# Differential Diagnosis between Sintilimab-related Autoimmune Myocarditis and Acute Myocardial Infarction

**Authors:** Yihe Wu, Jiayun Nian, Hongxu Liu, Xiaolei Lai, Zihao Liu, Tengfei Li, Shenglei Qiu

PMC · DOI: 10.1186/s12575-025-00267-4 · 2026-03-03

## TL;DR

This paper explores how to distinguish sintilimab-related autoimmune myocarditis from heart attacks, focusing on clinical features and diagnostic methods.

## Contribution

The paper provides key differential diagnosis criteria for sintilimab-related autoimmune myocarditis versus acute myocardial infarction.

## Key findings

- Sintilimab-related autoimmune myocarditis commonly affects elderly men aged 60–75 years.
- Non-specific symptoms like chest tightness and palpitations are common, with elevated cardiac biomarkers and ECG changes.
- Coronary angiography and cardiovascular magnetic resonance aid in diagnosis and differential diagnosis.

## Abstract

To analyze the regularities and clinical features of sintilimab-related autoimmune myocarditis, and to summarize the differential diagnosis key points between sintilimab-related autoimmune myocarditis and acute myocardial infarction.

The case reports about sintilimab-related autoimmune myocarditis were searched on databases from the establishment of the database to April 1st 2024. The relevant medical records were searched on the hospital information system of Beijing Hospital of Traditional Chinese Medicine in the past 3 years. The case reports and medical records were collected for statistical analysis.

Twenty three cases were collected including 22 case reports and 1 case record. Most of the sintilimab-related autoimmune myocarditis were in elderly men aged 60–75 years old and occurred between the end of the first dose of treatment to the beginning of the second dose. The symptom was nonspecific such as chest tightness and palpitation, sometimes with symptom of myasthenia as muscle weakness or myositisand as muscle soreness. Elevated cardiac biomarkers and changes in electrocardiogram were common, and decreased left ventricular ejection fraction was rarely seen in echocardiography. 9 cases underwent coronary angiography or computed coronary tomography angiography, and 3 cases underwent cardiovascular magnetic resonance.

The manifestations of sintilimab-related autoimmune myocarditis are not specific. The medication history and concomitant symptoms are of warning value. Coronary angiography or coronary computed coronary tomography angiography can be helpful when ruling out acute myocardial infarction. Cardiovascular magnetic resonance and myocardial biopsy can confirm the diagnosis. Cardiac biomarkers and the electrocardiogram can assist in diagnosis and prognosis assessment.

## Linked entities

- **Diseases:** autoimmune myocarditis (MONDO:0022519), acute myocardial infarction (MONDO:0004781)

## Full-text entities

- **Genes:** CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, CLEC3B (C-type lectin domain family 3 member B) [NCBI Gene 7123] {aka MCDR4, TN, TNA}, CD274 (CD274 molecule) [NCBI Gene 29126] {aka ADMIO5, B7-H, B7H1, PD-L1, PDCD1L1, PDCD1LG1}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}, MB (myoglobin) [NCBI Gene 4151] {aka MYOSB, PVALB}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}
- **Diseases:** ACS (MESH:D000168), atrioventricular block (MESH:D054537), ptosis (MESH:C564553), infection (MESH:D007239), cardiac adverse reactions (MESH:D002318), AMI (MESH:D009203), cerebral infarction (MESH:D002544), myocardial ischemia (MESH:D017202), Cardiac death (MESH:D003643), Hypertension (MESH:D006973), atherosclerosis (MESH:D050197), damage of myocardial tissue (MESH:D017695), hepatocellular carcinoma (MESH:D006528), ventricular escape (MESH:D014693), necrosis (MESH:D009336), esophageal cancer (MESH:D004938), Ventricular Tachycardia (MESH:D017180), QT interval prolongation (MESH:D008133), cardiac perforation (MESH:D057112), thymoma (MESH:D013945), muscle injury (MESH:D009135), heart disease (MESH:D006331), coronary artery calcification (MESH:D003324), muscle soreness (MESH:D063806), type 2 diabetes (MESH:D003924), depression (MESH:D003866), sinus tachycardia (MESH:D013616), abdominal infection (MESH:D000007), heart failure (MESH:D006333), lung cancer (MESH:D008175), shortness of breath (MESH:D004417), cancer (MESH:D009369), aortic dissection (MESH:D000784), bundle branch block (MESH:D002037), diabetes (MESH:D003920), muscle weakness (MESH:D018908), CHD (MESH:D003327), Acute Coronary Syndrome (MESH:D054058), inflammatory (MESH:D007249), myasthenia (MESH:D020294), respiratory infection (MESH:D012141), coronary artery stenosis (MESH:D023921), non-small cell lung cancer (MESH:D002289), cardiomyocytes damage (MESH:D020263), cardiotoxic (MESH:D066126), rhythm (MESH:D021081), kidney cancer (MESH:D007680), coronary thrombosis (MESH:D003328), Hodgkin's lymphoma (MESH:D006689), heart rupture (MESH:D006341), conduction block (MESH:D006327), fatigue (MESH:D005221), cachexia (MESH:D002100), dysarthria (MESH:D004401), myositis (MESH:D009220), chest pain (MESH:D002637), Primary diseases (MESH:D009202), hypercoagulability (MESH:D019851), Autoimmune Myocarditis (MESH:D009205), arrhythmia (MESH:D001145)
- **Chemicals:** antilotinib (-), Sintilimab (MESH:C000632826), steroids (MESH:D013256), Anthracyclines (MESH:D018943), Methylprednisolone (MESH:D008775)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12964628/full.md

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Source: https://tomesphere.com/paper/PMC12964628