Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Standard

Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest. / Wiberg, Sebastian; Stride, Nis; Bro-Jeppesen, John; Holmberg, Mathias J; Kjærgaard, Jesper; Larsen, Steen; Donnino, Michael W; Hassager, Christian; Dela, Flemming.

In: European Heart Journal: Acute Cardiovascular Care, Vol. 9, No. 4_suppl, 11.2020, p. S138-S144 .

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Wiberg, S, Stride, N, Bro-Jeppesen, J, Holmberg, MJ, Kjærgaard, J, Larsen, S, Donnino, MW, Hassager, C & Dela, F 2020, 'Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest', European Heart Journal: Acute Cardiovascular Care, vol. 9, no. 4_suppl, pp. S138-S144 . https://doi.org/10.1177/2048872618814700

APA

Wiberg, S., Stride, N., Bro-Jeppesen, J., Holmberg, M. J., Kjærgaard, J., Larsen, S., Donnino, M. W., Hassager, C., & Dela, F. (2020). Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest. European Heart Journal: Acute Cardiovascular Care, 9(4_suppl), S138-S144 . https://doi.org/10.1177/2048872618814700

CBE

Wiberg S, Stride N, Bro-Jeppesen J, Holmberg MJ, Kjærgaard J, Larsen S, Donnino MW, Hassager C, Dela F. 2020. Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest. European Heart Journal: Acute Cardiovascular Care. 9(4_suppl):S138-S144 . https://doi.org/10.1177/2048872618814700

MLA

Wiberg, Sebastian et al. "Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest". European Heart Journal: Acute Cardiovascular Care. 2020, 9(4_suppl). S138-S144 . https://doi.org/10.1177/2048872618814700

Vancouver

Wiberg S, Stride N, Bro-Jeppesen J, Holmberg MJ, Kjærgaard J, Larsen S et al. Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest. European Heart Journal: Acute Cardiovascular Care. 2020 Nov;9(4_suppl):S138-S144 . https://doi.org/10.1177/2048872618814700

Author

Wiberg, Sebastian ; Stride, Nis ; Bro-Jeppesen, John ; Holmberg, Mathias J ; Kjærgaard, Jesper ; Larsen, Steen ; Donnino, Michael W ; Hassager, Christian ; Dela, Flemming. / Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest. In: European Heart Journal: Acute Cardiovascular Care. 2020 ; Vol. 9, No. 4_suppl. pp. S138-S144 .

Bibtex

@article{c41c9b8e5586492c9deb3895ac220591,
title = "Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest",
abstract = "BACKGROUND:: While preclinical studies suggest that mitochondria play a pivotal role in ischaemia-reperfusion injury, the knowledge of mitochondrial function in human out-of-hospital cardiac arrest remains scarce. The present study sought to compare oxidative phosphorylation capacity in skeletal muscle biopsies from out-of-hospital cardiac arrest patients to healthy controls.METHODS:: This was a substudy of a randomised trial comparing targeted temperature management at 33°C versus 36°C for out-of-hospital cardiac arrest patients. Skeletal muscle biopsies were obtained from adult resuscitated comatose out-of-hospital cardiac arrest patients 28 hours after initiation of targeted temperature management, i.e. at target temperature prior to rewarming, and from age-matched healthy controls. Mitochondrial function was analysed by high-resolution respirometry. Maximal sustained respiration through complex I, maximal coupled respiration through complex I and complex II and maximal electron transport system capacity was compared.RESULTS:: A total of 20 out-of-hospital cardiac arrest patients and 21 controls were included in the analysis. We found no difference in mitochondrial function between temperature allocations. We found no difference in complex I sustained respiration between out-of-hospital cardiac arrest and controls (23 (18-26) vs. 22 (19-26) pmol O2/mg/s, P=0.76), whereas coupled complex I and complex II respiration was significantly lower in out-of-hospital cardiac arrest patients versus controls (53 (42-59) vs. 64 (54-68) pmol O2/mg/s, P=0.01). Furthermore, electron transport system capacity was lower in out-of-hospital cardiac arrest versus controls (63 (51-69) vs. 73 (66-78) pmol O2/mg/s, P=0.005).CONCLUSIONS:: Mitochondrial oxidative phosphorylation capacity in skeletal muscle biopsies was reduced in out-of-hospital cardiac arrest patients undergoing targeted temperature management compared to age-matched, healthy controls. The role of mitochondria as risk markers and potential targets for post-resuscitation care remains unknown.",
author = "Sebastian Wiberg and Nis Stride and John Bro-Jeppesen and Holmberg, {Mathias J} and Jesper Kj{\ae}rgaard and Steen Larsen and Donnino, {Michael W} and Christian Hassager and Flemming Dela",
year = "2020",
month = nov,
doi = "10.1177/2048872618814700",
language = "English",
volume = "9",
pages = "S138--S144 ",
journal = "European Heart Journal: Acute Cardiovascular Care",
issn = "2048-8726",
publisher = "SAGE Publications Ltd",
number = "4_suppl",

}

RIS

TY - JOUR

T1 - Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest

AU - Wiberg, Sebastian

AU - Stride, Nis

AU - Bro-Jeppesen, John

AU - Holmberg, Mathias J

AU - Kjærgaard, Jesper

AU - Larsen, Steen

AU - Donnino, Michael W

AU - Hassager, Christian

AU - Dela, Flemming

PY - 2020/11

Y1 - 2020/11

N2 - BACKGROUND:: While preclinical studies suggest that mitochondria play a pivotal role in ischaemia-reperfusion injury, the knowledge of mitochondrial function in human out-of-hospital cardiac arrest remains scarce. The present study sought to compare oxidative phosphorylation capacity in skeletal muscle biopsies from out-of-hospital cardiac arrest patients to healthy controls.METHODS:: This was a substudy of a randomised trial comparing targeted temperature management at 33°C versus 36°C for out-of-hospital cardiac arrest patients. Skeletal muscle biopsies were obtained from adult resuscitated comatose out-of-hospital cardiac arrest patients 28 hours after initiation of targeted temperature management, i.e. at target temperature prior to rewarming, and from age-matched healthy controls. Mitochondrial function was analysed by high-resolution respirometry. Maximal sustained respiration through complex I, maximal coupled respiration through complex I and complex II and maximal electron transport system capacity was compared.RESULTS:: A total of 20 out-of-hospital cardiac arrest patients and 21 controls were included in the analysis. We found no difference in mitochondrial function between temperature allocations. We found no difference in complex I sustained respiration between out-of-hospital cardiac arrest and controls (23 (18-26) vs. 22 (19-26) pmol O2/mg/s, P=0.76), whereas coupled complex I and complex II respiration was significantly lower in out-of-hospital cardiac arrest patients versus controls (53 (42-59) vs. 64 (54-68) pmol O2/mg/s, P=0.01). Furthermore, electron transport system capacity was lower in out-of-hospital cardiac arrest versus controls (63 (51-69) vs. 73 (66-78) pmol O2/mg/s, P=0.005).CONCLUSIONS:: Mitochondrial oxidative phosphorylation capacity in skeletal muscle biopsies was reduced in out-of-hospital cardiac arrest patients undergoing targeted temperature management compared to age-matched, healthy controls. The role of mitochondria as risk markers and potential targets for post-resuscitation care remains unknown.

AB - BACKGROUND:: While preclinical studies suggest that mitochondria play a pivotal role in ischaemia-reperfusion injury, the knowledge of mitochondrial function in human out-of-hospital cardiac arrest remains scarce. The present study sought to compare oxidative phosphorylation capacity in skeletal muscle biopsies from out-of-hospital cardiac arrest patients to healthy controls.METHODS:: This was a substudy of a randomised trial comparing targeted temperature management at 33°C versus 36°C for out-of-hospital cardiac arrest patients. Skeletal muscle biopsies were obtained from adult resuscitated comatose out-of-hospital cardiac arrest patients 28 hours after initiation of targeted temperature management, i.e. at target temperature prior to rewarming, and from age-matched healthy controls. Mitochondrial function was analysed by high-resolution respirometry. Maximal sustained respiration through complex I, maximal coupled respiration through complex I and complex II and maximal electron transport system capacity was compared.RESULTS:: A total of 20 out-of-hospital cardiac arrest patients and 21 controls were included in the analysis. We found no difference in mitochondrial function between temperature allocations. We found no difference in complex I sustained respiration between out-of-hospital cardiac arrest and controls (23 (18-26) vs. 22 (19-26) pmol O2/mg/s, P=0.76), whereas coupled complex I and complex II respiration was significantly lower in out-of-hospital cardiac arrest patients versus controls (53 (42-59) vs. 64 (54-68) pmol O2/mg/s, P=0.01). Furthermore, electron transport system capacity was lower in out-of-hospital cardiac arrest versus controls (63 (51-69) vs. 73 (66-78) pmol O2/mg/s, P=0.005).CONCLUSIONS:: Mitochondrial oxidative phosphorylation capacity in skeletal muscle biopsies was reduced in out-of-hospital cardiac arrest patients undergoing targeted temperature management compared to age-matched, healthy controls. The role of mitochondria as risk markers and potential targets for post-resuscitation care remains unknown.

U2 - 10.1177/2048872618814700

DO - 10.1177/2048872618814700

M3 - Journal article

C2 - 30854867

VL - 9

SP - S138-S144

JO - European Heart Journal: Acute Cardiovascular Care

JF - European Heart Journal: Acute Cardiovascular Care

SN - 2048-8726

IS - 4_suppl

ER -