Six weeks after a large transmural inferior MI, a 54-year-old man returns with fever, pleuritic chest pain, arthralgia, and elevated ESR. Pericardial and pleural effusions are present, cultures are sterile, and antimicrobial therapy has produced no benefit. The most likely mechanism is:

• A Progression of the infarct to ventricular aneurysm formation
• B Recurrent thrombotic occlusion of the right coronary artery
• C Seeding of the pericardium during the initial infarction
• D Autoimmune reaction to altered myocardial antigens ✓

Explanation

This is Dressler syndrome, a delayed pericarditis appearing 2 to 10 weeks after infarction, mediated by an autoimmune response against antigenically altered myocardial tissue exposed by necrosis. It responds to anti-inflammatory agents, not antibiotics, and cultures are sterile. Acute fibrinous pericarditis within the first few days is a direct extension of the infarct inflammation, whereas recurrent coronary occlusion would show recurrent ischemic symptoms and rising troponin, and aneurysm formation causes late heart failure and thrombus.

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

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Written and medically reviewed by the StethoPrep medical team.