Pathophysiological role of neutrophils in acute myocardial infarction
F Carbone1, A Nencioni, F Mach
1Fabrizio Montecucco, Cardiology Division, Department of Medicine, Geneva University Hospital, Foundation for Medical Researches, 64 Avenue Roseraie, 1211 Geneva, Switzerland, Tel.: +41 223827238, Fax: +41 223827245,
Insights
Neutrophils play a key role in acute myocardial infarction (AMI) pathogenesis, causing tissue damage and adverse cardiac remodeling. Targeting neutrophils offers a promising therapeutic strategy for improving outcomes in acute coronary syndromes.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Pathophysiology
Background:
- Acute myocardial infarction (AMI) involves systemic, intraplaque, and myocardial inflammatory processes.
- Neutrophils are increasingly recognized as critical immune cells in acute coronary syndromes (ACS).
- These cells contribute to myocardial damage and adverse cardiac remodeling post-infarction.
Purpose of the Study:
- To review the role of neutrophils in the pathogenesis of AMI.
- To discuss pharmacological strategies targeting neutrophil function in ACS.
- To highlight potential therapeutic interventions for reducing neutrophil-mediated damage and improving post-ischaemic outcomes.
Main Methods:
- This is a narrative review.
- Literature search on neutrophil involvement in AMI and ACS.
- Analysis of preclinical and clinical studies on neutrophil-targeted therapies.
Main Results:
- Neutrophils infiltrate coronary plaques and infarcted myocardium.
- They release matrix-degrading enzymes and reactive oxygen species, causing tissue damage.
- Neutrophils are implicated in post-infarction cardiac remodeling and neointima formation.
Conclusions:
- Neutrophils are central players in AMI pathogenesis and adverse outcomes.
- Pharmacological interventions targeting neutrophil recruitment or function show promise.
- Further research is warranted to translate preclinical findings into clinical practice for ACS treatment.
Abstract:
The pathogenesis of acute myocardial infarction is known to be mediated by systemic, intraplaque and myocardial inflammatory processes. Among different immune cell subsets, compelling evidence now indicates a pivotal role for neutrophils in acute coronary syndromes. Neutrophils infiltrate coronary plaques and the infarcted myocardium and mediate tissue damage by releasing matrix-degrading enzymes and reactive oxygen species. In addition, neutrophils are also involved in post-infarction adverse cardiac remodelling and neointima formation after angioplasty. The promising results obtained in preclinical modelswith pharmacological approaches interfering with neutrophil recruitment or function have confirmed the pathophysiological relevance of these immune cells in acute coronary syndromes and prompted further studies of these therapeutic interventions. This narrative review will provide an update on the role of neutrophils in acute myocardial infarction and on the pharmacological means that were devised to prevent neutrophil-mediated tissue damage and to reduce post-ischaemic outcomes.
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