Myocardial infarction – The Pathology

So far the following dynamic interactions have occurred:

1. severe coronary atheroscleroris

2. acute disruption to the atheromatous plaque  causing an acute change (rupture)  platelet activation leading to superimposed platelet aggregation  intracoronary thrombus overlying the plaque and vasospasm stimulation.

The details of step 2 is presented here:

• platelet aggregation cause release of thromboxane A2, serotonin, platelet factors 3 & 4 – these stimulate vasospasm.

Following an acute MI

• 2 mins after occlusion (REVERSIBLE)

  • loss of aerobic glycolysis, leads to inadequate ATP formation  accumulation of toxic products such as lactic acid. Ischaemia also has impact on contractility  this is lost.

• 15 mins after occlusion (REVERSIBLE)

  • Wrinkled fibres at infarct margin, and also electron microscopy shows mitochondrial swelling

• 15 hrs after occlusion (POINT OF IRREVERSIBLE DAMAGE)

  • Gross: dark mottling appearance, Light microscopy: coagulative necrosis, pyknosis of nuclei, myocyte hypereosinophilia, neutrophil infiltrates.

• 36hrs – 3 days

  • Gross: mottling with yellow-tan infarct centre with haemorrhagic border, Light microscopy: coagulative necrosis with loss of myocyte nuclei + striations, interstitial infiltrate of neutrophils.

• 7 days

  • Gross: maximally yellow tan and soft centre, with depressed red-tan margins, Light microscopy: phagocytosis of dead cells, granulation tissue at margins

• 1-3 wks

  • Gross: gray depressed infarct progresses from border to core of infarct, Light microscopy: granulation tissue with neovascularisation + collage deposition, decreased cellularity.

• > 2 mths:

  • Gross: white scar, Light microscopy: dense collagenous scar

Category: Pathology Notes