Obstructive sleep apnoea should be deemed a cardiovascular disease

Fuchs, Flávio Danni; Martinez, Dênis

doi:10.1136/heartjnl-2015-307879

Cited by 9 publications

(5 citation statements)

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“…Both basic and clinical research investigations have demonstrated OSAHS contributes to CAD initiation and progression [17-19]. OSAHS has been linked to cardiovascular disease via endothelial dysfunction, sympathetic activation, inflammation, and oxidative stress, but the precise responsible molecular mechanisms remain unclear [3, 20]. We report in the present study that OSAHS increased endothelial cells-derived MPs formation in CAD patients, which exacerbated endothelial dysfunction by increasing endothelial permeability and inflammatory cytokine expression.…”

Section: Discussionsupporting

confidence: 57%

Endothelial Cell-Derived Microparticles from Patients with Obstructive Sleep Apnea Hypoxia Syndrome and Coronary Artery Disease Increase Aortic Endothelial Cell Dysfunction

Jia

Fan²,

Cui

et al. 2017

Cell Physiol Biochem

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Background/Aims: Obstructive sleep apnea hypoxia syndrome (OSAHS) is an independent risk factor for coronary artery disease (CAD). Treatment of OSAHS improves clinical outcome in some CAD patients, but the relationship between OSAHS and CAD is complex. Microparticles (MPs) are shed by the plasma membrane by either physiologic or pathologic stimulation. In the current study, we investigated the role of MPs in the context of OSAHS. Methods and Results: 54 patients with both suspected coronary artery stenosis and OSAHS were recruited and underwent both coronary arteriography and polysomnography. Circulating MPs were isolated and analyzed by flow cytometry. CAD+OSAHS patients exhibited greater levels of total MPs (Annexin V⁺), erythrocyte-derived MPs (CD235⁺ Annexin V⁺), platelet-derived MPs (CD41⁺ Annexin V⁺), and leukocyte-derived MPs (CD45⁺ Annexin V⁺) compared to CAD alone patients or control. CAD+OSAHS patients expressed the greatest level of endothelial-derived MPs of all cellular origin types (CD144⁺ Annexin V ⁺). Treatment of human aortic endothelial cells (HAECs) with MPs isolated from CAD+OSAHS patients markedly increased HAEC permeability (as detected by FITC-dextran), and significantly upregulated mRNA levels of ICAM-1, VCAM-1, and MCP-1. Conclusion: OSAHS+CAD patients harbor increased levels of MPs, particularly the endothelial cell-derived subtype. When administered to HAECs, OSAHS+CAD patients MPs increase endothelial cell permeability and dysfunction.

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Section: Discussionsupporting

confidence: 57%

Endothelial Cell-Derived Microparticles from Patients with Obstructive Sleep Apnea Hypoxia Syndrome and Coronary Artery Disease Increase Aortic Endothelial Cell Dysfunction

Jia

Fan²,

Cui

et al. 2017

Cell Physiol Biochem

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“…The impact of OSA on the cardiovascular system in general has been well described [15][16][17]. The recurrent episodes of apnoea or hypopnoea associated with upper airway obstruction in OSA not only lead to negative inspiratory intrathoracic pressure, but also result in intermittent hypoxemia and hypercapnia, which in turn cause increased sympathetic drive and ultimately an arousal state that restores airway patency and ventilation.…”

Section: Sleep-disordered Breathingmentioning

confidence: 99%

Heart failure and sleep-disordered breathing

Zhai

Yip²,

Haddad³

2016

Current Opinion in Cardiology

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“… 3 OSA is more frequent in middle-aged male patients and in those with arterial hypertension, heart failure, ischemic heart disease, and stroke. 4 , 5 Previous studies have stated the estimated risk of coronary artery disease in OSA patients, especially males, as 37%. 6 …”

Section: Introductionmentioning

confidence: 99%