Autopsy of a patient who died 4 days after an acute MI shows a large area of yellow-tan softened myocardium surrounded by a hyperaemic border with neutrophilic infiltration giving way to macrophage infiltration. Coagulative necrosis is confirmed. Which temporal event in the pathologic healing sequence corresponds to peak risk of free wall rupture?
- A Hours 1–4 — peak contraction band necrosis before neutrophilic infiltration
- B Days 10–14 — granulation tissue formation causing focal weak zones
- C Weeks 6–8 — dense scar contraction producing mechanical stress at the scar border
- D Days 3–7 — maximal macrophage-mediated removal of necrotic myocytes with degradation of extracellular matrix before collagen deposition (the 'softening phase') ✓
Explanation
Free wall rupture (and papillary muscle rupture and ventricular septal defect) is most common between days 3 and 7 post-MI. During this interval, macrophages aggressively phagocytose necrotic debris and release matrix metalloproteinases (MMPs) that degrade the collagen ECM of the infarcted wall. Simultaneously, new collagen has not yet been deposited (granulation tissue with fibrous scarring begins around days 7–10). This 'enzymatic softening' or macrophage lysis phase creates the weakest point in the ventricular wall, predisposing to rupture. Contraction band necrosis occurs in reperfused infarcts (hours to days) but is not the peak rupture period; dense scar is the end-stage and is actually mechanically strong.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.