Protective Cardiovascular Effect of Sleep Apnea Severity in Obesity Hypoventilation Syndrome

Masa, Juan F.; Corral, Jaime; Romero, Odile; Caballero, Candela; Terán-Santos, Joaquín; Alonso-Álvarez, María Luz; Gómez-García, Teresa; González, Mónica; López-Martín, Soledad; Lucas, Pilar de; Marı́n, José Marı́a; Martí, Sergi; Díaz-Cambriles, Trinidad; Chiner, Eusebi; Merchan, Miguel; Egea, Carlos; Obeso, Ana; Mokhlesi, Babak; García-Ledesma, Estefanía; Sánchez-Quiroga, M-Ángeles; Ordax, Estrella; González-Mangado, Nicolás; Troncoso, María F.; Martínez-Martínez, María-Ángeles; Cantalejo, Olga; Ojeda, Elena; Carrizo, Santiago; Gallego, Begoña Carazo; Pallero, Mercedes; Ramón, M Antonia; Díaz-de-Atauri, Josefa; Muñoz-Méndez, Jesús; Senent, Cristina; Sancho-Chust, José N.; Ribas-Solis, Francisco Javier; Barrot, Emilia; Benítez, José María; Sánchez-Gómez, Jesús; Golpe, Rafael; Santiago-Recuerda, Ana; Gómez, Sílvia; Bengoa, Mónica

doi:10.1016/j.chest.2016.02.647

Cited by 57 publications

(31 citation statements)

References 40 publications

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“…Besides the need for expanded research on this issue, the cumulative findings to date may account for some of the contrasting results reported by clinical studies addressing the interaction between sleep apnea and heart diseases. Indeed, in obesity hypoventilation syndrome, the prevalence of chronic heart failure had the strongest negative association with the highest tertile of oxygen desaturation index (14). More intriguingly, treatment of severe central sleep apnea with adaptive servo-ventilation in patients with HF was associated with an increase in all-cause and cardiovascular mortality (15).…”

Section: Discussionmentioning

confidence: 99%

Chronic Sleep Fragmentation Mimicking Sleep Apnea Does Not Worsen Left-Ventricular Function in Healthy and Heart Failure Mice

et al. 2020

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Aims: Obstructive sleep apnea (OSA) has been associated with heart failure (HF). Sleep fragmentation (SF), one of the main hallmarks of OSA, induces systemic inflammation, oxidative stress and sympathetic activation, hence potentially participating in OSA-induced cardiovascular consequences. However, whether SF per se is deleterious to heart function is unknown. The aim of this study was to non-invasively evaluate the effect of SF mimicking OSA on heart function in healthy mice and in mice with HF. Methods and Results: Forty C57BL/6J male mice were randomized into 4 groups: control sleep (C), sleep fragmentation (SF), isoproterenol-induced heart failure (HF), and mice subjected to both SF+HF. Echocardiography was performed at baseline and after 30 days to evaluate left ventricular end-diastolic (LVEDD) and end-systolic (LVESD) diameters, left ventricular ejection fraction (LVEF) and fraction shortening (FS). The effects of SF and HF on these parameters were assessed by two-way ANOVA. Mice with isoproterenol-induced HF had significant increases in LVEDD and LVESD, as well as a decreases in LVEF and FS (p = 0.013, p = 0.006, p = 0.027, and p = 0.047, respectively). However, no significant effects emerged with SF (p = 0.480, p = 0.542, p = 0.188, and p = 0.289, respectively). Conclusion: Chronic SF mimicking OSA did not induce echocardiographic changes in cardiac structure and function in both healthy and HF mice. Thus, the deleterious cardiac consequences of OSA are likely induced by other perturbations associated with this prevalent condition, or result from interactions with underlying comorbidities in OSA patients.

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Section: Discussionmentioning

confidence: 99%

Chronic Sleep Fragmentation Mimicking Sleep Apnea Does Not Worsen Left-Ventricular Function in Healthy and Heart Failure Mice

et al. 2020

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“…As such, it leads to a higher prevalence and more severe pulmonary hypertension and metabolic syndrome and a higher risk of other cardiovascular events and mortality compared to eucapnic obese patients 30,45 . 28,47,48 .…”

Section: Barcelona Respiratory Networkmentioning

confidence: 99%

“…A cross-sectional analysis 48 examined the association between cardiovascular morbidity and OSA severity in patients with OHS, based on tertiles of oxygen desaturation index (ODI). In patients with OHS, the highest OSA severity phenotype was associated with reduced risk of cardiovascular morbidity.…”

Section: Barcelona Respiratory Networkmentioning

confidence: 99%

Obesity Hypoventilation Syndrome: New Insights

Molina¹,

Jiménez²,

Terreros³

2021

BRN

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Obesity hypoventilation syndrome (OHS) is an obesity-dependent sleep disorder that has acquired great importance worldwide due to its prevalence and the fact that its features may lead to an increase in morbidity and mortality whilst reducing life quality. This condition is characterised by the presence of chronic hypercapnic respiratory failure not secondary to other causes, alveolar hypoventilation during sleep and with or without apnoeic episodes. In this review, we have gone over new insights about OHS, diagnosis and the role of positive airway pressure, in particular the mechanisms that provide general improvement, physical relief, clinical applications, and management.

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“…In addition to possible different treatment responses, there appears to be differential clinical features of these patient groups. 30 Patients with predominant OSA tend to be younger, are more likely to be male and paradoxically have lower cardiovascular co-morbidity. The reasons for this are not clear, although they can be postulated to relate to different responses to intermittent rather than sustained hypoxia.…”

Section: Clinical Phenotypes Of Obese Patients With Hypercapnic Respimentioning

confidence: 99%

Non‐invasive ventilation for obese patients with chronic respiratory failure: Are two pressures always better than one?

2019

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Obesity‐related respiratory failure is increasingly common but remains under‐diagnosed and under‐treated. There are several clinical phenotypes reported, including severe obstructive sleep apnoea (OSA), isolated nocturnal hypoventilation with or without severe OSA and OSA complicating chronic obstructive pulmonary disease (COPD). The presence of hypercapnic respiratory failure is associated with poor clinical outcomes in each of these groups. While weight loss is a core aim of management, this is often unachievable, and treatment of sleep‐disordered breathing with positive airway pressure (PAP) therapy is the mainstay of clinical practice. Although there are few long‐term clinical efficacy trials, the lack of equipoise would prevent the utilization of an untreated control group. The current data support the use of PAP therapy to improve respiratory failure and is associated with improvements in health‐related quality of life, reduced healthcare utilization and reduced mortality. Both continuous PAP (CPAP) and non‐invasive ventilation (NIV) appear safe and effective in patients with obesity‐related respiratory failure and OSA, with or without COPD, and the current evidence would not support a single therapy choice in all patients. There are no studies of CPAP in patients with isolated nocturnal hypoventilation, and NIV would be the current recommendation in this patient group. Whichever starting therapy is used, titration should be performed to correct sleep‐disordered breathing and reverse chronic respiratory failure, with consideration of step‐down of the treatment based on a clinical re‐evaluation. In contrast, failure to reach physiological and clinical treatment targets should lead to the consideration of treatment escalation.

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Protective Cardiovascular Effect of Sleep Apnea Severity in Obesity Hypoventilation Syndrome

Cited by 57 publications

References 40 publications

Chronic Sleep Fragmentation Mimicking Sleep Apnea Does Not Worsen Left-Ventricular Function in Healthy and Heart Failure Mice

Chronic Sleep Fragmentation Mimicking Sleep Apnea Does Not Worsen Left-Ventricular Function in Healthy and Heart Failure Mice

Obesity Hypoventilation Syndrome: New Insights

Non‐invasive ventilation for obese patients with chronic respiratory failure: Are two pressures always better than one?

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