1. MYOCARDIAL INFARCTION
DR.SAMINA QAMAR
ASSISTANT PROFESSOR HISTOPATHOLOGY.

2. The major underlying cause of MI is atherosclerosis .
Myocardial ischemia-an imbalance between cardiac blood supply (perfusion) and myocardial oxygen demand.
Infarction is tissue death /necrosis caused by a local lack of oxygen, due to an obstruction of the tissue's blood supply.

3. Blockade of arterial supply.

4. What causes the blockade?
Sudden disruption of an atheromatous plaque,
Intraplaque hemorrhage,
Erosion,
Ulceration, or
Rupture/ fissuring-exposing subendothelial collagen .
Platelets come and adhere to it and occlude the lumen.

5. Myocardial response to ischemia.
Coronary artery obstruction blocks the myocardial blood supply.
Within seconds of vascular obstruction, aerobic glycolysis ceases in cardiac myocyte leading to accumulation of lactic acid.
Severe ischemia lasting at least 20 to 40 minutes causes irreversible injury and myocyte death results in coagulative necrosis .

6. Myocardial response
Necrotic myocytes release protiens that are normally present inside them, and can be measured in blood.
Troponin I and T (bound to actin) are considered to be most specific serological markers of MI.
Raised levels of Creatinin Kinase, an enzyme is another marker of MI in blood.

7. Can Myocyte be revived?
Reperfusion: If myocardial blood flow is restored earlier(within 20 minutes), cell viability may be preserved.
This provides the rationale for early clinical detection of acute MI, and prompt intervention by angioplasty or thrombolysis, to restore blood flow.
YES IN INFARCTION, NO IN NECROSIS.

8. Occlusion results in cell death/necrosis.
Necrosis begins in a small zone of the subendocardial ISCHEMIC ZONE.
A very narrow zone of myocardium immediately beneath the endocardium is spared because it can be oxygenated by diffusion from the ventricle.
The end result of obstruction to blood flow is coagulative necrosis of the muscle.

9. Gross appearance of infarct.
Yellow tan softened area rimmed by hyperemic zone usually in left ventricle and/or ventricular septum.

10. How coagulative necrosis appears?
First day of myocardial infarction is contraction band and necrosis.
The myocardial fibers are beginning to loose cross striations and the nuclei.
Many irregular darker pink wavy contraction bands extending across the fibers, appear.

11. 1-2 days old infarct.
The myocardial fibers have dark red contraction bands and their nuclei disappear.
Neutrophils appear to show acute inflammation.
Clinically, changes in the ECG and a rise in the MB fraction of creatine kinase can be seen in blood.

12. 1-2 day old infarct.
Recent myocardial infarction, can also show extensive hemorrhage after reperfusion.

13. 3-4 day old infarct.
There is an extensive acute inflammatory infiltrate and the myocardial fibers are so necrotic that the outlines of them are only barely visible.

14. 7-14 days old infarct. Normal myocardial fibers at the top.
Below these fibers macrophages have appeared along with numerous capillaries and collagen, collectively called GRANULATION TISSUE.

15. 7-14 days
Macrophages completely remove necrotic myocytes by phagocytosis (7-10 days).

16. More than 2 week old .
There is pale white extensive collagen deposition within the interstitium between myocardial fibers.
Inflammation has disappeared.

17. Summary: N,M,G,C. Necrotic myocardium invites Neutrophils .
Macrophages come to remove necrotic myocytes and neutrophil fragments.
The infarcted zone is progressively replaced by Granulation tissue .
Later, dense Collagenous scar is formed.