Background: Myocardial ischemia, the most common kind of cardiovascular disease, and the leading cause of mortality worldwide. It is caused mostly by cardiac muscle necrosis caused by an abrupt coronary artery occlusion. Smoking and obesity are two major risk factors for myocardial infarction. Chest pain and dyspnea are common symptoms caused by a reduction in blood flow to the myocardium. Objective:  glycogen (GP) modulates glucose metabolism by mobilizing intracellular glycogen. Heart and brain tissues express it, which generates energy during muscle contraction. Myocardial ischemia activates Glycogen phosphorylase BB, which promotes glycogen breakdown. Subjects and Methods:  A case-control study was used in this investigation. These investigations comprise 160 Iraqi volunteers ranging in age from 25 to 75 years (50 with ST- elevation, 50 without ST- elevation, and 60 in the normal healthy control group). Results: Glycogen phosphorylase BB (GPBB) Activity by spectrophotometer technique. There were significant differences in GPBB activity among the groups the mean of GPBB for Control (3.25± 0.97) was significantly smaller than for both STEMI (12.54± 2.85), p < .001 and non ST-elevation myocardial infarction (NSTEMI) (6.51± 0.73), p < .001. The mean of GPBB for ST-elevation myocardial infarction (STEMI) (12.54± 2.88) was significantly larger than for NSTEMI (6.51± 0.73), p < .001. A significant negative correlation was observed between GPBB and high sensitive troponin I (hs-troponin I) and a negative correlation was observed between GPBB and TC in the NSTEMI group.  Conclusion: higher serum glycogen phosphorylase levels with higher troponin I levels were both observed in myocardial infarction patients and there was a significant correlation between them.