Does OSA Upregulate Cardioprotective Pathways to an Ischemic Insult?

[摘要] Figures Figure 1 The clinical consequences of intermittent hypoxia (IH) are determined by a complex interaction between multiple factors, including the extent of the maladaptive and adaptive responses to IH as well as the individual patient susceptibility to the deleterious effects of IH and the specific organ or vascular bed. CAD = coronary artery disease; EPCs = endothelial progenitor cells; HIF-1α = hypoxia-inducible factor-1α; HSPs = heat shock proteins; LVH = left ventricular hypertrophy; VEGF = vascular endothelial growth factor. The literature regarding intermittent hypoxia (IH) and OSA is undergoing a sea change. For many years, the prevailing paradigm was that IH uniformly exerts deleterious cardiovascular effects that initiate or accelerate the progression of cardiovascular conditions (eg, stroke, myocardial infarction, and sudden cardiac death).¹ More recently, it has become increasingly evident that IH can elicit a multitude of adaptive cardiovascular pathways, collectively termed preconditioning.^2,3 This refers to the resistance or tolerance conferred by potentially deleterious stimuli applied repeatedly in a sequential order near or below the threshold of damage (or both), preventing or reducing injury to the organism with prolonged or more severe exposure (or both) to the same noxious stimuli.

[学科分类] 呼吸医学