Targeting Inflammation After Acute Myocardial Infarction

Abstract

Despite advances in secondary prevention, adverse cardiovascular events still occur after acute myocardial infarction (AMI). Contributing to residual cardiovascular risk, acute and persistent inflammation is a stronger predictor of recurrent events and mortality than low-density lipoprotein cholesterol. The inflammatory response following AMI is a finely regulated, multiphase process, beginning with a proinflammatory phase followed by a reparative phase. Disruptions in its regulation lead to persistent low-grade inflammation and worse clinical outcomes. Modulating inflammation has emerged as a promising secondary prevention strategy, with several drugs being tested with conflicting results regarding their efficacy and safety. Recently, novel approaches have reignited the interest in anti-inflammatory strategies after AMI. However, key knowledge gaps remain regarding potential class effects, drug choice, patient selection, and the optimal administration timing. This review provides an updated and comprehensive overview of inflammatory mechanisms after AMI and critically appraises the evolving clinical evidence surrounding anti-inflammatory therapies for secondary cardiovascular prevention.

Keywords: anti-inflammatory drugs; inflammation; myocardial repair; residual cardiovascular risk; targeted therapy.