**3. Histopathological findings**

between different geographical locations around the world. For example among South Asian populations, Pakistani people have the highest known rate of CAD. According to careful estimates nearly 100,000 individuals suffered from acute myocardial infarction (AMI) in

Acute MI is commonly presented with chest pain or discomfort, weakness, sweating, nausea, vomiting, and arrhythmias, sometimes loss of consciousness and syncope. It occurs with the sudden interruption of coronary blood flow and it is a life-threatening medical emergency

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

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

Total coronary occlusion leading decreased myocardial oxygen supply results with the dam-

• After 10–15 min of coronary occlusion necrosis of the myocardial tissue starts and since myocardial cells are strongly differentiated cells they have so weak regenerative abilities. Thus, according the size of the necrotic tissue the heart becomes a permanently weaker

• The injured myocardial tissue may cause ventricular arrhythmias (e.g. ventricular tachycardias or ventricular fibrillation) by re-entry mechanism. This is the most common under-

lying mechanism of the sudden cardiac death resulting from MI [17, 18].

Pakistan, in 2002 [2].

24 Myocardial Infarction

**2. Pathophysiology**

MI [13, 14].

age of myocytes [15, 16].

which requires quick management [3, 4].

in oxygen demand and a reduction in supply [5–8].

This decreased blood supply has the following consequences:

pump for the rest of the individual's life;

Examination of the heart shows that there is a well-defined circumscribed area of ischemic necrosis (coagulative necrosis). In the first 12–48 h, myocardial fibers are still well delineated with concentrated eosinophilic cytoplasm, but lose their transversal striations and the nucleus along with red blood cells which infiltrate the interstitial space. Later (5–10 days after the initial event), during healing of the myocardial tissue, the area with coagulative necrosis shows histologically preserved myocardial fibers with intensely eosinophilic cytoplasm, transverse striations and nuclei which are completely lost. The interstitium of the infarcted area is primarily infiltrated with neutrophils, then later with lymphocytes and macrophages to phagocytose the necrotic myocyte debris. The necrotic area is peripherally surrounded and gradually infiltrated by granulation tissue, which ultimately replace the infarct with a fibrous scar [19].
