Obstructive sleep apnoea (OSA) is a highly prevalent disease and associated with the development of various cardiovascular diseases which represents a significant public health burden. OSA comprises various pathophysiological triggers for cardiovascular diseases, which include sleep fragmentation, intrathoracic pressure swings and recurrent hypercapnia. However, there is now strong evidence that the unique form of intermittent hypoxia (IH) observed in OSA, with repetitive short cycles of desaturation followed by rapid reoxygenation, plays a pivotal role in the development of cardiovascular co-morbidities. The pathogenesis is likely multifactorial and our current concept involves sympathetic nervous system overactivity, systemic inflammation and oxidative stress leading to endothelial dysfunction, and possibly metabolic dysfunction as the most important pathways.Inflammatory processes are central in this pathogenesis and there is ample evidence – arising from both cell culture and in vivo models – that IH preferentially activates the transcription factor nuclear factor-kappa B (NF-κB). NF-κB is a key player in inflammatory and innate immune responses and when chronically activated contributes to atherosclerosis through driving production of inflammatory mediators such as tumour necrosis factor alpha (TNF-α), interleukin (IL)- 8 and IL-6 and these mediators have been found to be upregulated in OSA patients. OSA and obesity are closely linked and there is increasing evidence that white adipose tissue is a potent source organ of inflammatory mediators in OSA. A greater understanding of the basic mechanisms of cardiovascular complications in OSA should lead to the identification of therapeutic targets and therefore, further translational studies involving cell, animal and human models are strongly required.