Wang, Shihan

Background Obstructive sleep apnea ( OSA ) is an important risk factor for the development of cardiovascular diseases including myocardial infarction ( MI ). The aim of this study was to investigate the effects of OSA on prognosis after MI , and to determine which specific measures of OSA severity best predicted outcomes. Methods and Results We performed a prospective study, in which 112 patients without a prior diagnosis of sleep apnea underwent comprehensive polysomnography within a median of 7 days after MI . Patients were followed up at 6‐monthly intervals (±2 weeks) for a total of 48 months. Patients classified with central apnea (n=6) or those using continuous positive airway pressure (n=8) after polysomnography were excluded from analyses. The primary end point was major adverse cardiac events, including death from any cause, recurrent MI , unstable angina, heart failure, stroke, and significant arrhythmic events. Forty of 98 patients (41%) had OSA (apnea‐hypopnea index ≥15 events/h). OSA patients had higher major adverse cardiac event rates when compared to those without OSA (47.5% versus 24.1%; χ 2 =5.41, P =0.020). In a multivariate model that adjusted for clinically relevant variables including age, left ventricular ejection fraction, diabetes mellitus, oxygen desaturation index, and arousal index, significant hypoxemia, as defined by nocturnal nadir oxygen saturation ≤85%, was an independent risk factor for major adverse cardiac events (hazard ratio=6.05, P =0.004) in follow‐up 15 months after baseline. Conclusions Nocturnal hypoxemia in OSA is an important predictor of poor prognosis for patients after MI . These findings suggest that routine use of low‐cost nocturnal oximetry may be an economical and practical approach to stratify risk in post‐ MI patients.

Obstructive and central sleep apnea have been associated with increased risk of adverse cardiovascular events and mortality. Sympathetic dysregulation occurring as a result of the respiratory disturbance is thought to play a role in this increased risk. Sleep apnea increases the risk of arrhythmias, myocardial ischemia/infarction, stroke, and heart failure, all of which may increase mortality risk. A higher incidence of nocturnal arrhythmias, cardiac ischemia, and sudden death has been noted in subjects with sleep-disordered breathing (SDB). In this review, the association between SDB and each of these conditions is discussed, as well as the potential mechanisms underlying these risks and the effects of treatment of SDB. Particular emphasis is placed on the relationship between SDB and nocturnal atrial and ventricular arrhythmias, myocardial ischemia/infarction and sudden death.

New Findings What is the topic of this review? This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex‐mediated pathophysiology in obstructive and central sleep apnoea. What advances does it highlight? Chemoreflex mechanisms are thought to contribute significantly to the pathophysiology and adverse outcomes seen in sleep apnoea. Clinical implications of altered chemoreflex function in sleep apnoea from recent studies in humans, including cardiac arrhythmias, coronary artery disease, systolic/diastolic heart failure and sudden cardiac death are highlighted. Activation of the chemoreflex in response to hypoxaemia results in an increase in sympathetic neural outflow. This process is predominantly mediated by the peripheral chemoreceptors in the carotid bodies and is potentiated by the absence of the sympatho‐inhibitory influence of ventilation during apnoea, as is seen in patients with sleep apnoea. In these patients, repetitive nocturnal hypoxaemia and apnoea elicit sympathetic activation, which may persist into wakefulness and is thought to contribute to the development of systemic hypertension and cardiac and vascular dysfunction. Chemoreflex activation could possibly lead to adverse cardiovascular outcomes, such as nocturnal myocardial infarction, systolic and/or diastolic heart failure, cardiac arrhythmias and sudden death in patients with sleep apnoea. This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex‐mediated pathophysiology in obstructive and central sleep apnoea. Measurement of the chemoreflex response may serve as a potential avenue for individualized screening for cardiovascular disease. Whether modulation of this response in sleep apnoea may aid in the prevention and treatment of adverse cardiovascular consequences will require further study.