The cardioprotective effects of pharmacological postconditioning with mangafodipir in ST-elevation myocardial infarction, a 4–7 years follow up study

Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): Futurum - the academy for health and care, Jönköping. Background/Introduction The prevalence of heart failure is increasing as more patients survive a myocardial infarction (MI). MI scar extent is a strong predictor of the development of heart failure due to left ventricular adverse remodeling. Reperfusion injury occurs in the early phase of reperfusion and is linked to the increase of reactive oxygen species (ROS) with calcium overload disrupting the mitochondrial structure, which in turn results in further cell necrosis. Manganese dipyridoxyl diphosphate (mangafodipir) has superoxide dismutase mimetics and may act as a ROS scavenger in the acute phase of myocardial ischemia, hence supporting the myocardial cells in the neutralization of the chemically reactive molecules reducing the MI extent [1–3]. Purpose Our aim was to investigate the cardioprotective role of pharmacological postconditioning with mangafidipir in patients with ST-elevation myocardial infarction (STEMI). Methods Twenty patients with acute STEMI were enrolled between 2009–2014 and followed up 2017. The subjects were randomized in the cath lab into blinded treatment with i.v mangafodipir or control treatment receiving i.v saline prior to restoration of blood flow in the occluded coronary artery. Cardiac magnetic resonance imaging (CMR) at baseline and at follow-up (4–7 years) was performed to evaluate MI scar, LV end diastolic volume (LVEDV), LV end systolic volume (LVESV), LV stroke volume (LVSV), LV ejection fraction (LVEF) and LV mass (LVM). The study was approved by the ethical review board in Linkoping (Dnr 2016/212-31) and registered in the public database at clinicaltrials.gov (NCT 00966563). Results There was no significant difference between the groups in MI scar or LV geometrical and functional properties at baseline, although the duration of ischemia was significantly longer in the mangafodipir group (206 min vs. 144 min, p < 0.05) and a better TIMI grade before pPCI was observed in the control group. The group that underwent pharmacological postconditioning with mangafodipir had lower volumes and higher LVEF (p < 0.05) at follow-up, while the placebo group showed increased LV volumes, see Table 1 and Figure 1. Conclusion Pharmacological postconditioning with mangafodipir in STEMI may have a cardioprotective role in the development of left ventricular adverse remodeling. Due to the limited number of participants, the benefit of mangafodipir needs confirmation in larger studies.