Acute-on-chronic inflammation in acute myocardial infarction.

Abstract

Purpose of review: Acute myocardial infarction (AMI) is heralded by chronic inflammation and entails an excessive burst of acute-on-chronic inflammation (AoCI). This review describes the evolution from understanding atherosclerosis as a chronic inflammatory disease, to recent efforts in optimizing anti-inflammatory therapy to patients with AMI. It highlights the challenges and opportunities in selecting the optimal patient with AMI to derive maximal benefit from early anti-inflammatory therapy.

Recent findings: The causal role of inflammation in atherosclerosis has been proven in large outcome trials. Since then, several smaller trials have sought to translate the concept of anti-inflammatory therapy targeting residual inflammatory risk to the dynamic early phase of AoCI after AMI. Current evidence highlights the importance of selecting patients with a high inflammatory burden. Surrogate criteria for large AMI (e.g., angiographic or electrocardiographic), as well as novel point-of-care biomarker testing may aid in selecting patients with particularly elevated AoCI. Additionally, patients presenting with AMI complicated by pro-inflammatory sequelae (e.g., atrial fibrillation, acute heart failure, left ventricular thrombosis) may dually profit from anti-inflammatory therapy.

Summary: Improved understanding of the mechanisms and dynamics of acute and chronic inflammatory processes after AMI may aid the strive to optimize early anti-inflammatory therapy to patients with AMI.