Background: Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular complications. OSA and coronary artery disease (CAD) share the same risk factors and coexist in many patients. In previous studies, repeated nocturnal cardiac ischemic events in OSA patients with CAD have been reported. Hypothesis: We hypothesized that OSA may precipitate myocardial ischemia, evidenced by ST-segment depression and elevated N-terminal brain natriuretic peptide (NT-proBNP) and high-sensitivity troponin T (hs-TropT) levels in patients with severe OSA and concomitant CAD. We also aimed to evaluate if the effects could be reversed by continuous positive airway pressure (CPAP) therapy. Methods: Twenty-one patients with severe OSA (apnea-hypopnea index >15/h, nadir oxygen desaturation ≤80%), and coexisting CAD underwent in-hospital polysomnography at baseline and under CPAP. Blood samples for hs-TropT and NT-proBNP measurements were drawn prior and immediately after sleep. ST-segment depression was measured at the time of maximum oxygen desaturation during sleep. Results: CPAP significantly decreased elevated NT-proBNP levels from 475 ± 654 pg/mL before sleep to 353 ± 573 pg/mL after sleep and attenuated ST-segment depression during sleep. hs-TropT was not elevated and did not differ after nocturnal oxygen desaturation at baseline and after CPAP. Conclusions: CPAP significantly reduced NT-proBNP in patients suffering from severe OSA and coexisting CAD. Repeated nocturnal myocardial ischemia did not cause myocyte necrosis evidenced by elevated hs-TropT or ST-segment depression.

Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia during sleep. We tested the hypothesis that nocturnal myocardial ischemia is detectable by ST segment depression and elevation of high sensitive troponin T (hsTrop T) and B-type natriuretic peptide (NT-proBNP) in patients with OSA and coexisting coronary artery disease (CAD). Twenty-one patients with OSA and CAD and 20 patients with OSA alone underwent in-hospital polysomnography. Blood samples for hsTrop T and NT-proBNP measurements were drawn before and after sleep. ST segment depression was measured at the time of maximum oxygen desaturation during sleep. The apnea-hypopnea-index (AHI), oxygen saturation nadir, and time in bed with oxygen saturation of ≤80% were similar in both groups. Levels of hsTrop T and NT-proBNP did not differ significantly before and after sleep but NT-proBNP levels were significantly higher in patients suffering from OSA and CAD compared to patients with OSA alone. No significant ST depression was found at the time of oxygen saturation nadir in either group. Despite the fact that patients with untreated OSA and coexisting CAD experienced severe nocturnal hypoxemia, we were unable to detect myocardial ischemia or myocyte necrosis based on significant ST segment depression or elevation of hsTrop T and NT-proBNP, respectively.

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