subgroup, patients with CA were older, more comorbid and with greater hemodynamic impairment while, in the HFmrEF and HFpEF subgroups, they had higher left atrial volumes and more severe diastolic dysfunction, respectively. When compared to patients with NB, those with OA were older and more comorbid independently from background EF.Conclusions: Across the whole spectrum of HF, CA prevalence increases and OA decreases as left ventricular systolic dysfunction progresses. Different predictors and specific clinical characteristics might help to identify patients at risk of developing CA or OA in different HF phenotypes.

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Section: Introductionmentioning

confidence: 99%

Central and Obstructive Apneas in Heart Failure With Reduced, Mid-Range and Preserved Ejection Fraction

Borrelli

Gentile

Sciarrone

et al. 2019

Front. Cardiovasc. Med.

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“…In addition, there is an increased risk for arrhythmogenesis due to autonomic dysfunction in patients with OSA 56. OSA is an independent risk factor for atrial fibrillation 57.…”

Section: Cardiovascular Diseasesmentioning

confidence: 99%

An update on cardiovascular effects of obstructive sleep apnoea syndrome

Uyar

Davutoğlu

2016

Postgraduate Medical Journal

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Obstructive sleep apnoea syndrome is an important health problem which may cause or worsen systemic diseases. Chronic intermittent hypoxia during repetitive airflow cessations may cause endothelial dysfunction. Sleep apnoea is also shown to be associated with hypercoagulability which may be due to decreased nitric oxide levels and impaired vasodilatation. Endothelial dysfunction, increased systemic inflammation, sympathetic nervous system activation, increased oxidative stress and dysglycaemia may all contribute to cardiovascular processes such as hypertension, arrhythmia, stroke, heart failure and coronary artery disease in patients with obstructive sleep apnoea. Treatment approaches in patients with obstructive sleep apnoea mainly focus on maintaining upper airway patency either with positive airway pressure devices or upper airway appliances. Strategies involving positive airway pressure therapy are associated with decreased morbidity and mortality. Obstructive sleep apnoea should be suspected as an underlying mechanism in patients with cardiovascular disease and warrants appropriate treatment.

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“…OSA is accompanied by impressive levels of intrathoracic pressure alterations approaching negative 65mmHg which has been specifically observed in those with OSA and HF 37 . These OSA-induced increasingly negative intrathoracic pressures have direct mechanical effects on the heart resulting in increased juxtacardiac and transmural pressures and increased ventricular afterload and myocardial oxygen demand 38 . These OSA-related perturbations with cyclic changes in venous return in HF can challenge the already vulnerable heart and contribute to HF progression.…”

Section: Common Underlying Pathophysiologic Mechanisms Linking Sleep mentioning

confidence: 99%

Targeting Sleep Disordered Breathing to Prevent Heart Failure: What is the Evidence?

Kusunose

Mehra

2014

Curr Cardiovasc Risk Rep

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The inter-relationships of sleep disordered breathing (SDB) and heart failure (HF) are becoming increasingly well-characterized. The pathways linking the two entities are likely bi-directional and key underlying pathophysiological mechanisms at play include autonomic nervous system fluctuations, intermittent hypoxia, intrathoracic cardiac mechanical influences, rostral fluid shifts and up-regulation of systemic inflammation and oxidative stress. Given the increased morbidity and mortality which accompanies heart failure, the recognition and treatment of factors such as sleep disordered breathing is paramount in order to mitigate these untoward downstream health consequences. Recently, the management of HF requires combining several treatments including pharmacotherapy, electrophysiologic therapy, and cardiac surgery to target the various complex facets of HF. Despite the development of HF treatments, HF remains to pose a great challenge to the general cardiologist. Herein we review several interventional studies highlighting the effects of treating SDB on HF morbidity and mortality with a notable predominance of literature focusing on HF reduced ejection fraction (HF-REF) as well as emerging data describing SDB treatment effects in HF preserved EF (HF-PEF). These data are compelling yet with intrinsic limitations which underscore the need for appropriately powered clinical trials employing rigorous clinical trials methodology to examine the effect of SDB treatment on HF progression and associated adverse outcomes.

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Arrhythmia Risk Associated with Sleep Disordered Breathing in Chronic Heart Failure

Cited by 20 publications

References 89 publications

Central and Obstructive Apneas in Heart Failure With Reduced, Mid-Range and Preserved Ejection Fraction

Central and Obstructive Apneas in Heart Failure With Reduced, Mid-Range and Preserved Ejection Fraction

An update on cardiovascular effects of obstructive sleep apnoea syndrome

Targeting Sleep Disordered Breathing to Prevent Heart Failure: What is the Evidence?

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