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Introduction: Sepsis is common and associated with high morbidity and mortality; novel prognostic biomarkers are needed. The association of myocardial injury with mortality in sepsis has not been fully characterized. Hypothesis: We hypothesized that elevated plasma high-sensitivity troponin I (hs-TnI) would be associated with 60-day mortality in patients with sepsis and acute respiratory distress syndrome (ARDS). Methods: We conducted a retrospective multicenter cohort study of subjects from the MI-ARDS study with ARDS and sepsis. The exposure variable was plasma hs-TnI on intubation (Day 0) and Day 3. Hs-TnI was measured using Abbott Laboratories’ ARCHITECT STAT assay. Patients were divided into four hs-TnI (ng/L) groups (Grp): GrpA: <2 (undetectable), GrpB: ≥2-<26 (<99 th percentile of population), GrpC: ≥26-<130 (<5 times upper limit of normal [ULN]), GrpD: ≥130 (>5 times ULN). The primary outcome was 60-day mortality. We determined the association between hs-TnI and mortality using Cox proportional hazards models. Results: Of 320 subjects, there were 15 (4%) in GrpA, 97 (30%) in GrpB, 88 (28%) in GrpC, and 120 (38%) in GrpD. Mean age was 50 years and 172 subjects (54%) required vasopressors. Higher plasma levels of hs-TnI were associated with higher SOFA score and creatinine, and more vasopressor use. Overall mortality was 33%. There was no significant difference in 60-day survival between clinical categories of Day 0 hs-TnI (Fig 1-A). Rising troponin between Day 0 and Day 3 was associated with a higher risk of mortality after adjusting for age, sex, trial assignment, and SOFA score (HR: 1.75, CI: 1.11-2.77, p=0.02) (Fig 1-B), and additionally adjusting for Day 0 hs-TnI (HR: 1.72, CI: 1.03-2.85, p=0.04). Conclusions: Initial hs-TnI in patients with sepsis and ARDS was not associated with mortality. Increase in hs-TnI of at least 20% by Day 3 was associated with 60-day mortality. Future studies should assess mechanism and treatment of myocardial injury in sepsis.

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Case Presentation: A 42-year-old male with a past medical history of recurrent myopericarditis treated with a combination of NSAIDs, colchicine, and steroids presented for left-sided chest pain. The pain first recurred when he attempted a prednisone taper and he was started on Anakinra. Upon presentation, physical examination and laboratory findings were within normal limits. Echocardiography and electrocardiogram were within normal limits. Cardiac magnetic resonance imaging (CMR) showed transmural enhancement of the basal-mid inferolateral segments and patchy mid-myocardial enhancement in the basal-mid anterolateral segments. Nuclear medicine PET showed FDG uptake in the basal anteroseptal, anterolateral, inferolateral, inferior, and apical segments suggestive of active inflammation. Initially, the diagnosis was thought to be recurrent myopericarditis of unknown etiology. Subsequent right heart catheterization with endomyocardial biopsy (EMB) showed mononuclear infiltrates in the interstitium associated with myocyte infiltration and focal moderate interstitial fibrosis. Due to his clinical, imaging, and pathologic findings, he was diagnosed with lymphocytic myocarditis. His anti-inflammatory therapy regimen was reinstated, and he was started on Mycophenolate Mofetil. On follow-up, the patient had significant symptomatic improvement. Discussion: Lymphocytic myocarditis is a pattern of myocardial inflammation that is typically associated with autoimmune and idiopathic causes. Myocarditis frequently manifests with signs and symptoms of heart failure, including chest pain, dyspnea, and arrhythmias. Diagnosis of myocarditis is often supported by CMR and FDG-PET findings, however, EMB is the gold standard for the diagnosis of myocarditis. Treatment is generally supportive, though immunomodulatory therapies have gained increased popularity due to benefits in treating symptoms and preventing complications of heart failure.

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