Why the study?
Postinfarction mechanical complications are rare in the primary PCI era, and the role of persistent Staphylococcus aureus bacteremia in silent cardiac rupture is not well characterized.
Persistent Staphylococcus aureus bacteremia after myocardial infarction warrants structured echocardiographic surveillance to detect silently evolving mechanical complications.
May prompt vigilance for silent contained rupture in immunosuppressed post-MI patients with bacteremia; hypothesis-generating and should not yet change practice.
BACKGROUND: Postinfarction mechanical complications are rare in the primary percutaneous coronary intervention era. We report a silent, contained left ventricular free wall rupture driven by persistent staphylococcal bacteremia in an immunomodulated patient. CASE SUMMARY: A 64-year-old man with active ulcerative colitis on corticosteroids and vedolizumab presented with an anterior ST-segment elevation myocardial infarction, complicated by early stent thrombosis. He developed persistent Staphylococcus aureus bacteremia; transesophageal echocardiography excluded endocarditis. Although clinically stable, routine echocardiography on postinfarction day 24 detected a silent contained free wall rupture. Surgery revealed hemato-purulent pericardial effusion with culture-confirmed Saureus. After initial recovery, a ventricular septal defect developed, requiring percutaneous closure. The patient died 2 months postinfarction. DISCUSSION: To our knowledge, this is the first antemortem diagnosis of sequential postinfarction mechanical complications driven by confirmed staphylococcal infection of necrotic myocardium without endocarditis. TAKE-HOME MESSAGES: Persistent Saureus bacteremia after infarction warrants comprehensive evaluation beyond endocarditis. Structured echocardiographic surveillance can detect silently evolving mechanical complications.
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Neuhalfen et al. (2026) studied this question.
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