Abstract and Introduction
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.
Introduction
A therosclerotic cardiovascular disease remains a leading cause of morbidity and mortality worldwide, with acute myocardial infarction (AMI) as the primary contributor to cardiovascular death.[1] Despite significant advances in reperfusion strategies, pharmacologic therapy, and the management of modifiable risk factors such as diabetes, dyslipidemia, and hypertension, adverse cardiovascular events continue to occur after AMI.[2,3,4,5] The determinants of this residual risk (ie, the risk that persists despite optimal control of known modifiable factors) remain uncertain. Among these determinants, inflammation plays a complex but increasingly recognized role. Recent studies suggest that residual inflammatory risk, as indicated by a high-sensitivity C-reactive protein (hs-CRP) level >2 mg/L, is a stronger predictor of recurrent events and mortality than residual elevation of lowdensity lipoprotein (LDL) cholesterol despite statin therapy.[6,7]
The inflammatory response following AMI follows a biphasic process, beginning with a proinflammatory phase that transitions into a reparative phase.[8] Dysregulation of this balance can lead to persistent inflammation, adverse left ventricular remodeling, and worse clinical outcomes.[9] This pathophysiological concept has spurred growing interest in anti-inflammatory strategies as a component of secondary prevention after AMI. However, although various anti-inflammatory agents have been investigated in this context, results have been heterogeneous, and their overall efficacy and safety remain debated. Currently, colchicine is the only antiinflammatory agent recommended by guidelines for secondary prevention in patients with coronary artery disease, though supporting evidence is mixed.[10,11] More selective anti-inflammatory agents are under investigation, but several key questions remain unresolved, not only regarding which inflammatory pathways should be targeted and with which drug and dose but also concerning the accurate patient selection and optimal timing of intervention. In fact, given the dynamic nature of post-AMI inflammation and its context-dependent protective and harmful effects, the timing of therapy may be critical in effectively modulating residual inflammatory risk and improving clinical outcomes.
In this review we examine the rationale for antiinflammatory therapy through the full spectrum of AMI, from the acute event to long-term secondary prevention, and summarize current evidence on available and upcoming treatments and their potential clinical applications.
J Am Coll Cardiol. 2026;86(15):1146–1169 © 2026
Cite this: Targeting Inflammation After Acute Myocardial Infarction - Medscape - Jan 16, 2026.
