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Myocardial Ischemia and Myocardial Infarction (MI)

Pathogenesis
  • Thrombosis superimposed on a complicated stenosing atheroma is the basic cause of acute myocardial ischemia and myocardial infarction.
  • The risk factors of atherosclerosis are hypercholesterolemia, cigarette smoking, diabetes mellitus, physical inactivity, and the use of oral contraceptives. Checkout risk factors.
  • Myocardial necrosis begins within approximately 20-30 minutes after coronary artery occlusion.
  • The subendocardial region of myocardium is the most poorly perfused region of the ventricular wall and therefore myocardial infarct typically begins in the subendocardial region. The infarct usually reaches its full size within a period of 3-6 hours (During this period of infarction in evolution lysis of thrombus by the administration of thrombolytic agents e.g. streptokinase or tissue plasminogen activator may limit the size of the infarct.
  • Location of infarct depends on the coronary artery involved e.g.
    • Occlusion of the anterior descending artery (LAD) leads to an infarction in anterior and apical areas of the left ventricle and adjacent anterior 2/3 of the interventricular septum.
    • Occlusion of the right coronary artery (RCA) leads to an infarction in the posterior wall of the left ventricle, posterior 1/3 of the interventricular septum.
    • Occlusion of the left circumflex artery (LCx) leads to an infarction in the lateral wall of the left ventricle.
  • Size of infarct depends on the following factors:
    • Which segment of the artery is blocked: Occlusion of proximal segments of the coronary arteries produces larger infarcts, involving the full thickness of the myocardium. Conversely, occlusion in more distal arterial branches tends to cause smaller infarcts.
    • Degree of collateral circulation: In patients with long-standing coronary atherosclerosis, collateral circulation may develop over time in response to chronic ischemia. Such collateral vessels may limit the size of the infarct.

Consequences of Acute Myocardial Ischemia

There are four possible consequences:
  1. It may only induce an attack of angina.
  2. More severe ischemia may result in myocardial infarction limited to inner 1/2  some portion or the entire circumference of the left ventricular wall to produce subendocardial foci of ischemic necrosis, also called a subendocardial infarct.
  3. The ischemic necrosis (infarction) may traverse the entire thickness of some portion of the left ventricular wall, creating transmural infarct.
  4. Sudden cardiac death.

Morphology

  1. Transmural infarct: Greater than 2.5 cm and traverses from endocardium to subepicardial myocardium. It is more common than a subendocardial one.
  2. Subendocardial infarct: Multifocal area of necrosis confined to inner 1/3 – 1/2 of the left ventricular wall.
  3. The sequence of Morphologic Changes in Transmural Infarct
Morphologic changes in myocardial infarction depend on the time passed from the onset. There is coagulation necrosis and inflammation followed by the formation of granulation tissue, resorption of necrotic material, and finally the organization of the granulation tissue to form a fibrous scar.

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