It Happened While You Were Sleeping

P redicting shortand long-term risk for adverse outcomes after an acute coronary syndrome (ACS; STsegment elevation myocardial infarction, non–ST-segment elevation myocardial infarction, and unstable angina) has been the focus of numerous modeling efforts over many years. Nevertheless, risk models can reflect only the variables that were systematically available in the population databases used to derive the models. The most widely used models for risk stratification of ACS patients in clinical practice today are limited to a handful of clinical and laboratory data routinely available in the context of clinical care. As we enter the “big data era,” the numbers, types, and availability and novelty of descriptive variables for any given population will expand rapidly through multiple sources (eg, electronic health records, social media, geospatial information systems, and continuous monitoring via wearable devices). As new bioinformatics and analysis methods evolve to integrate this increasing volume and variety of data, the potential exists to inform the components of risk models in both expected and unexpected ways and, perhaps, to suggest new targets for intervention to mitigate risk. The pathophysiology of sleep disturbances and the importance of information gathered while we are sleeping are dimensions of cardiovascular risk that have been explored but not fully appreciated or integrated into risk assessment previously. In this issue of the Journal of the American Heart Association, Mazaki and colleagues expanded what is known of the relationship between sleep-disordered breathing and adverse cardiovascular outcomes to long-term follow-up (median 5.6 yr) of patients with ACS. Among 257 consecutive post-ACS patients who were treated with percutaneous coronary intervention at a single center in Japan, 241 had full data from an overnight sleep study conducted within 1 week of the index ACS event. Interestingly, more than half (52%) of this population had sleep-disordered breathing (defined as an apnea–hypopnea index of ≥5 events per hour of apnea [at least 10 seconds] or oxygen desaturation [at least 4%]). Using this definition, sleep-disordered breathing was associated with a significant increase in death, recurrence of ACS, nonfatal stroke, and hospital admission for congestive heart failure in multivariable modeling (hazard ratio 2.28, 95% CI 1.06–4.92). Despite the limited number of events available for modeling, these observations were consistent using a number of statistical approaches and sensitivity analyses, including multivariable modeling in a propensity score–matched cohort and incorporating the apnea–hypopnea index as a continuous variable. Because sleep-disordered breathing is potentially treatable, and given the high prevalence of sleep-disordered breathing observed among ACS patients, the findings of the study by Mizaki et al are not simply of academic interest. In this regard, however, their study did not distinguish obstructive sleep apnea from central sleep apnea, which may have different relationships with outcomes and necessitate different modes of treatment. Furthermore, the presence of clinical heart failure was not reported, but the mean left ventricular ejection fraction in the group with sleep-disordered breathing was 53 10%. Consequently, although the majority of patients had a normal left ventricular ejection fraction, 15% to 20% of patients had a left ventricular ejection fraction ≤45%; treatment with continuous positive airway pressure has not been shown to be effective in this group, and adaptive servoventilation may be harmful. In the Treatment of Sleep Disordered Breathing with Predominant Central Sleep Apnea by Adaptive Servo Ventilation in Patients with Heart Failure (SERVE-HF) trial, compared with no treatment, the use of adaptive servoventilation resulted in an increase in all-cause mortality (hazard ratio 1.28, 95% CI 1.06–1.55) and cardiovascular mortality (hazard ratio 1.34, 95% CI 1.09–1.65) among symptomatic patients with chronic heart failure (left The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Division of Cardiology, Department of Medicine and Duke Clinical Research Institute, Duke University Medical Center, Durham, NC. Correspondence to: L. Kristin Newby, MD, MHS, P.O. Box 17969, Durham, NC 27715-7969. E-mail: [email protected] J Am Heart Assoc. 2016;5:e003748 doi: 10.1161/JAHA.116.003748. a 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.