Effect of CPAP on Oxidative Stress and Circulating Progenitor Cell Levels in Sleep Patients With Apnea-Hypopnea Syndrome

Murri, Mora; García-Delgado, R.; Alcázar-Ramírez, José D.; Fernández-Ramos, Ana; Alcaide, Juan; Cardona, Fernando; Tinahones, Francisco J.

doi:10.4187/respcare.01081

Cited by 24 publications

(24 citation statements)

References 26 publications

(24 reference statements)

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“…It should also be pointed out that investigators in different studies assessed circulating EPCs through different methods. Whereas some studies assessed circulating EPCs using flow cytometry alone, 35,40 another study assessed circulating EPCs by the assay of endothelial colony-forming units. 35 In addition, the EPCs studied by one group are not necessarily the same cell type as those of another.…”

Section: Discussionmentioning

confidence: 99%

Systematic and Endothelial Inflammation and Endothelial Progenitor Cell Levels in Emphysematous Rats Exposed to Intermittent Hypoxia

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Systematic and Endothelial Inflammation and Endothelial Progenitor Cell Levels in Emphysematous Rats Exposed to Intermittent Hypoxia

et al. 2015

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“…[4][5][6] Myocardial oxidative stress and ischemia are the main explanations for these disturbances. 7,8 The LV wall is not homogenous and is composed of 3 layers of fibers. Opposite orientation of the myocardial fibers in the subendocardial and subepicardial layer is important for the equal redistribution of stress and strain in the heart.…”

Section: Introductionmentioning

confidence: 99%

A Novel Method for Sensitive Determination of Subclinical Left-Ventricular Systolic Dysfunction in Subjects With Obstructive Sleep Apnea

et al. 2015

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BACKGROUND: This study was to evaluate the subclinical left-ventricular (LV) systolic dysfunction with 2-dimensional speckle-tracking echocardiography in subjects with obstructive sleep apnea (OSA) with normal left ventricular ejection fraction and without any confounding disease that can cause myocardial dysfunction. METHODS: Nineteen healthy individuals and 60 subjects with OSA were included in this study. According to the severity of disease, OSA subjects were examined in 3 groups: mild, moderate, and severe OSA. LV apical views (for longitudinal strain) and short-axis views (for circumferential strain) were acquired for evaluation. Three-layer longitudinal strain values and circumferential strain values were determined for each view, and averages of these were used in comparison with other groups. RESULTS: Three-layer longitudinal strain values of the subjects with OSA were lower than those of the healthy individuals, and these values were decreased along with the OSA severity. The difference was significant between severe OSA and all other groups. Three-layer circumferential strain values of the OSA subjects were lower than those of the healthy individuals, and the difference was significant between the control group and all other groups. The apnea hypopnea index was found to be correlated with the 3-layer longitudinal strain (r ‫؍‬ ؊0.74, P < .001; r ‫؍‬ ؊0.72, P < .001; r ‫؍‬ ؊0.69, P ‫؍‬ <.001). CONCLUSIONS: Three-layer longitudinal and circumferential LV systolic functions in OSA subjects with normal left ventricular ejection fraction are deteriorated in the subclinical stage. Two-dimensional speckle-tracking echocardiography can be used as an effective method in the determination of subclinical myocardial dysfunction in subjects with OSA. Key words: obstructive sleep apnea; speckle-tracking echocardiography; myocardial strain. [Respir Care 2016;61(3):366 -375.

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“…Murri et al44 found that EPCs (CD34+ CD133+ VEGFR2+ cells) were lower in the patients with OSA than in the control patients. There was a significant negative correlation between EPC levels and the severity of OSA, and the EPC levels correlated negatively with the levels of oxidative stress markers, but positively with markers of protection against oxidation.…”

Section: Bone Marrow–derived Epc Studies In Patients With Osamentioning

confidence: 97%

“…One of the major limitations in studying EPCs is the lack of unifying phenotypic markers that are employed by different investigators. Thus, different investigators employ different marker combinations for the assessment of EPCs: CD34+ VEGFR2+,41 CD34+ 133+,42,44,46 or CD34+ CD133+ VEGFR2+ 43–45. Third, the recruited participants are different.…”

Section: Bone Marrow–derived Epc Studies In Patients With Osamentioning

confidence: 99%

Obstructive sleep apnea and endothelial progenitor cells

Wang¹,

Wu²,

Feng³

et al. 2013

PPA

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BackgroundObstructive sleep apnea (OSA) occurs in 4% of middle-aged men and 2% of middle-aged women in the general population, and the prevalence is even higher in specific patient groups. OSA is an independent risk factor for a variety of cardiovascular diseases. Endothelial injury could be the pivotal determinant in the development of cardiovascular pathology in OSA. Endothelial damage ultimately represents a dynamic balance between the magnitude of injury and the capacity for repair. Bone marrow–derived endothelial progenitor cells (EPCs) within adult peripheral blood present a possible means of vascular maintenance that could home to sites of injury and restore endothelial integrity and normal function.MethodsWe summarized pathogenetic mechanisms of OSA and searched for available studies on numbers and functions of EPCs in patients with OSA to explore the potential links between the numbers and functions of EPCs and OSA. In particular, we tried to elucidate the molecular mechanisms of the effects of OSA on EPCs.ConclusionIntermittent hypoxia cycles and sleep fragmentation are major pathophysiologic characters of OSA. Intermittent hypoxia acts as a trigger of oxidative stress, systemic inflammation, and sympathetic activation. Sleep fragmentation is associated with a burst of sympathetic activation and systemic inflammation. In most studies, a reduction in circulating EPCs has emerged. The possible mechanisms underlying the decrease in the number or function of EPCs include prolonged inflammation response, oxidative stress, increased sympathetic activation, physiological adaptive responses of tissue to hypoxia, reduced EPC mobilization, EPC apoptosis, and functional impairment in untreated OSA. Continuous positive airway pressure (CPAP) therapy for OSA affects the mobilization, apoptosis, and function of EPCs through preventing intermittent hypoxia episodes, improving sleep quality, and reducing systemic inflammation, oxidative stress levels, and sympathetic overactivation. To improve CPAP adherence, the medical staff should pay attention to making the titration trial a comfortable first CPAP experience for the patients; for example, using the most appropriate ventilators or proper humidification. It is also important to give the patients education and support about CPAP use in the follow-up, especially in the early stage of the treatment.

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Effect of CPAP on Oxidative Stress and Circulating Progenitor Cell Levels in Sleep Patients With Apnea-Hypopnea Syndrome

Cited by 24 publications

References 26 publications

Systematic and Endothelial Inflammation and Endothelial Progenitor Cell Levels in Emphysematous Rats Exposed to Intermittent Hypoxia

Systematic and Endothelial Inflammation and Endothelial Progenitor Cell Levels in Emphysematous Rats Exposed to Intermittent Hypoxia

A Novel Method for Sensitive Determination of Subclinical Left-Ventricular Systolic Dysfunction in Subjects With Obstructive Sleep Apnea

Obstructive sleep apnea and endothelial progenitor cells

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