Chitra Lal and Charlie Strange
The significant adverse sequelae of Obstructive Sleep Apnea Syndrome (OSAS) include a higher incidence of stroke, myocardial infarction and neurocognitive deficits. A link between the intermittent hypoxia of OSAS and endothelial dysfunction may explain many of the macrovascular and microvascular complications of OSAS. The pathogenesis of endothelial dysfunction involves an alteration in the levels of pro-inflammatory and pro-atherogenic mediators. As a form of ischemia/reperfusion injury to the endothelium, intermittent hypoxia induces reactive oxygen species and dysregulatesbolites including pathways of nitric oxide synthesis. In addition, hypercoagulability and altered leucocyte migration contribute to the sp vasoactive metaectrum of endothelial dysfunction. The tools for measurement of endothelial dysfunction and its clinical implications are discussed. Endothelial dysfunction can be in part reversed with continuous positive airway pressure. Thus, early recognition and aggressive treatment of OSAS may prevent associated endothelial dysfunction and subsequent complications of this syndrome.
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