Abstract
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.
Highlights
Despite significant improvements in the care of patients with acute myocardial infarction (AMI) in the recent decades, AMI remains associated with high morbidity and mortality [1]
The plasma samples previously acquired in the course of a randomized controlled trial investigating the effects of remote ischemic conditioning (RIC) on myocardial damage in patients with acute ST elevation AMI were analyzed
It needs to be emphasized that based on our study design, it is not possible to deduce if AMI causes higher MG levels or if reperfusion by primary percutaneous coronary intervention (pPCI) causes them
Summary
Biomedicines 2022, 10, 605 no intervention has yielded a convincing effect that would result in its implementation in the clinical routine, as reviewed previously [2] One of these interventions is remote ischemic conditioning (RIC), whereby brief and repetitive ischemia and reperfusion cycles in a remote tissue or organ lead to tissue protection. Preclinical results have been promising [5,6], and preconditioning is impossible for the treatment of AMI in humans, but large clinical trials applying per- or postconditioning strategies have failed to show the cardioprotective effect of RIC in patients with ST elevation myocardial infarction [7,8]. 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. 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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