Obstructive sleep apnea during acute coronary syndrome is related to myocardial necrosis and wall stress

The relative contribution of pathophysiological mechanisms in acute coronary syndrome (ACS) towards obstructive sleep apnea (OSA) is not well-studied. We examined the correlation between severity of OSA and inflammation, myocardial necrosis, wall stress, and fibrosis.

A total of 89 patients admitted with ACS underwent a sleep study during index admission. Plasma levels of high-sensitivity C-reactive protein (hs-CRP), troponin I, 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.

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. 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 (versus 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 atrial diameter measured on echocardiography (p = 0.029). Likewise, the severe OSA group had higher plasma levels of hs-CRP (p = 0.004), troponin I (p = 0.017), and NT-proBNP (p = 0.004), but not ST2 (p = 0.10). After adjustment for the effects of confounding variables, OSA was independently associated with troponin I (ie, myocardial necrosis; p = 0.001) and NT-proBNP (ie, myocardial wall stress; p = 0.008).

Severe OSA during the acute phase of ACS was associated with extensive myocardial necrosis and high myocardial wall stress, but not with inflammation and myocardial fibrosis.