Cardiovascular disease: pathophysiological mechanisms

OSA is a common disease that affects approximately 10% of the middle-aged population and becomes more prevalent with age. It is caused by intermittent and repetitive collapse of the UA during sleep. The main acute physiological consequences of OSA are oxygen desaturation, intrathoracic pressure changes and arousals. OSA is associated with significant cardiovascular morbidity and mortality and is an independent risk factor for CVD. The pathogenesis of CVD in OSA is not completely understood but is likely to be multifactorial, involving a diverse range of closely interrelated and detrimental intermediate mechanisms that predispose patients to atherosclerosis, including oxidative stress, sympathetic activation, inflammation, hypercoagulability, endothelial dysfunction and metabolic dysregulation. IH is considered to lead to increased oxidative stress, systemic inflammation and sympathetic stimulation. Despite the existence of these detrimental mechanisms, there are epidemiological studies that suggest that some protective mechanisms could also be activated in OSA patients. This chapter describes the underlying mechanisms linking OSA with CVD.