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:
i. Coronary Atherosclerosis(~90%)
ii. 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).

5. 1. 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

6. ii. Hemorrhage into the central core of plaque
Increases the plaque size
Sudden occlusion of lumen.
Ischemia and necrosis
PATHOGENESIS

7. 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

8. 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

9. 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

10. 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

11. MORPHOLOGY
1. 0-30 minutes: Reversible injury
• Gross: None
• Light microscopy: None
• Electron microscopy: relaxation of myofibrils, glycogen loss,
mitochondrial swelling
2. 0.5-6 hours:
• Gross: None
• Light microscopy: Usually none
variable waviness of fibers at border
• Electron microscopy: sarcolemmal disruption, mitochondrial amorphous
densities

12. 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

13. 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

14. 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

15. 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

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