Clinical Risks and Underlying Mechanisms of Atrial Fibrillation after Myocardial Infarction.

Atrial Fibrillation (AF) following Myocardial Infarction (MI) is a common clinical complication that significantly impairs patient prognosis and quality of life. This review examines the clinical risks and underlying pathophysiological mechanisms of post-MI AF. The pathophysiology of AF after MI involves multiple maladaptive processes, particularly atrial structural and electrical remodeling, which collectively establish the arrhythmogenic substrate. This review summarizes the molecular mechanisms contributing to AF in the post-infarction setting. Furthermore, it was synthesized current evidence on pharmacological interventions targeting this substrate, highlighting four primary mechanisms of action: anti-fibrotic effects, modulation of calcium homeostasis, endogenous hormone regulation, and anti-inflammatory actions. Consequently, elucidating the complex and dynamic pathophysiological changes that drive atrial fibrillation after myocardial infarction may inform the development of targeted therapeutic strategies for post-infarction AF.