Showing papers by "Peretz Lavie published in 2006"

Sleep medicine--time for a change.

Abstract: The growing awareness of obstructive sleep apnea and its profound impact on patients' quality of life and health has resulted in an unprecedented growth in sleep medicine in the last 2 decades. The present paper argues that, based on recently accumulated knowledge about the pathophysiology of cardiovascular morbidity in sleep apnea, the practice of sleep medicine must be changed in order to improve patients' care. The diagnosis of sleep apnea should be performed when patients are aged 25 to 30 years, far younger than the approximately 50 years of age, which is when most patients usually receive a diagnosis now, and programs of regular follow-up visits to assess patients' condition and compliance with treatment should be incorporated into the everyday practice of sleep specialists. Because of the wide gap between the number of sleep specialists and sleep clinics and the prevalence of sleep apnea in the general population, an alliance between sleep medicine and family practitioners is necessary to ensure such changes. A proposal for such an alliance is presented.

Oxidative Stress – The Culprit of Obstructive Sleep Apnea Syndrome

Abstract: Obstructive sleep apnea, characterized by intermittent and recurrent pauses in respiration during sleep resulting in a decreased oxygen saturation and sleep fragmentation, is closely associated with cardiovascular morbidity.There is accumulated evidence that hypoxia/reoxygenation, such that is characteristic of sleep apnea, promotes the formation of reactive oxygen species that activate critical redox-sensitive signaling pathways and transcription factors.This facilitates the expression of sets of genes that encode proteins essential to adaptation to hypoxia, as well those that elicit inflammatory pathways such as adhesion molecules and inflammatory cytokines. Consequently, inflammatory and immune responses are aggravated, thus resulting in the activation of endothelial cells/leukocytes/platelets. These activated cells express adhesion molecules and proinflammatory cytokines that in turn may further exacerbate inflammatory responses and cause endothelial cell injury and dysfunction.These may lead to the development of cardio- and cerebrovascular morbidities in sleep apnea. Evidence supporting the existence of endothelial dysfunction and early clinical signs of atherosclerosis in patients with sleep apnea provides firm support to the above chain of events.This newly acquired insight into the pathophysiology of cardiovascular morbidity in OSA has important implications regarding the diagnosis and treatment of the syndrome.