Myocardial infarction remains a significant worldwide public health issue, primarily owing to its mortality and morbidity rates. This condition is due to myocardial ischemia, appearing once the heart's blood flow is obstructed or significantly reduced, causing the death of heart muscle cells. Reperfusion prevents further death of cardiomyocytes, restoring coronary flow. However, the initial lack of coronary blood flow and the subsequent restoration induce ischemia/reperfusion injury (IRI) due to abrupt metabolic and biochemical changes, such as calcium overload, activation of inflammatory cells, and oxidative stress (OS). OS is associated with damage to cellular biomolecules such as proteins, lipids, DNA, or carbohydrates and with organelles such as mitochondria, activating mitochondrial dynamics. These oxidative conditions may also trigger ferroptosis, cell death linked to cellular oxidation. While ferroptosis induction is desirable in certain diseases like cancer, it is not beneficial in situations such as myocardial IRI. Although considerable research has been conducted on ferroptosis in myocardial IRI, the potential impact of reducing ferroptosis via mitochondrial dynamics in IRI remains to be reviewed. Consequently, this review concentrates on mitochondrial dynamics during myocardial ferroptosis in IRI and explores the potential therapy to inhibit myocardial ferroptosis by targeting mitochondrial dynamics to mitigate IRI.