Impact of Obstructive Sleep Apnea on Cardiac Troponin I: Comparisons of the Effects of Nasal O2 and Positive Airway Pressure on this Biomarker

Sleep apnea is a common disorder and is known to impact myocardial stress and increase morbidity and mortality. The concentrations of cardiac highly sensitive troponin I (hs-TnI) are currently in clinical use as markers of myocardial injury. That obstructive sleep apnea (OSA) may lead to myocardial injury and elevated cardiac troponin levels suggests that the treatment of sleep apnea with positive airway pressure (PAP) should decrease myocardial injury. We studied 114 patients with a diagnosis of moderate-to-severe OSA who were referred to our cardiovascular department. None of the patients had a history of cardiovascular problems and diabetes. The mean age was 30.653.96 years. The patients were divided into 2 groups: the first group (the O2 group) received nasal O2 for 2 weeks, and the second group (the PAP group) received PAP for about 2 weeks. The concentrations of hs-TnI were measured in evening blood samples in ed patients. After 2 weeks of treatment with O2 or PAP, the serum hs-TnI level was rechecked and compared with the baseline and between the 2 groups. The level of hs-TnI did not differ significantly between the 2 groups. No patients in either O2 or PAP group showed elevated troponin levels before the treatment. The cardiac biomarker, hs- TnI, was detectable (≥1 ng/L) in none of the patients in the O2 group before and after the treatment and only in 2 (3%) patients in the PAP group after treatment. There was no significant difference in the hs-TnI level before and after the treatment with nasal O2 (P=0.4). Although OSA is well known to impact myocardial stress, we did not find increased amounts of cardiac hs-TnI as a biomarker of myocardial damage even in the severe form of OSA. PAP did not cause any myocardial damage detectable with the hs-TnI level and it was somewhat more effective than was O2 in decreasing the baseline level of troponin.