Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities: Fig. 1—

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.

Inflammation contributes to the atherogenic role of intermittent hypoxia in apolipoprotein-E knock out mice

“…carotid artery intima-media thickening, carotid plaques and arterial stiffness) that are independent of other cardiovascular or metabolic risk factors 4,5 , and are reversible in some patients by continuous positive airway pressure (CPAP) therapy 6 . OSA is a clinical situation with dyslipidemia 7 , hypertension 8 and systemic inflammation 9 which are in part imputable to the main component of OSA, i.e. intermittent hypoxia (IH).…”

“…intermittent hypoxia (IH). These several OSA-consequences could promote cardiac and vascular disease such as atherosclerosis 2,8 . However, their respective contribution is unknown.…”

Impact of obstructive sleep apnoea on diastolic function

“…In recent years, intensive research has revealed multiple negative consequences of obstructive sleep apnoea (OSA) on the cardiovascular system [8,9]. The pathophysiological interaction between OSA and cardiovascular disease is complex and comprises sympathetic activation, inflammation, oxidative stress, endothelial dysfunction and clock gene dysfunction [9][10][11].…”

Bone mineral density in patients with obstructive sleep apnea syndrome

“…All these intermediate mechanisms may help to explain the contribution of OSAS to several diseases, including hypertension, stroke, diabetes, and cardiac arrhythmias and the increased mortality associated with the disease [3][4][5][6]. Cardiovascular morbidity and mortality associated with sleep apnea have been extensively studied in the last decade [4,7,8]. Furthermore, several former and recent studies have indicated strong association between cardiovascular diseases and osteoporosis [9][10][11][12][13], with the above intermediate mechanisms of OSAS to have a critical role in the common pathophysiological pathway of both diseases.…”