Send to

Choose Destination
Sleep Breath. 2014 May;18(2):351-8. doi: 10.1007/s11325-013-0892-6. Epub 2013 Sep 17.

Obstructive sleep apnea: no independent association to troponins.

Author information

Department of Cardiology, Lovisenberg Diakonale Hospital, 0440, Oslo, Norway,



Cardiac troponins (cTn) are to date the most sensitive and specific biochemical markers of myocardial injury. Abnormal breathing patterns in patients with obstructive sleep apnea (OSA) may cause myocardial cell stress detectable by novel cTn assays. The objectives of this study were to investigate whether a new single-molecule cTnI (S-cTnI) assay and a commercially available high-sensitivity cTnT (hs-cTnT) assay would detect myocyte injury in individuals evaluated for possible OSA, and to explore their relation to variables of disordered breathing during sleep.


Consecutive individuals referred to Lovisenberg Diakonale Hospital's sleep laboratory between 1 October 2009 and 1 March 2010 were included. We measured cTn in specimens collected the morning after sleep and studied these in relation to variables recorded during polygraphy or polysomnography.


All 222 (100 %) individuals had measurable cTn levels using either assay. Stratified into categories according to the apnea-hypopnea index (AHI), patients with OSA (AHI ≥5) had a different distribution of S-cTnI (P = 0.036) and hs-cTnT (P = 0.002) compared to those without (AHI <5). The median (quartiles 1-3) were 3.0 (1.9-6.0) versus 2.3 (1.6-3.8) ng/l for S-cTnI, and 7.0 (5.5-8.7) versus 6.2 (4.9-7.2) ng/l for hs-cTnT. However, in multiple median regression analyses adjusted for conventional predictors, neither S-cTnI (P = 0.57) nor hs-cTnT (P = 0.80) were significantly associated with AHI.


This study reveals no association independent of conventional predictors between OSA and myocardial cell injury measured by S-cTnI and hs-cTnT assays. Our findings support a search for novel biomarkers for prognostication of OSA.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center