Article

Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities.

Respiratory Sleep Disorders Unit, St. Vincent's University Hospital, Elm Park, Dublin 4, Ireland.
European Respiratory Journal (Impact Factor: 7.13). 02/2007; 29(1):156-78. DOI: 10.1183/09031936.00027406
Source: PubMed

ABSTRACT Considerable evidence is available in support of an independent association between obstructive sleep apnoea syndrome (OSAS) and cardiovascular disease, which is particularly strong for systemic arterial hypertension and growing for ischaemic heart disease, stroke, heart failure, atrial fibrillation and cardiac sudden death. The pathogenesis of cardiovascular disease in OSAS is not completely understood but likely to be multifactorial, involving a diverse range of mechanisms including sympathetic nervous system overactivity, selective activation of inflammatory molecular pathways, endothelial dysfunction, abnormal coagulation and metabolic dysregulation, the latter particularly involving insulin resistance and disordered lipid metabolism. The present report, which arose out of a European Union Cooperation in the field of Scientific and Technical Research (COST) action on OSAS (COST B26), reviews the current evidence for an independent association and proposes research priorities to identify the underlying mechanisms involved, with a view to identifying novel therapeutic strategies. Large-scale collaborative studies of carefully defined patient populations with obstructive sleep apnoea syndrome, adequately controlled for potential confounders, are needed. Such studies carry the prospect of evaluating potential interactions between different basic mechanisms operating in obstructive sleep apnoea syndrome and cardiovascular disease, and interactions with other related disorders, such as obesity, diabetes and dyslipidaemia. Furthermore, translational studies involving cell culture and animal models linked to studies of obstructive sleep apnoea syndrome patients are necessary to integrate basic mechanisms with the clinical disorder.

0 Bookmarks
 · 
96 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Systemic hypertension is associated with obstructive sleep apnoea syndrome (OSAS) but the pathophysiological mechanisms are incompletely understood. A collaborative European network of 24 sleep centres established a European Sleep Apnoea Database to evaluate cardiovascular morbidity associated with OSAS. 11 911 adults referred with suspected OSAS between March 2007 and September 2013 underwent overnight sleep studies, either cardiorespiratory polygraphy or polysomnography. We compared the predictive value of the apnoea-hypopnoea index (AHI) and 4% oxygen desaturation index (ODI) for prevalent hypertension, adjusting for relevant covariates including age, smoking, obesity, dyslipidaemia and diabetes. Among patients (70% male, mean±sd age 52±12 years), 78% had AHI >5 events·h(-1) and 41% systemic hypertension. Both AHI and ODI independently related to prevalent hypertension after adjustment for relevant covariates (p<0.0001 for linear trend across quartiles (Q) of severity for both variables). However, in multiple regression analysis with both ODI and AHI in the model, ODI was, whereas AHI was not, independently associated with prevalent hypertension: odds ratios (95% CI) for Q4 versus Q1 regarding ODI were 2.01 (1.61-2.51) and regarding AHI were 0.92 (0.74-1.15) (p<0.0001 and p = 0.3054, respectively). This cross sectional study suggests that chronic intermittent hypoxia plays an important role in OSAS-related hypertension.
    European Respiratory Journal 08/2014; · 7.13 Impact Factor
  • Source
  • [Show abstract] [Hide abstract]
    ABSTRACT: To assess distal/alveolar inflammation in patients with suggestive symptoms of obstructive sleep apnoea (OSA) using exhaled nitric oxide (NO) measured by two-compartment model (2-CM) after correction for axial NO back-diffusion (trumpet model). Ninety five patients suspected for OSA prospectively underwent pulmonary function test, overnight polysomnography (PSG), and exhaled NO measurement. Patients with apnoea-hypopnoea index (AHI) <5/hour were included in non-OSA group. Exhaled NO was repeatedly measured after PSG in 21 OSA patients and 8 non-OSA subjects. Alveolar NO concentration (CANO) was significantly higher in OSA patients (n=71; 4.07±1.7ppb) as compared with non-OSA subjects (n=24; 2.24±1.06ppb; p<0.0001) whilst maximal bronchial NO flux (J'awNO) and fractional exhaled NO (FENO) did not differ between the two groups. CANO was strongly associated to AHI (r=0.701; p<0.0001) and to recording time with SaO2<90% (ST-90%; r=0.659; p<0.0001) in OSA patients but not in non-OSA persons. The area under ROC curve for screening patients with OSA and significant nocturnal oxygen desaturation (ST-90%>1%) was 0.865±0.036 (95% IC, 0.793-0.937; p<0.0001). CANO at 4.5 ppb could detect these patients with specificity of 94% and sensitivity of 46%. Increase of CANO measured after PSG was significantly related to oxygen desaturation index (ST-90%) in OSA patients. Increased alveolar NO concentration was related to the severity of nocturnal oxygen desaturation in patients with OSA, linking the distal airway inflammation to intermittent hypoxia. (250 words). Copyright © 2015. Published by Elsevier Inc.
    Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society. 01/2015;