Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk - Scorecard - MDSpire
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Mechanisms and biomarkers of immune checkpoint inhibitor-associated myocarditis: from T cell imbalance to multicellular crosstalk
Clinical Scorecard: Pathophysiological Mechanisms and Biomarkers of Myocarditis Induced by Immune Checkpoint Inhibitors: Insights into T Cell Dysregulation and Multicellular Interactions
At a Glance
Category
Detail
Condition
Key Mechanisms
T-cell dysregulation, macrophage polarization, and multicellular interactions leading to myocardial inflammation, including cGAS–STING and STAT1/NF-κB pathways.
Target Population
Care Setting
Key Highlights
ICI-MC is a rare but life-threatening toxicity with mortality rates approaching 50%.
Pathogenesis involves α-myosin-driven clonal expansion of cytotoxic CD8+ T cells.
Crosstalk among immune cells amplifies myocardial inflammation.
A five-phase multicellular framework summarizes disease evolution.
Candidate biomarkers and targeted therapies are being explored for precision strategies.
Future studies are needed to refine diagnosis and develop cardioprotective interventions.
Guideline-Based Recommendations
Diagnosis
Management
Implement strategies to mitigate cardiotoxicity associated with ICIs, including corticosteroids.
Monitoring & Follow-up
Risks
Patient & Prescribing Data
Patients with cancer undergoing treatment with immune checkpoint inhibitors.
ICIs can induce myocarditis, necessitating careful monitoring and management.
Clinical Best Practices
Recognize the potential for immune-related adverse events in patients on ICIs, including atypical presentations.
Utilize a multidisciplinary approach involving oncology and cardiology for management.
Stay updated on emerging biomarkers and therapeutic targets for ICI-MC.
