Abstract     Myocardial ischemia results from reduction of coronary flow to such an extent that supply of oxygen to the myocardium does not meet the oxygen demand of myocardial tissue. When this ischemia is prolonged and irreversible the myocardial cell death and necrosis occurs which is defined as myocardial infarction. Oxygen deprivation due to prolonged ischemia leads to a cascade in metabolism in myocardial tissues beginning from anaerobic glycolysis, inhibition of ATP- dependent transport process in cell membrane, electrolyte shift, cellular edema and finally loss of cell membrane integrity. Due to increased glycolysis there is increased lactate concentration. This decreases the intracellular pH, resulting in release and activation of lysosomal proteolytic enzymes and thereby disintegrating intracellular structure and structurally bound proteins. The release and appearance of these ischemia affected biomolecules in blood stream is an outcome of these metabolic changes. Elevated enzyme activity associated with disease is generally assumed to reflect activity of enzyme released from injured tissue. In most of the conditions, the same enzymes with which an injured organ is richly endowed are those exhibiting elevated activity in serum following organ injury. Time course of depletion of enzyme activity from a damaged organ parallels time course of increase of activity of same enzyme in serum following insult. Early and accurate identification of myocardial necrosis in patients experiencing symptoms suggestive of myocardial infarction is a common and important clinical challenge. Since the clinical symptoms are not very reliable, ECG is the most widely used method of diagnosis of myocardial infarction. But many a times ECG shows inconclusive pattern in such a situation the importance of serum biochemical markers of myocardial injury.