Abstract
Introduction
Obstructive sleep apnea (OSA) is prevalent and carries prognostic implication in patients with acute coronary syndrome (ACS). The relative contribution of pathophysiological mechanisms in ACS towards OSA is not well-studied. We examined the correlation between severity of OSA and myocardial necrosis, inflammation, wall stress, and fibrosis.
Methods
A total of 89 patients admitted with ACS underwent an overnight sleep study during index admission. Plasma levels of peak troponin I, high-sensitivity C-reactive protein (hs-CRP), N-terminal pro-brain natriuretic peptide (NT-proBNP), and suppression of tumorigenicity 2 (ST2) were prospectively analyzed. Two patients diagnosed with central sleep apnea were excluded.
Results
The recruited patients were divided into no (AHI <5 events/hour, 9.2%), mild (5-<15, 27.6%), moderate (15-<30, 21.8%), and severe (≥30, 41.4%) OSA. The respective Epworth Sleepiness Scale scores were 3.8±3.7, 5.3±4.9, 4.0±2.8, and 5.5±4.5 (p=0.734). Compared to the no, mild and moderate OSA groups, the severe OSA group had a higher body mass index (p=0.005). They were also more likely to present with ST-segment elevation ACS (vs non-ST-segment elevation ACS) (p=0.041), have undergone previous coronary artery bypass grafting (p=0.013), demonstrate complete coronary occlusion during baseline coronary angiography (p=0.049), and have a larger left atrium diameter measured on echocardiography (p=0.029). Likewise, the severe OSA group had higher plasma levels of troponin I (10584±13078, 11699±20130, 19280±30670, 37571±31269 µg/L; p=0.017), hs-CRP (8.1±9.2, 23.1±52.3, 9.3±17.1, 39.4±44.7 mg/L; p=0.004), and NT-proBNP (667±604, 765±856, 636±728, 1395±1220 pg/mL; p=0.004), but not ST2 (p=0.10). After adjusting for the effects of the confounding variables, severe OSA was independently associated with troponin I (i.e., myocardial necrosis; OR 1.00003, 95% CI 1.000013-1.000048; p=0.001) and NT-proBNP (i.e., myocardial wall stress; OR 1.00081, 95% CI 1.00021-1.00141; p=0.008).
Conclusion
Severe OSA during the acute phase of ACS was associated with extensive myocardial necrosis and myocardial wall stress, but not with inflammation and myocardial fibrosis.
Support
Nil