This review article summarizes the results of histopathological and clinical imaging studies to assess myocardial necrosis in humans. Different histopathological features of myocardial cell necrosis are reviewed. In addition, the present role of echocardiographic techniques in assessing irreversible myocardial damage is briefly summarized.By myocardial cell damage we mean a primary damage of the myocardial cell. In fact, the myocardium includes several other structures as vessels (arteries, veins, lymphatics), nerves, collagen matrix, interstitium, which can be primarily altered with subsequent secondary damage of myocardial cells. In general, both clinicians and pathologists believe in a unique pattern of myocardial necrosis due to ischemia; less frequently to inflammatory processes or rarely to storage diseases. In reality, three types of myocardial cell necrosis can be recognized [1][2][3][4] in relation to contraction cycle.The myocardial cell may irreversibly arrest in: 1. relaxation 2. contraction 3. after progressive failure.1. In the first condition the early histologic pattern is characterized by mild eosinophilia, increased length of sarcomeres and elongation of nuclei. This myocellular stretching is due to the action of intraventricular pressure on these elements in flaccid paralysis and visible within 30 minutes. The lesion is pathognomonic for myocardial infarct with its sequelae, namely a polymorphonuclear leukocytic infiltration which starts after 6-8 hours and disappears within 5 days, centripetal removal of necrotic tissue by macrophages and substitution by collagen ending in acellular and avascular, dense, scar (Fig. 1). No repair by granulation tissue is observed. In humans the infarct is monofocal and its size ranges from less than 10% to more than 50% of the total left ventricular mass. Erroneously named "coagulation necrosis" (coagulation never occurs), is better defined as infarct or ischemic necrosis. In contrast to the current belief oriented to reduce or avoid expansion of an infarct, death due to a myocardial infarct is not related to its size. About half of these cases have a size less than 20% of the left ventricular mass (Tab. 1). The same table show that: a) infarct size is not related to severity of coronary atherosclerotic lumen reduction and number of main vessels with sever stenosis; b) long survival (interval from the beginning to death) prevails in large infarcts; c) extensive myocardial fibrosis, as expression of chronic disease, does not correlate with infarct size; and d) the frequency of an occlusive thrombus is significantly higher in the largest infarcts supporting its secondary formation [5].2. The opposite pattern is seen when the myocytes stop in contraction or better in hypercontraction (Fig. 2). In less than 10 minutes the hypercontracted myocardial cells