Pack Allan I, Gislason Thorarinn
Center for Sleep and Respiratory Neurobiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-3403, USA.
Prog Cardiovasc Dis. 2009 Mar-Apr;51(5):434-51. doi: 10.1016/j.pcad.2009.01.002.
Data from animal and human studies provide a biological plausibility to the notion that obstructive sleep apnea activates pathways that lead to insulin resistance, atherosclerosis and hypertension. Sleep apnea thus activates the same pathways as does obesity. That obstructive sleep apnea is a risk factor for cardiovascular disease is supported by epidemiological association studies. Longitudinal cohort studies also provide evidence that patients with untreated severe sleep apnea have an increased rate of cardiovascular events. But these studies, while highly suggestive, do not provide the evidence needed to convince the skeptic. This would only be obtained by randomized treatment trials with hard cardiovascular endpoints such as cardiac events and deaths. While such studies are in the planning stages, they will be challenging. There are issues about randomizing individuals with severe sleep apnea and excessive sleepiness into no therapy, since they are at known increased risk for car crashes. Thus, lack of therapy puts others on the road at risk as well as the subject with sleep apnea. There is, moreover, the concern that treating obstructive sleep apnea in very obese individuals will have little impact, since any effect of therapy for OSA will be overwhelmed by the effects of obesity itself. Data from randomized treatment trials for cardiovascular endpoints will likely not be available for many years. In the interim, physicians need to consider how to treat such patients. It is proposed that given that CPAP treatment for obstructive sleep apnea is highly effective and essentially totally safe, and that the evidence is suggestive that sleep apnea is a risk factor for cardiovascular disease, then we propose all patients with severe sleep apnea should be treated to reduce cardiovascular risk.
来自动物和人体研究的数据为阻塞性睡眠呼吸暂停激活导致胰岛素抵抗、动脉粥样硬化和高血压的通路这一观点提供了生物学合理性。因此，睡眠呼吸暂停与肥胖一样激活相同的通路。阻塞性睡眠呼吸暂停是心血管疾病的危险因素这一观点得到了流行病学关联研究的支持。纵向队列研究也提供了证据，表明未经治疗的严重睡眠呼吸暂停患者心血管事件发生率增加。但这些研究虽然极具启发性，却没有提供足以说服怀疑者的证据。只有通过以心脏事件和死亡等硬性心血管终点进行的随机治疗试验才能获得此类证据。虽然此类研究正处于规划阶段，但它们将具有挑战性。将患有严重睡眠呼吸暂停和过度嗜睡的个体随机分为不接受治疗组存在问题，因为他们已知发生车祸的风险增加。因此，不进行治疗不仅会使睡眠呼吸暂停患者自身处于危险之中，也会使其他道路使用者面临风险。此外，还有人担心在非常肥胖的个体中治疗阻塞性睡眠呼吸暂停效果甚微，因为肥胖本身的影响会掩盖阻塞性睡眠呼吸暂停治疗的任何效果。关于心血管终点的随机治疗试验数据可能在许多年内都无法获得。在此期间，医生需要考虑如何治疗此类患者。鉴于阻塞性睡眠呼吸暂停的持续气道正压通气（CPAP）治疗非常有效且基本完全安全，并且有证据表明睡眠呼吸暂停是心血管疾病的危险因素，我们建议所有严重睡眠呼吸暂停患者都应接受治疗以降低心血管风险。
