B71-14 Hypoxia-driven Myocardial Injury Mimicking Acute Coronary Syndrome in Legionella Pneumonia

Abstract Introduction Legionella pneumophila represents an uncommon yet clinically significant cause of community-acquired pneumonia, distinguished by its systemic inflammatory potential. Beyond respiratory compromise, Legionella infection can precipitate secondary myocardial injury through hypoxemia, cytokine surge, and oxygen supply-demand mismatch. Elevated cardiac biomarkers in this context frequently lead to misclassification as acute coronary syndrome (ACS), resulting in unnecessary invasive testing. Differentiating true ischemia from infection-driven myocardial stress is essential for accurate diagnosis and appropriate management. This case highlights how Legionella-associated hypoxia can imitate ischemic myocardial injury and underscores the importance of clinical discernment in interpreting elevated troponin values during severe pneumonia. Case Presentation An 83-year-old African American woman with known coronary artery disease and a history of tobacco use presented with a two-day history of worsening dyspnea. Initial arterial blood gas demonstrated severe hypoxemia, and high-sensitivity troponin I was markedly elevated at 3342 ng/L, decreasing to 1604 ng/L within 24 hours. Electrocardiography revealed no ischemic changes, and mean arterial pressure remained stable at 73 mm Hg. Despite initial improvement on nasal cannula, she developed recurrent desaturation necessitating BiPAP support. Urinary Legionella antigen testing confirmed Legionella pneumophila infection. She was treated with intravenous fluoroquinolone therapy, leading to steady respiratory and biochemical recovery. Planned cardiac catheterization was deferred given the absence of ischemic evidence and improving troponin trend. Discussion Cardiac injury occurs in a significant proportion of patients with severe community-acquired pneumonia and is associated with higher mortality. In this patient, the rapid decline in troponin following antimicrobial therapy, absence of ECG changes, and preserved hemodynamics suggest a Type 2 myocardial infarction secondary to hypoxia rather than coronary plaque rupture. The body’s systemic inflammatory response likely amplified myocardial oxygen imbalance. Recognizing infection-induced myocardial strain is critical, as misinterpretation may prompt unnecessary interventions and delay appropriate management.This case illustrates how severe hypoxemia from pneumonia can mimic acute coronary syndrome and cause marked troponin elevation without ischemia. The distinction between infection-mediated myocardial stress and true ischemic injury has major diagnostic and therapeutic implications. Clinicians should maintain a high index of suspicion for Legionella in elderly or high-risk patients with elevated troponin and pneumonia, ensuring that cardiac workup is guided by clinical context rather than biomarker elevation alone. Early identification and targeted antimicrobial therapy can prevent iatrogenic harm and improve patient outcomes. This abstract is funded by: None