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SGLT2 inhibition reduces myocardial oxygen consumption




TekijätSøndergaard Esben, Lauritzen Esben S, Lauritsen Katrine M, Åkerblom Axel, Nuutila Pirjo, Oldgren Jonas, Gormsen Lars C

KustantajaElsevier

Julkaisuvuosi2022

JournalMetabolism open

Tietokannassa oleva lehden nimiMetabolism open

Lehden akronyymiMetabol Open

Artikkelin numero100207

Vuosikerta15

ISSN2589-9368

eISSN2589-9368

DOIhttps://doi.org/10.1016/j.metop.2022.100207

Verkko-osoitehttps://www.sciencedirect.com/science/article/pii/S2589936822000457?via%3Dihub

Rinnakkaistallenteen osoitehttps://research.utu.fi/converis/portal/detail/Publication/177975645


Tiivistelmä

Aims/hypothesis: SGLT2 inhibition is associated with a reduced risk of cardiac disease that is still largely unexplained. According to one hypothesis, improved myocardial energetics may explain the cardioprotective effects of SGLT2i. However, recent mechanistic studies that have addressed this question have lacked the power to detect discrete but still clinically significant effects.
Methods:We pooled data from two recent randomized clinical trials and performed a meta-analysis to determine the effect of SGLT2 inhibition on myocardial oxygen consumption and myocardial external efficiency measured by positron emission tomography.
Results:SGLT2 inhibition reduced myocardial oxygen consumption (−1.06 [95%CI: 0.22–1.89] mL/100 g/min (n = 59, p = 0.01)), but did not affect myocardial external efficiency (2.22 [95%CI: 0.66-5.11] % (n = 59, p = 0.13))
Conclusions: /interpretation SGLT2 inhibition reduces myocardial oxygen consumption at rest, which may contribute to the drugs’ cardioprotective effects.


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Last updated on 2025-27-03 at 22:05