Original ArticleThe influence of timing of polysomnography on diagnosis of obstructive sleep apnea in patients presenting with acute myocardial infarction and stable coronary artery disease
Introduction
Obstructive sleep apnea (OSA) is characterized by recurrent upper airway collapse and intermittent apnea or hypopnea episodes during sleep. Apart from causing disruptive snoring and excessive daytime somnolence, there is evidence that OSA is associated with adverse effects on cardiovascular physiology [1], [2], [3]. Epidemiologic studies have shown that the prevalence of OSA was significantly higher in patients with cardiovascular disease than in the general population [4], [5] and that untreated OSA leads to untoward cardiovascular events [6], [7], [8]. The results from these studies highlight the importance of diagnosing concomitant OSA in patients presenting with cardiovascular disease [9].
Overnight polysomnography (PSG) is a simple and noninvasive investigation for diagnosing OSA. However, the optimal time to perform PSG for patients admitted with coronary heart disease has not been well-defined. There have been a few studies describing how PSG performed at different times seemed to have affected the results. In a study of 18 patients admitted to the coronary care unit for a variety of cardiac conditions, the prevalence of OSA reduced from 56% during the acute phase to 18% at 6-week follow-up [10]. Likewise, in 28 patients presenting with acute coronary syndrome and diagnosed with OSA during hospitalization, repeat PSG at 6-month follow-up showed resolution of OSA in most patients [11]. This finding suggests that the timing of PSG may influence the diagnosis of OSA. However, these studies were too small to be conclusive, and the lower prevalence of OSA at the repeat PSG could be due to measures taken by the patients when receiving the diagnosis after the first PSG. Moreover, the small sample size precluded analysis based on different clinical presentations.
Determining the optimal timing of PSG in patients is crucial in correctly identifying patients with OSA, and therefore optimizing resource allocation. In our study, we sought to determine if the timing of PSG affected the diagnosis of OSA. We also evaluated if the relationship differed for patients presenting with acute myocardial infarction (AMI) vs stable coronary artery disease (CAD).
Section snippets
Study design and patient population
Our study was a single-center study conducted at a university-affiliated hospital. We prospectively recruited 160 consecutive patients who had undergone coronary angiography and intervention for either AMI (n = 80) or stable CAD (n = 80). Recruited patients were scheduled to undergo a PSG during in-hospital or postdischarge period in a 1:1 ratio. We first recruited 80 consecutive patients (AMI [n = 40]; stable CAD [n = 40]) in a parallel manner for in-hospital PSG, followed by recruiting another 80
Study profile and patient characteristics
The study profile is shown in Fig. 1. A total of 160 consecutive patients presenting with coronary heart disease were recruited and scheduled to undergo in-hospital (n = 80) or postdischarge (n = 80) PSG. The demographic and clinical characteristics of the patients are shown in Table 1 stratified by timing of sleep study. Most of the patients were men. The ethnic composition of the recruited patients was consistent with the overall ethnic composition of Singapore.
All of the PSG studies were
Discussion
We studied the influence of the timing of PSG on the diagnosis of OSA in 160 consecutive patients admitted with coronary heart disease. The overall prevalence of OSA was 37%, and patients diagnosed with OSA were more likely to have the PSG done during the in-hospital period. The most important finding of our study was that PSG conducted during the in-hospital period was an independent predictor of OSA in patients presenting with AMI but not in those with stable CAD. This difference remained
Conclusion
Our study indicated that the conduction of PSG at different timings post-AMI affects the diagnosis of OSA; however, it does not affect the diagnosis of OSA in patients presenting with stable CAD. Our findings suggest that OSA in the acute phase of AMI may be a transient phenomenon related to myocardial stunning. Further studies to investigate the complex relationships between the evolution of myocardial dysfunction post-AMI and OSA are warranted.
Funding sources
Our study was funded by the Clinician Scientist Program, National University Health System, Singapore (Grant No.: R172-000-239-112). Dr. Thet Hein was supported by funding from the Cardiovascular Research Institute, National University of Singapore.
Conflict of interest
The ICMJE Uniform Disclosure Form for Potential Conflicts of Interest associated with this article can be viewed by clicking on the following link: http://dx.doi.org/10.1016/j.sleep.2013.03.025.
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