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Introduction Coronary microembolization (CME), resulting from atherosclerotic plaque debris and thrombotic materials, is one of the main causes of the no-reflow phenomenon ( Ferroptosis is a novel form of programmed cell death characterized by the iron-mediated accumulation of lipid peroxidation ( The enzyme prostaglandin-endoperoxide synthase-2 (Ptgs2) is pivotal in modulating the expression levels of prostaglandins, which are the master mediators of the inflammatory response ( Hypoxia-inducible factor 1 subunit alpha (Hif1a) is a transcriptional activator that functions as a master regulator in maintaining oxygen homeostasis ( Atorvastatin (ATV) remains the cornerstone of pharmacological treatment for atherosclerotic cardiovascular diseases ( In the present study, we hypothesize that ATV could attenuate ferroptosis-dependent myocardial injury and inflammation following CME by inhibiting the Hif1a/Ptgs2 pathway