A 55-year-old diabetic man undergoes coronary angioplasty for an acute STEMI. Following reperfusion of the ischemic myocardium, pathology shows focal hypercontraction bands, mitochondrial swelling, and calcium overload in previously ischemic myocytes despite restoration of flow. This is best described as:
- A Coagulative necrosis — irreversible cell injury from ischemia preceding reperfusion
- B Contraction band necrosis due to massive catecholamine surge from cardiac failure
- C Apoptosis — activated by Bcl-2 downregulation during ischemia-reperfusion
- D Ischemia-reperfusion injury — lethal reperfusion injury in cells sublethally injured during ischemia ✓
Explanation
Ischemia-reperfusion (I/R) injury occurs when oxygen delivery resumes to ischemic (but not yet irreversibly injured) cells. The sudden influx of oxygen generates reactive oxygen species (superoxide via xanthine oxidase), mitochondrial permeability transition pore (mPTP) opening is triggered by calcium overload, and hypercontraction bands form from uncontrolled myofibril contraction when ATP is restored in the presence of elevated calcium. This 'lethal reperfusion injury' kills cells that survived ischemia. While contraction band necrosis is the morphological feature of I/R injury, it can also occur in catecholamine storm but the clinical scenario points to reperfusion as the cause.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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