Prevalence of Sleep Apnea in Patients with Carotid Artery Stenosis

Nahorecki, Artur; Postrzech-Adamczyk, Katarzyna; Święcicka-Klama, Agnieszka; Skomro, Robert; Szuba, Andrzej

doi:10.1007/5584_2019_397

Cited by 2 publications

(1 citation statement)

References 28 publications

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“…This meta-analysis, confirmed that CIMT was higher in OSA patients compared to healthy controls (SMD = 0.810 CI: 0.676-0.943; P < 0.001) with a fair correlation between AHI and CIMT (R = 0.389; 95% CI: 0.315-0.459; P < 0.001). Further studies published after these two metaanalyses deserve to be reported [55][56][57][58][59][60][61][62][63][64]. A total of 206 adults newly diagnosed with OSA (AHI of 15-75 events/h) and 53 controls with AHI < 10 were studied by Kim et al [55].…”

Section: Carotid Atherosclerosismentioning

confidence: 99%

Targeting subclinical organ damage in obstructive sleep apnea: a narrative review

et al. 2020

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Subclinical abnormalities in cardiac and vascular structure reflect the adverse effects triggered by a variety of risk factors on the cardiovascular (CV) system thereby representing an intermediate step in the cardiovascular continuum; such alterations are recognized as reliable markers of increased cardiovascular risk in different clinical settings including obstructive sleep apnea (OSA). The mechanisms underlying subclinical organ damage (OD) in the OSA setting are multifactorial. Hypoxemia and hypercapnia, induced by repeated collapses of upper airways, have been suggested to trigger a cascade of events such as activation of the sympathetic tone, renin-angiotensin-aldosterone system leading to endothelial dysfunction, vasoconstriction, myocardial and vascular remodeling, and hypertension. Furthermore, coexisting non-haemodynamic alterations such as increased oxidative stress, release of inflammatory substances, enhanced lipolysis and insulin resistance have been reported to play a role in the pathogenesis of both cardiac and extra-cardiac OD. In this article we reviewed available evidence on the association between OSA and subclinical cardiac (i.e., left and right ventricular hypertrophy, left atrial dilatation) and extracardiac organ damage (i.e., carotid atherosclerosis, arterial stiffness, microvascular retinal changes, and microalbuminuria). This association is apparently stronger for cardiac and carotid subclinical damage than for other markers (i.e., arterial stiffness and retinal changes) and mostly evident in the setting of severe OSA.

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