Stroke alert: sleep disordered breathing predicts survival?

Stoke is a very widespread disease, a leading cause of death, and generates high healthcare costs due to causing considerable disability. The aetiology and outcomes of stroke are various. Ischemic stroke dominates and differs pathogeneti-cally from haemorrhagic stroke, the latter having a poorer prognosis. Several modifiable risk factors, including hyper-tension, diabetes, hyperlipidemia, smoking, and arterial fibri-llation, have been defined in stroke. However, these traditional risk factors do not fully explain the occurrence of stroke and new risk factors including inflammatory markers, infection and homocysteine have been proposed [1]. Other data have identified sleep disordered breathing (SDB) as a potential risk factor. SDB is a common condition affecting 10–20% of the adult population and an even higher incidence has been reported in the elderly. Obstructive sleep apnoea (OSA) is by far the most common type of SDB, whereas central SDB, such as Cheyne-Stokes respiration, is more frequent in patients suffering from acute stroke and cardiac failure. There is ongoing debate on the causal role of SDB in vascular disease. Several epidemiological studies identified an association between SDB and ischemic heart disease and stroke, but the causality remained unresolved. Recent data on the incidence of fatal and nonfatal cardiovascular events clearly suggest that coexisting SDB increased event rate [2, 3]. The risk impact varies between studies but is generally low-to-moderate. However, the high prevalence of SDB implied that even a minor risk increase may have considerable implications for public health. The epidemiological data contrasts with results from pathophy-siological case control studies mainly performed in OSA patients. These studies suggest a far stronger link between SDB and vascular disease. OSA has a profound cardio-vascular impact by increased sympathetic activity, reduced vascular endothelial function, neuro-endocrine activation, and as a trigger of systemic vascular inflammation. The resulting haemodynamic instability and recurrent nocturnal oxygenation/re-oxygenation have been proposed as the main trigger mechanisms for vascular and cardiac stress during sleep. Other studies have demonstrated that elimination of OSA by nasal continuous positive airway pressure (CPAP) normalised vascular or cardiac dysfunction, hypercoaguable state, oxygen radical release and inflammatory cell activation. However, it should be kept in mind that far from all SDB/ OSA patients appear to develop a manifest cardiovascular disease even after years of apnoeic events. It is therefore likely that yet unidentified compensatory mechanisms of genetic/ environmental origin play an important role for susceptibility of vascular disease in SDB patients. Patients with manifest cerebrovascular disease (ischaemic …