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Obstructive sleep apnea: no independent association to troponins

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Abstract

Background

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.

Methods

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.

Results

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.

Conclusions

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.

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Abbreviations

AHI:

Apnea–hypopnea index

cTn:

Cardiac troponin

CVD:

Cardiovascular disease

EMG:

Electromyogram

hs-cTnT:

High-sensitivity cardiac troponin T

LoB:

Limit of blank

LoD:

Limit of detection

LoQ:

Limit of quantification

OSA:

Obstructive sleep apnea

PG:

Polygraphy

PSG:

Polysomnography

S-cTnI:

Single-molecule cardiac troponin I

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Acknowledgments

The authors want to acknowledge the Ear–Nose–Throat department at Lovisenberg Diakonale Hospital for their support and assistance throughout the study. We also acknowledge Michael J. Conrad (TIMI Clinical Trials Laboratory) and May Lill Madsen (Lovisenberg Diakonale Hospital) for their contribution on the biomarker analyses, and Christian Hall for valuable discussions and advice throughout the project. The study was supported by grants from Lovisenberg Diakonale Hospital’s research fund and the South-Eastern Norway Regional Health Authority. TSH also received a scholarship from AstraZeneca that funded some of the biomarker analyses. These institutions had no other involvement in the study.

Declaration of interest

PJ has consulted for T2 Biosystems and Quanterix and has received grant support from Abbott, AstraZeneca, Daiichi Sankyo, Merck, Roche Diagnostics and Waters Technologies. JH is an employee of Boehringer Ingelheim Norway, with the company not being involved in this study. SA has received speakers’ honoraria from AstraZeneca, Boehringer Ingelheim, Orion Pharma, Pfizer and Siemens. DA has received speakers’ honoraria from Siemens. The other authors have no disclosures.

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Correspondence to Trygve Sørdahl Hall.

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Hall, T.S., Herrscher, T., Jarolim, P. et al. Obstructive sleep apnea: no independent association to troponins. Sleep Breath 18, 351–358 (2014). https://doi.org/10.1007/s11325-013-0892-6

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  • DOI: https://doi.org/10.1007/s11325-013-0892-6

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