Timely restoration of blood supply after myocardial infarction is crucial for saving the infarcted myocardium. So far, the most effective method is to restore myocardial oxygenation and coronary blood flow through coronary interventional therapy. However, reperfusion may also lead to greater heart damage due to the reintroduction of molecular oxygen. New treatments are needed to protect the heart from myocardial ischemia-reperfusion injury (MIRI) to improve clinical outcomes in patients with acute myocardial infarction and heart failure (HF). A deeper understanding of the mechanisms of MIRI and the search for new treatments could provide key evidence to mitigate myocardial damage and improve patient survival. At present, it has been found that copper, as a trace element in human body, can have a significant protective effect on MIRI. Copper can reduce apoptosis in cardiomyocytes, that is, control the self-destruction process of cell, so as to reduce the degree of myocardial injury. However, the potential relationship between abnormal copper ion metabolism as well as cuproptosis and MIRI as well as HF has not been explored. In this review, we focus on potential therapeutic strategies for MIRI and understand the metabolic pathways of copper in the human body, so as to provide more options and hope for the treatment of cardiovascular diseases.