Four- to seven-year follow-up of pharmacological postconditioning with mangafodipir as an adjunct to primary PCI in ST-segment elevation myocardial infarction.

Introduction: Adverse left ventricular remodelling (AR) develops over time in approximately 30% of patients with a history of coronary artery disease. AR manifests as a structural change in the left ventricle (LV) in terms of increased volumes and reduced left ventricular ejection fraction (LVEF). Manganese dipyridoxyl diphosphate (mangafodipir) has demonstrated interesting cardioprotective features in acute myocardial ischaemia.

Corrigendum: A head-to-head comparison of myocardial strain by fast-strain encoding and feature tracking imaging in acute myocardial infarction.

[This corrects the article DOI: 10.3389/fcvm.2022.

A head-to-head comparison of myocardial strain by fast-strain encoding and feature tracking imaging in acute myocardial infarction.

Background: Myocardial infarction (MI) is a major cause of heart failure. Left ventricular adverse remodeling is common post-MI. Several studies have demonstrated a correlation between reduced myocardial strain and the development of adverse remodeling.

Mangafodipir as a cardioprotective adjunct to reperfusion therapy: a feasibility study in patients with ST-segment elevation myocardial infarction.

Aims: The aim of the present study was to examine the feasibility of applying the catalytic antioxidant mangafodipir [MnDPDP, manganese (Mn) dipyridoxyl diphosphate] as a cardioprotective adjunct to primary percutaneous coronary intervention (pPCI) in patients with ST-segment elevation (STE) myocardial infarction (STEMI). Both MnDPDP and a metabolite (Mn dipyridoxyl ethyldiamine) possess properties as mitochondrial superoxide dismutase mimetics and iron chelators, and combat oxidative stress in various tissues and conditions.

Methods And Results: The study tested MnDPDP (n = 10) vs.