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Association of Plasma Methylglyoxal Increase after Myocardial Infarction and the Left Ventricular Ejection Fraction.
Heber, Stefan; Haller, Paul M; Kiss, Attila; Jäger, Bernhard; Huber, Kurt; Fischer, Michael J M.
Afiliação
  • Heber S; Institute of Physiology, Center for Physiology and Pharmacology, Medical University of Vienna, 1090 Vienna, Austria.
  • Haller PM; Department of Cardiology, University Heart & Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
  • Kiss A; German Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, 20151 Hamburg, Germany.
  • Jäger B; Center for Biomedical Research and Translational Surgery, Ludwig Boltzmann Institute for Cardiovascular Research, Medical University of Vienna, 1090 Vienna, Austria.
  • Huber K; 3rd Department of Medicine, Cardiology and Intensive Care Medicine, Klinik Ottakring, 1016 Vienna, Austria.
  • Fischer MJM; 3rd Department of Medicine, Cardiology and Intensive Care Medicine, Klinik Ottakring, 1016 Vienna, Austria.
Biomedicines ; 10(3)2022 Mar 04.
Article em En | MEDLINE | ID: mdl-35327407
Background: Preclinical studies suggest that methylglyoxal (MG) increases within the myocardium upon acute myocardial infarction (AMI) and thereafter contributes to adverse postinfarct remodeling. The aims of this study were to test whether MG increases in plasma of humans after AMI and whether this increase is related to the left ventricular ejection fraction (LVEF). Methods: The plasma samples of 37 patients with ST elevation AMI undergoing primary percutaneous coronary intervention (pPCI) acquired in a previously conducted randomized controlled trial testing remote ischemic conditioning (RIC) were analyzed by means of high-performance liquid chromatography. Time courses of the variables were analyzed by means of mixed linear models. Multiple regression analyses served to explore the relationship between MG levels and the LVEF. Results: Compared to the MG levels upon admission due to AMI, the levels were increased 2.4-fold (95% CI, 1.6−3.6) 0.5 h after reperfusion facilitated by pPCI, 2.6-fold (1.7−4.0) after 24 h and largely returned to the baseline after 30 d (1.1-fold, 0.8−1.5). The magnitude of the MG increase was largely independent of that of cardiac necrosis markers. Overall, the highest MG values within 24 h after AMI were associated with the lowest LVEF after 4 d. While markers of myocardial necrosis and stretch quantified within the first 24 h explained 52% of the variance of the LVEF, MG explained additional 23% of the variance (p < 0.001). Conclusions: Considering these observational data, it is plausible that the preclinical finding of MG generation after AMI negatively affecting the LVEF also applies to humans. Inhibition of MG generation or MG scavenging might provide a novel therapeutic strategy to target post-AMI myocardial remodeling and dysfunction.
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Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Clinical_trials / Prognostic_studies / Risk_factors_studies Idioma: En Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Clinical_trials / Prognostic_studies / Risk_factors_studies Idioma: En Ano de publicação: 2022 Tipo de documento: Article