A patient undergoes successful primary angioplasty for an acute myocardial infarction. Histological examination of the reperfused myocardium later shows hypercontracted sarcomeres with transverse bands of densely eosinophilic material crossing the myocytes. What is the underlying mechanism of this lesion?

• A Calcium influx through restored sarcolemmal membranes causing hypercontraction of myofibrils ✓
• B Coagulative necrosis from prolonged ATP depletion before reperfusion
• C Neutrophil-mediated proteolytic digestion of dead myocytes
• D Granulation tissue ingrowth from the endocardial surface

Explanation

Contraction band necrosis is the hallmark of reperfusion injury. On restoration of flow, damaged sarcolemmal membranes allow massive calcium entry, producing hypercontracted sarcomeric segments that appear as transverse eosinophilic contraction bands. Coagulative necrosis without bands reflects irreversible injury before reperfusion, neutrophils dominate at 1 to 3 days as part of inflammation rather than this lesion, and granulation tissue appears only after about a week.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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