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The focus in cardiovascular research is shifting from determining mass HDL cholesterol levels toward investigating HDL functionalities as biomarker for cardiovascular disease. Myeloperoxidase (MPO), a main effector enzyme of the innate immune system, is increasingly implicated to negatively impact HDL function by various chemical modifications of HDL-associated proteins. This review summarizes recent insights how MPO affects HDL function in the setting of acute myocardial infarction (MI), mainly focusing on human data.First the mechanisms how MPO renders HDL particles dysfunctional and the usefulness of MPO as prospective biomarker for MI incidence and outcomes are described. Then the evidence for MPO causing specific HDL function impairments in MI and the clinical value of these observations is discussed in the context of the different HDL function assays employed.MPO modification of HDL in acute MI generates dysfunctional HDL. Features of HDL dysfunction can be used to stratify MI patients and seem associated with outcomes. More prospective studies are warranted to explore, if MPO-modified HDL is causally linked to severity and outcomes of MI. If this could be established, MPO would represent an attractive target to improve HDL dysfunction in MI and provide clinical benefit for patients.