Floras John S
University Health Network and Mount Sinai Hospital Division of Cardiology, Canada; Faculty of Medicine, University of Toronto, Canada.
J Cardiol. 2014 Jan;63(1):3-8. doi: 10.1016/j.jjcc.2013.08.009. Epub 2013 Sep 29.
Sleep apnea is evident in approximately 10% of adults in the general population, but in certain cardiovascular diseases, and in particular those characterized by sodium and water retention, its prevalence can exceed 50%. Although sleep apnea is not as yet integrated into formal cardiovascular risk assessment algorithms, there is increasing awareness of its importance in the causation or promotion of hypertension, coronary artery disease, heart failure, atrial arrhythmias, and stroke, and thus, not surprisingly, as a predictor of premature cardiovascular death. Sleep apnea manifests as two principal phenotypes, both characterized by respiratory instability: obstructive (OSA), which arises when sleep-related withdrawal of respiratory drive to the upper airway dilator muscles is superimposed upon a narrow and highly compliant airway predisposed to collapse, and central (CSA), which occurs when the partial pressure of arterial carbon dioxide falls below the apnea threshold, resulting in withdrawal of central drive to respiratory muscles. The present objectives are to: (1) review the epidemiology and patho-physiology of OSA and CSA, with particular emphasis on the role of renal sodium retention in initiating and promoting these processes, and on population studies that reveal the long-term consequences of untreated OSA and CSA; (2) illustrate mechanical, autonomic, chemical, and inflammatory mechanisms by which OSA and CSA can increase cardiovascular risk and event rates by initiating or promoting hypertension, atherosclerosis, coronary artery disease, heart failure, arrhythmias, and stroke; (3) highlight insights from randomized trials in which treating sleep apnea was the specific target of therapy; (4) emphasize the present lack of evidence that treating sleep apnea reduces cardiovascular risk and the current clinical equipoise concerning treatment of asymptomatic patients with sleep apnea; and (5) consider clinical implications and future directions of clinical research and practice.
在普通人群中，约10%的成年人存在明显的睡眠呼吸暂停，但在某些心血管疾病中，尤其是那些以钠水潴留为特征的疾病，其患病率可超过50%。尽管睡眠呼吸暂停尚未被纳入正式的心血管风险评估算法，但人们越来越意识到它在高血压、冠状动脉疾病、心力衰竭、房性心律失常和中风的病因或发展过程中的重要性，因此，毫不奇怪，它可作为心血管过早死亡的预测指标。睡眠呼吸暂停表现为两种主要类型，均以呼吸不稳定为特征：阻塞性（OSA），当睡眠相关的对上气道扩张肌的呼吸驱动力减弱叠加在易于塌陷的狭窄且顺应性高的气道上时发生；中枢性（CSA），当动脉血二氧化碳分压降至呼吸暂停阈值以下时发生，导致中枢对呼吸肌的驱动减弱。当前的目标是：（1）回顾阻塞性睡眠呼吸暂停和中枢性睡眠呼吸暂停的流行病学和病理生理学，特别强调肾钠潴留在启动和促进这些过程中的作用，以及揭示未经治疗的阻塞性睡眠呼吸暂停和中枢性睡眠呼吸暂停长期后果的人群研究；（2）阐述阻塞性睡眠呼吸暂停和中枢性睡眠呼吸暂停通过启动或促进高血压、动脉粥样硬化、冠状动脉疾病、心力衰竭、心律失常和中风来增加心血管风险和事件发生率的机械、自主神经、化学和炎症机制；（3）强调以治疗睡眠呼吸暂停为特定治疗目标的随机试验的见解；（4）强调目前缺乏治疗睡眠呼吸暂停可降低心血管风险的证据，以及目前关于无症状睡眠呼吸暂停患者治疗的临床平衡；（5）考虑临床意义以及临床研究和实践的未来方向。
