Ischemic heart disease is mainly caused by atherosclerosis and its complications. Platelets have important role in initiation of atherosclerotic lesions. Increase platelet activation and aggregation within coronary circulation initiate thrombus formation at a ruptured or eroded plaque. Large platelets are enzymatically and metabolically more active and have a higher potential thrombosis ability than smaller one. There is growing evidence that myocardial cell injury not only is related to platelet activation of neutrophils (PMNs). PMNs have been demonstrated to release myeloperoxidase (MPO) into coronary circulation. MPO promotes destabilization and rupture of the atherosclerotic plaque surface, impairing vasodilatory and anti-inflammatory function.