Myocardial ischemia results from imbalance between the needs of cardiac tissue and oxygenated blood supplied by the coronary circulation. This imbalance causes a deficit in tissue supplies of oxygen and of metabolizable substrates which leads, to varying degrees according to the severity of the ischemic process, to a decrease in the production of energy. This production rapidly becomes insufficient to ensure normal function. Furthermore, the accumulation of metabolic waste products causes the development of progressive cellular acidosis with inhibitory functional and metabolic effects. These metabolic and functional changes in the cell are accompanied by changes in structure and arrhythmias, as well as modifications in all-energy dependent mechanisms, particularly clearly marked in relation to membrane systems responsible for ion transport. The degree of these various disturbances is dependent upon the severity of the ischemic process as well as its duration. Reversibility can be ensured if normal perfusion is restored early. If reperfusion occurs later, it is generally incapable of ensuring the recovery of normal cell function and the ischemic cell is then destined to necrosis. Among the possible factors responsible for irreversible ischemic injury, an increase in cellular free-calcium concentration or an over-production of oxygen free-radicals, have been largely suggested. A number of therapeutic measures (metabolic or pharmaceutical) have been suggested with the aim of prolonging the duration of tolerable ischemia before the development of irreversible changes which render reperfusion ineffective. This is particularly the case of anti-ischemic drugs, the prototype of which is for instance trimetazidine.