Abstract: The coronary artery lesion caused by myocardial ischemia (MI) is one of the important factors of cardiac structural changes and functional disorders. At the same time, the ischemia and hypoxia of myocardial tissue can also cause myocardial energy metabolism disorder. Drugs optimizing energy metabolism have become therapeutic targets and hot spots for the prevention and control of MI. As the energy of myocardial cells mainly comes from adenosine triphosphate (ATP) in mitochondria, adjusting the biosynthesis of mitochondria is an important way to improve myocardial energy metabolism, especially to promote glycolysis of myocardial tissue and inhibit the oxidation of free fatty acid, which are conducive to the reduction of the myocardial cell injury caused by MI and the improvement of the function of myocardial tissue. This article briefly summarizes and reviews the mechanism research of ischemic myocardial energy metabolism and also the research progress in clinical drug treatment.