**2. Pathophysiology**

Myocardial ischemia may occur either from increased demand of oxygen by the myocardium, or decreased oxygen supply to the myocardium, or both. During exercise, tachycardia or emotions, myocardial oxygen requirement is increased and if there is coronary obstruction, it will lead to a transitory imbalance. This condition is often termed demand ischemia and is responsible for most episodes of chronic stable angina. In other conditions, this imbalance occurs due to acute decrease of oxygen supply because of increased coronary vascular tone (i.e., coronary vasospasm) or obvious reduction or occlusion of coronary artery as a result of platelet aggregates or thrombi. This condition which is known as supply ischemia may lead to MI and unstable angina (UA). In many conditions, ischemia is a result of both an increase in oxygen demand and a reduction in supply [5–8].

The leading cause of MI, by far, is atherosclerosis, a progressive accumulation of cholesterol and fibrous tissue in plaques present within the arterial wall, spanning over decades [9–12]. Nevertheless atherosclerotic plaques may become unstable, rupture, and form a thrombus that occludes the artery. When a significant plaque rupture occurs in the coronary vessels, it leads to thrombosis and total vascular occlusion which concludes with the occurrence of MI [13, 14].

Total coronary occlusion leading decreased myocardial oxygen supply results with the damage of myocytes [15, 16].

This decreased blood supply has the following consequences:

