Pathogenesis And Morphological changes of Myocardial Infarction

This presentation slide deals with Pathogenesis And Morphological changes of Myocardial Infarction

1. MYOCARDIAL INFARCTION Pathogenesis & Morphological changes

2. INTRODUCTION Myocardial infarction is a coagulative type of necrosis of cardiac muscle and is due to prolonged severe ischemia . Risk Factors Race : Any race can be affected. Age: Its frequency rises progressively with age. Peak is between 40 to 65 years of age. Sex : Males > females(during the reproductive period) Risk factors for atherosclerosis ( hyperlipidemia , hypertension, diabetes and cigarette smoking).

3. PATHOGENESIS Causes: Coronary Atherosclerosis(~90%) Non- atheromatous causes -Vasospasm without coronary atherosclerosis Emboli Ischemia due to other causes: – Vasculitis – Hematologic disorders like sickle cell disease – Amyloid deposition in vascular walls – Vascular dissection – Lowered systemic blood pressure (e.g. shock).

4. Acute plaque change : i ) Erosion/Ulceration, Rupture , fissuring of plaque exposes highly thrombogenic plaque sudden thrombus formation sudden occlusion of lumen . Ischemia and necrosis PATHOGENESIS

5. ii . Hemorrhage into the central core of plaque I ncreases the plaque size Sudden occlusion of lumen . Ischemia and necrosis PATHOGENESIS

6. 2. Formation of microthrombi : Exposure of thrombogenic subendothelial Collagen platelets adhere to the site platelet activation and aggregation Formation of microthrombi on the atheromatous plaque partial or complete occlusion of the affected coronary artery. PATHOGENESIS

7. 3. Vasospasm : Release of mediators by activated platelets, endothelial cell and inflammatory cells vasospasm at the sites of atheroma further narrowing of the lumen. PATHOGENESIS

8. 4. Activation of the coagulation pathway: Release of tissue factor at the site of rupture activates coagulation system increase the size of the thrombus Occlusion of blood vessel Necrosis PATHOGENESIS

9. 5. Tukotsubo cardiomyopathy - Broken heart syndrome: Drugs or endogenous catechols Vasospasm Increase heart rate, myocardial contractility, excerbating ischemia Sudden cardiac death or dilated cardiomyopathy PATHOGENESIS

10. MORPHOLOGY 0-30 minutes: Reversible injury Gross: None Light microscopy: None Electron microscopy: relaxation of myofibrils, glycogen loss, mitochondrial swelling 0.5-6 hours: Gross: None Light microscopy: Usually none variable waviness of fibers at border Electron microscopy: sarcolemmal disruption, mitochondrial amorphous densities

11. MORPHOLOGY 3. 6-12 hours: Gross: Dark mottling (occasional ) Light microscopy: Early coagulative necrosis, edema, hemorrhage 4. 12-24 hours: Gross: Dark mottling Light microscopy: Progression of coagulation necrosis, pyknotic nuclei, increased eosinophilia of cytoplasm, contraction band necrosis at margins, beginning of neutrophilic infiltrate

12. MORPHOLOGY 5. 1-3 days: Gross: Mottling with yellow-tan infarct center Light microscopy: Coagulation necrosis, with loss of nuclei and striations, increased interstitial infiltration of neutrophils 6. 3-7 days: Gross: Hyperemic border, central yellow-tan softening Light microscopy: Beginning disintegration of dead myocardial cells, with dying neutrophils , early phagocytosis of dead cells by macrophages at infarct border

13. MORPHOLOGY 7. 7–10 days: Gross: Maximally yellow-tan and soft , with depressed red tan margins Light microscopy: Well-developed phagocytosis of dead cells, formation of fibrovascular granulation tissue at margins 8. 10-14 days: Gross: Red-gray depressed infarct borders Light microscopy: Red-gray depressed infarct borders

14. MORPHOLOGY 9. 2-8 weeks: Gross: Gray-white scar, progressive from border around infarct Light microscopy: Increased collagen deposition, with decreased cellularity 10. >2 months: Gross: Scarring complete Light microscopy: Dense collagenous scar

15. REFERENCES General And Systemic Pathology- Ramadas Nayak Robbins And Cotran Pathologic Basis Of Disease Robbins Basic Pathology Textbook of Pathology- Harsh Mohan

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