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Supplemental oxygen therapy does not affect the systemic inflammatory response to acute myocardial infarction
Author(s) -
Hofmann R.,
Tornvall P.,
Witt N.,
Alfredsson J.,
Svensson L.,
Jonasson L.,
Nilsson L.
Publication year - 2018
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/joim.12716
Subject(s) - medicine , myocardial infarction , randomized controlled trial , randomization , troponin , systemic inflammation , inflammation , cardiology , troponin t , troponin i
Background Oxygen therapy has been used routinely in normoxemic patients with suspected acute myocardial infarction ( AMI ) despite limited evidence supporting a beneficial effect. AMI is associated with a systemic inflammation. Here, we hypothesized that the inflammatory response to AMI is potentiated by oxygen therapy. Methods The DET ermination of the role of Oxygen in suspected Acute Myocardial Infarction ( DETO 2X‐ AMI ) multicentre trial randomized patients with suspected AMI to receive oxygen at 6 L min −1 for 6–12 h or ambient air. For this prespecified subgroup analysis, we recruited patients with confirmed AMI from two sites for evaluation of inflammatory biomarkers at randomization and 5–7 h later. Ninety‐two inflammatory biomarkers were analysed using proximity extension assay technology, to evaluate the effect of oxygen on the systemic inflammatory response to AMI . Results Plasma from 144 AMI patients was analysed whereof 76 (53%) were randomized to oxygen and 68 (47%) to air. Eight biomarkers showed a significant increase, whereas 13 were decreased 5–7 h after randomization. The inflammatory response did not differ between the two treatment groups neither did plasma troponin T levels. After adjustment for increase in troponin T over time, age and sex, the release of inflammation‐related biomarkers was still similar in the groups. Conclusions In a randomized controlled setting of normoxemic patients with AMI , the use of supplemental oxygen did not have any significant impact on the early release of systemic inflammatory markers.

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