Abstract:Obstructive sleep apnoea (OSA) is associated with atherosclerosis and cardiovascular events. Peripheral arterial disease (PAD) represents severe atherosclerosis with a high mortality after vascular surgery. The role of OSA in the prognosis of these patients is not yet established.84 patients (aged 67¡9 years) scheduled for sub-inguinal surgical revascularisation were enrolled for preoperative polysomnography. The threshold for significant OSA was an apnoea/hypopnoea index o20 events?h -1 . Major adverse cardio… Show more
“…In patients with OSAS with significant characteristics of upper airway collapse (19) and effects on the circulatory system, the primary mechanism involves the excitement of sympathetic nerves (3), increase of endothelin levels (20), vascular endothelial function, abnormalities in vascular active substances (21), vascular tension (22) and excessive renin secretion causing sustained hypertension (23). In previous studies, plasma levels of CRP and other inflammatory cytokines in patients with OSAS caused by inflammation have been reported to promote cardiovascular and cerebrovascular diseases (24), including AS.…”
Obstructive sleep apnea syndrome (OSAS) is known to be a risk factor for atherosclerosis (AS), derived from a series of chronic inflammatory reactions caused by hypoxia. However, the association between chronic inflammation and high blood pressure caused by hypoxia remains to be fully elucidated. The aim of the present study was to investigate the effect of continuous positive airway pressure (CPAP) therapy on inflammatory cytokines and AS. A total of 100 patients with OSAS and 50 healthy control subjects were enrolled. Fresh venous blood samples were collected prior to and following a 3‑months period of CPAP treatment. The inflammatory factors, interleukin (IL)‑18 and tumor necrosis factor (TNF)‑α, C‑reactive protein (CRP), intercellular cell adhesion molecule 1 (ICAM‑1), vascular cell adhesion molecule 1 (VCAM‑1), E‑selectin and P‑selectin, were detected using standard enzyme‑linked immunosorbent assay kits. Intima‑media thickness (IMT), brachial‑ankle pulse wave velocity (Ba‑PWV), apnea‑hypopnea index (AHI) and transcutaneous oxygen saturation (SpO2) were also detected to compare differences prior to and following treatment. The results showed that, compared with the pre‑treatment data, the expression levels of IL‑8, TNF‑α, CRP, ICAM‑1, VCAM‑1, E‑selectin and P‑selectin were significantly decreased following treatment (P<0.05). The AHI, IMT, blood pressure and Ba‑PWV values were significantly decreased (P<0.05), and the SpO2 was increased (P<0.05). Taken together, by comparing the pre‑ and post‑intervention data, it was confirmed that inflammatory factors were involved in the process of AS in patients with OSAS. Following CPAP treatment, blood pressure and primary indicators in the patients improved.
“…In patients with OSAS with significant characteristics of upper airway collapse (19) and effects on the circulatory system, the primary mechanism involves the excitement of sympathetic nerves (3), increase of endothelin levels (20), vascular endothelial function, abnormalities in vascular active substances (21), vascular tension (22) and excessive renin secretion causing sustained hypertension (23). In previous studies, plasma levels of CRP and other inflammatory cytokines in patients with OSAS caused by inflammation have been reported to promote cardiovascular and cerebrovascular diseases (24), including AS.…”
Obstructive sleep apnea syndrome (OSAS) is known to be a risk factor for atherosclerosis (AS), derived from a series of chronic inflammatory reactions caused by hypoxia. However, the association between chronic inflammation and high blood pressure caused by hypoxia remains to be fully elucidated. The aim of the present study was to investigate the effect of continuous positive airway pressure (CPAP) therapy on inflammatory cytokines and AS. A total of 100 patients with OSAS and 50 healthy control subjects were enrolled. Fresh venous blood samples were collected prior to and following a 3‑months period of CPAP treatment. The inflammatory factors, interleukin (IL)‑18 and tumor necrosis factor (TNF)‑α, C‑reactive protein (CRP), intercellular cell adhesion molecule 1 (ICAM‑1), vascular cell adhesion molecule 1 (VCAM‑1), E‑selectin and P‑selectin, were detected using standard enzyme‑linked immunosorbent assay kits. Intima‑media thickness (IMT), brachial‑ankle pulse wave velocity (Ba‑PWV), apnea‑hypopnea index (AHI) and transcutaneous oxygen saturation (SpO2) were also detected to compare differences prior to and following treatment. The results showed that, compared with the pre‑treatment data, the expression levels of IL‑8, TNF‑α, CRP, ICAM‑1, VCAM‑1, E‑selectin and P‑selectin were significantly decreased following treatment (P<0.05). The AHI, IMT, blood pressure and Ba‑PWV values were significantly decreased (P<0.05), and the SpO2 was increased (P<0.05). Taken together, by comparing the pre‑ and post‑intervention data, it was confirmed that inflammatory factors were involved in the process of AS in patients with OSAS. Following CPAP treatment, blood pressure and primary indicators in the patients improved.
“…In a 1-year follow-up study in 84 patients undergoing surgical revascularization for peripheral artery disease, an AHI $ 20 was predictive of major adverse cardiovascular and cerebrovascular events (hazard ratio, 5.1). 35 Lastly, a study in 471 patients who had undergone various noncardiac or upper airway surgeries under general anesthetic, Kaw et al 36 reported that a diagnosis of OSA (as defined by an AHI $ 5 events per hour) was associated with increased risk of postoperative hypoxemia, admission to the ICU, and longer hospital length of stay. No relationship between the AHI and postoperative complications was reported.…”
In the surgical setting, OSA is associated with an increased risk of postoperative complications. At present, risk stratification using OSA-associated parameters derived from polysomnography
“…A further 525 records were removed after screening by titles and abstracts. We carefully read the full texts of the remaining 16 papers and then excluded 8 additional articles [11][12][13][14][15][16][17][18] for the following reasons: (1) a review, (2) no extractable data, (3) overlapping data, (4) Burger disease, and (5) PAD not clearly identified as a cardiovascular event. Ultimately, the review included 8 articles.…”
Introduction: Sleep-disordered breathing (SDB) is associated with atherosclerosis. Peripheral arterial disease (PAD) is a manifestation of atherosclerosis in lower extremity arteries. No systematic review addressing the relationship between PAD and SDB was found. We performed this study aimed to summarize the relationship between SDB and PAD described in current clinical studies. Material and Methods: PubMed and Embase electronic databases were searched for clinical articles (published before 3 April, 2019) describing studies that evaluated the association between SDB and PAD. We showed the results involved in the association in clinical studies. Results: In total, 8 clinical studies have been included, and most of them were cross-sectional studies. Six articles demonstrated the coexistence of SDB and PAD, evidenced by high prevalence of SDB in patients with PAD and vice versa. Meanwhile, the included studies exhibited independent positive associations between SDB or sleep parameters and PAD after adjusting for multiple confounders. Conclusion: From present clinical prospective, positive association between SDB and PAD was shown. More prospective, randomized controlled studies are needed to establish the cause–effect relationships involved.
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