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Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide. Ischemic heart disease and diabetic cardiomyopathy are two CVDs characterized by prominent myocardial injuries. Calcium overload, mitochondrial damage, the accumulation of reactive oxygen species (ROS), and abnormal programmed cell death (PCD) pathways, such as autophagy, pyroptosis, apoptosis, and ferroptosis, are recognized as the major mechanisms of myocardial injury. Dexmedetomidine (DEX) is a selective α2-adrenergic receptor agonist that is often administered to surgical patients due to the associated sedative, analgesic, and anxiolytic properties. Recent studies have indicated that DEX can exhibit more beneficial effects in patients, including reducing myocardial and vascular damage in CVD patients. Mechanistically, DEX reduces levels of oxidative stress markers and inflammatory cytokines and improves mitochondrial function. Numerous studies have revealed novel regulatory roles for DEX in mediating ferroptosis. This study summarizes the expression and functions of ferroptosis in ischemic heart disease and diabetic cardiomyopathy and discusses the regulatory mechanism of DEX in ferroptosis.