Key result
Inflammation plays a pivotal role in the pathogenesis of arrhythmias following acute myocardial infarction by contributing to electrical instability, structural remodeling, and autonomic imbalance.
Why the study?
Arrhythmias are the most common complication after acute myocardial infarction that can worsen disease progression and lead to sudden cardiac death, requiring prompt diagnosis and effective treatment.
This review outlines the inflammatory mechanisms underlying post-AMI arrhythmias, highlighting the potential of targeted anti-inflammatory therapies to reduce arrhythmia burden.
Should not yet change post-AMI arrhythmia management; extends mechanistic understanding while leaving clinical translation open.
Acute myocardial infarction (AMI) remains a leading cause of cardiovascular death. Arrhythmias are the most common complication after AMI and can worsen disease progression and lead to sudden cardiac death (SCD). Therefore, prompt and accurate diagnosis, together with proactive and effective treatment, is crucial. This article reviews the mechanisms of inflammation in post-AMI arrhythmias, including inflammatory cell infiltration, cytokine release, oxidative stress, cardiac structural remodeling, and neuroimmune interactions. Additionally, this review discusses the predictive value of inflammatory markers and the clinical prospects of anti-inflammatory therapy, thereby providing a reference for future research and clinical prevention.
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Guo et al. (2026) conducted a review in Acute Myocardial Infarction and Arrhythmias. Inflammation was evaluated. Inflammation plays a pivotal role in the pathogenesis of arrhythmias following acute myocardial infarction by contributing to electrical instability, structural remodeling, and autonomic imbalance.
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