A patient dies 10 days after acute myocardial infarction. Autopsy shows a ventricular free wall rupture with haemopericardium. Histologically, the infarcted zone shows maximal neutrophilic infiltration at this timepoint. Which pathological process is responsible for rupture?
- A Calcification of the infarct zone causing brittleness
- B Granulation tissue contraction causing wall thinning
- C Re-occlusion of the culprit vessel causing extension
- D Neutrophil-released metalloproteinases (collagenases) degrading the necrotic myocardium before fibrous replacement ✓
Explanation
Free wall rupture peaks at day 3-7 (range up to 14 days) post-STEMI, corresponding to the phase of maximum collagenolysis by neutrophil-derived MMPs (MMP-1, -2, -9) and macrophage-derived MMPs during the inflammatory removal of necrotic tissue. At this point, dead myocardium lacks structural integrity but has not yet been replaced by fibrous scar — making the wall mechanically weakest. Calcification is a dystrophic change appearing in organized old infarcts. Granulation tissue forms from day 7 onward and actually begins to restore wall strength. Re-occlusion extension is a separate entity from free wall rupture.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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Written and medically reviewed by the StethoPrep medical team.