Key result
High-dose methylprednisolone resolves acute respiratory failure within ~24 hours and markedly lowers troponin.
Why the study?
Immune checkpoint inhibitor-associated myocarditis is an uncommon but potentially fatal adverse event whose diagnosis is often challenging because its clinical manifestations overlap with more common cardiovascular conditions such as ACS, heart failure, and other treatment-related cardiotoxicities.
Case Report (n=1)
No
Answers are grounded in this paper and cite their sources.
This case highlights the importance of multimodality imaging and prompt high-dose corticosteroid therapy in ICI-associated myocarditis, while identifying a potential temporal association between myocardial injury and reversible lactic acidosis.
Immune checkpoint inhibitor (ICI)-associated myocarditis is an uncommon but potentially fatal immune-related adverse event characterised by high morbidity and mortality despite a relatively low incidence. Diagnosis is often challenging because clinical manifestations overlap with more common cardiovascular conditions, including acute coronary syndrome (ACS), heart failure and other forms of treatment-related cardiotoxicity. Early recognition and prompt immunosuppressive therapy are critical to improving outcomes. A man in his 80s with metastatic human epidermal growth factor receptor 2-positive distal oesophageal adenocarcinoma receiving pembrolizumab, trastuzumab and leucovorin, fluorouracil and oxaliplatin (FOLFOX) chemotherapy presented with acute hypoxaemic respiratory failure and marked myocardial injury. Initial evaluation revealed diffuse pulmonary oedema, high-sensitivity troponin elevation (11 374 ng/L, peaking at 34 066 ng/L), elevated lactate (4.4 mmol/L, peaking at 6.0 mmol/L) and mildly reduced left ventricular systolic function. ACS was initially suspected; however, serial electrocardiograms demonstrated no dynamic ischaemic changes, and transthoracic echocardiography showed only mildly reduced ejection fraction. Cardiac MRI revealed focal subepicardial late gadolinium enhancement and myocardial oedema consistent with acute myocarditis. Given the recent pembrolizumab exposure and exclusion of alternative aetiologies, a diagnosis of ICI-associated myocarditis was established. High-dose methylprednisolone (1000 mg daily for 3 days) was initiated approximately 23 hours after presentation, resulting in rapid clinical improvement, resolution of respiratory failure and marked decline in cardiac biomarkers. Notably, serial lactate levels rose following peak troponin elevation and normalised after corticosteroid therapy, closely paralleling clinical recovery. This case highlights the diagnostic complexity of ICI-associated myocarditis and underscores the importance of multimodality cardiac evaluation and early corticosteroid therapy. In addition, the temporal association between myocardial injury and reversible lactic acidosis raises the possibility that lactate kinetics may serve as a complementary marker of disease activity in severe ICI-associated myocarditis, a finding that warrants further investigation.
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Kim et al. (2026) conducted a case report in Immune checkpoint inhibitor-associated myocarditis (n=1). Methylprednisolone was evaluated on Clinical recovery, high-sensitivity troponin, and whole-blood lactate levels. High-dose methylprednisolone resolved acute respiratory failure within 24 hours, reduced hs-troponin from 34,066 to 7,894 ng/L, and decreased lactate from 6.0 to 2.4 mmol/L.
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