Fulminant Myocarditis

Foreword
Foreword
Foreword
Preface
Contents
Contributors
1: Introduction: Accumulating More Knowledge and Ability in Treating Fulminant Myocarditis to Save More Lives
References
2: The Epidemiology of Fulminant Myocarditis
2.1 Introduction
2.2 The Incidence of Fulminant Myocarditis
2.3 The Prognosis of Patients with Fulminant Myocarditis
References
3: Pattern Recognition Receptors and Fulminant Myocarditis
3.1 Brief Introduction
3.2 Pattern Recognition Receptors (PRRs)
3.2.1 Membrane-Bound TLRs
3.2.2 TLR1–2 and TLR6
3.2.3 TLR4
3.2.4 TLR5
3.2.5 TLR3 and TLR7-9
3.2.6 TLR10
3.2.7 NLRs
3.2.8 NLRP3 Inflammasome
3.2.9 RLRs
3.2.10 Cytoplasmic DNA Sensors
3.2.11 CLRs
3.2.12 Non-pattern Recognition Receptors
3.2.13 RAGE
3.2.14 PRMs
3.2.15 Myeloid Cells’s Triggering Receptors
3.2.16 G-Protein-Coupled Receptors
3.2.17 Actions of PRRs
3.2.18 Phagocytosis and TLRs
3.2.19 TLR Signaling Pathways
3.3 Pyroptosis and its Pathway
3.3.1 Expression of PRRs and Responses to Ligands in Heart
References
4: Etiology and Pathogenesis of Fulminant Myocarditis
4.1 Etiology of Fulminant Myocarditis
4.1.1 Infectious Factors
4.1.1.1 Enterovirus
4.1.1.2 Adenovirus
4.1.1.3 Parvovirus
4.1.1.4 Human Herpes Virus
4.1.2 Non-infectious Factors
4.2 Pathogenesis of FM
4.3 Laboratory Test
4.3.1 Enterovirus
4.3.2 Adenovirus
4.3.3 Parvovirus
4.3.4 Human Herpes Virus
4.3.4.1 Enzyme-Linked Immunosorbent Assay
4.3.4.2 Flow Cytometry
4.3.4.3 Liquid Cytokine Chip
4.4 COVID-19 Pandemic-Related Etiology
References
5: Pathophysiology and Mechanisms of Fulminant Myocarditis
5.1 Animal Models of Fulminant Myocarditis
5.1.1 Mouse Selection
5.1.2 Virus Selection
5.1.2.1 Modeling Method
5.1.3 Establishment and Evaluation of Common Animal Models of Fulminant Myocarditis
5.2 Cytokine Storm in Fulminant Myocarditis
5.2.1 Interferons
5.2.1.1 Type I Interferon (IFN I)
5.2.1.2 Type II Interferon (IFN II)
5.2.2 Interleukins
5.2.2.1 IL-1 Family
5.2.2.2 IL-2
5.2.2.3 IL-6 Family
5.2.2.4 IL-10
5.2.3 Chemokines
5.2.4 Tumor Necrosis Factor
5.3 Pathogenesis of Cytokine Storm in Fulminant Myocarditis
5.4 Possible Mechanisms of Cytokine Storm-Induced Cardiac Dysfunction
5.5 In the Future
References
6: Pathology of Fulminant Myocarditis
6.1 Overview of the Pathology of Myocarditis and Fulminant Myocarditis
6.1.1 Infectious Myocarditis
6.1.2 Non-infectious Myocarditis
6.2 Pathological Characteristics of Myocarditis of Different Etiologies
6.2.1 Viral Myocarditis
6.2.2 Bacterial Myocarditis
6.2.3 Fungal Myocarditis
6.2.4 Systemic Disease-Associated Myocarditis
6.2.5 Granulomatous Myocarditis
6.2.6 Allergic Myocarditis
6.2.7 Toxic Myocarditis from Snake Venom
6.3 Typical Cases
6.3.1 Case 1
6.3.2 Case 2
6.3.3 Case 3
6.3.4 Case 4
6.3.5 Case 5
References
7: Clinical Manifestations of and Laboratory Tests for Myocarditis and Fulminant Myocarditis
7.1 Clinical Manifestations
7.1.1 Predisposing Factors
7.1.2 Early Symptoms
7.1.2.1 Respiratory Symptoms
7.1.2.2 Gastrointestinal Symptoms
7.1.2.3 Systemic Symptoms
7.1.2.4 Symptoms of Myocardial Damage
7.1.3 Progressive Symptoms
7.1.3.1 Symptoms of Myocardial Damage
Chest Pain and Tightness
Painless Myocarditis
Arrhythmia
7.1.3.2 Hemodynamic Disorder
Acute Heart Failure
Cardiogenic Shock
Adams–Stokes Syndrome
7.1.3.3 Manifestations of Multiple Organ Involvement
7.2 Physical Signs
7.2.1 Vital Signs
7.2.1.1 Fever
7.2.1.2 Hypotension
7.2.1.3 Breathing Changes
7.2.1.4 Heart Rate and Heart Rhythm Changes
7.2.2 Heart-Related Signs
7.2.2.1 Cardiac Size
7.2.2.2 Heart Sounds and Murmurs
7.2.2.3 Cardiac Insufficiency
7.2.3 Lung Signs
7.3 Laboratory Examination
7.3.1 Myocardial Injury Marker Cardiac Troponin I or T (cTnI or cTnT) Assessment
7.3.2 Brain Natriuretic Peptide (BNP) Assessment
7.3.3 Blood Routine Examination
7.3.4 General Biochemical Tests
7.3.5 Coagulation Function Tests
7.3.6 Inflammatory Indicator Assessment
7.3.7 Pathogen Detection
7.3.8 ECG
7.4 Case Reports
References
8: Diagnostic Values and Clinical Application of Endomyocardial Biopsy in Fulmiant Myocarditis
8.1 EMB
8.1.1 Preoperative Preparation
8.1.2 Approach Selection and Equipment Preparation
8.1.3 Several Common EMB Operation Processes
8.1.3.1 Transradial Left Ventricular EMB
8.1.3.2 Transfemoral Left Ventricular EMB
8.1.3.3 Transfemoral Right Ventricular EMB
8.2 Management and Analysis of Myocardial Intimal Tissue
8.2.1 Light Microscopic Examination and Staining of Myocardial Intimal Tissues
8.2.2 Molecular Study of Myocardial Intimal Tissue
8.2.3 Molecular Biological Detection of the Virus Genome in Myocardium Tissue
8.2.4 Immunohistochemistry of the Myocardium
8.3 Clinical Application of EMB in Fulminant Myocarditis
References
9: Association between Histological Changes and Clinical Manifestations of Fulminant Myocarditis
9.1 Lymphocytic Myocarditis
9.1.1 Stage 0 (Pre-Infection Stage)
9.1.2 Stage 1 (Acute Stage)
9.1.2.1 Entry of Virus into Cardiomyocytes
9.1.2.2 Replication of Virus
9.1.2.3 Direct Viral Damage to Cardiomyocytes
9.1.2.4 Host Defense—Innate Immune Response
Interferons
TLRs
RNA Helicases
9.1.2.5 Host Defense–Acquired Immune Response
9.1.2.6 Damage to Host Cells by Host Immune Response
9.1.3 Stage 2 (Subacute Stage)
9.1.4 Stage 3 (Chronic Stage)
9.2 Giant Cell Myocarditis
9.3 Eosinophilic Myocarditis
9.4 Sarcoidosis Myocarditis
9.5 Connective Tissue Disease-Induced Autoimmune Myocarditis
9.6 Immune Checkpoint Inhibitor-Induced Myocarditis
References
10: Changes of Electrpcardiography in Patients with Fulminant Myocarditis
10.1 Mechanism of Arrhythmias in Viral Myocarditis
10.2 Common ECG Findings of Fulminant Myocarditis
10.2.1 Sinus Arrhythmia
10.2.2 Atrial Arrhythmia
10.2.3 Changes in the Cardiac Conduction System
10.3 Arrhythmias and Prognosis of Myocarditis
References
11: Echocardiography in Fulminant Myocarditis
11.1 Introduction
11.2 Two-Dimensional Echocardiography
11.2.1 Left Ventricular (LV) Function
11.2.2 Left Ventricular Dimension and Wall Thickness
11.2.3 Right Ventricular (RV) Function
11.2.4 Pericardial Effusion and Intra-cardiac Thrombus
11.3 Speckle-Tracking Echocardiography (STE)
11.4 Proposed Echocardiographic Scan Protocols
11.5 Utility of Echocardiography in Treating FM with Extracorporeal Membrane Oxygenation (ECMO)
11.6 Prognostic Value of Echocardiographic Measurements in FM
11.7 Conclusions
References
12: Cardiac Magnetic Resonance in Fulminant Myocarditis
12.1 Introduction
12.2 Utility of CMRI in Acute Myocarditis
12.3 Lake Louise Criteria (LCC)
12.4 Novel CMR Mapping Techniques
12.5 Functional Abnormalities
12.6 Pericardial Abnormalities
12.7 Update to the LCC
12.8 Utility of CMRI in FM
12.9 Prognostic Value of CMRI in Myocarditis
12.10 Limitations of CMRI in FM
12.11 Conclusion
References
13: Diagnosis and Differential Diagnosis of Fulminant Myocarditis
13.1 Clinical Diagnosis of Fulminant Myocarditis
13.2 Pathological Classification of Fulminant Myocarditis
13.3 Differential Diagnosis of Fulminant Myocarditis
References
14: Novel Conceptions in Treatments of Fulminant Myocarditis
14.1 New Understanding of Pathophysiology of Fulminant Myocarditis
14.2 Design of Treatment Regimen
14.3 Treatment Regimen
14.4 Life Support Treatment
14.4.1 ECMO
14.4.2 IABP
14.4.3 Percutaneous Left Ventricular Assist Device
14.5 Immunomodulatory Therapy
14.5.1 Intravenous Gamma Globulin
14.5.2 GCs
14.5.3 Cytotoxic Immunosuppressive Drugs
14.5.4 CRRT
14.6 Antiviral Treatment
References
15: Treatments of Fulminant Myocarditis in Acute Phase
15.1 Treatment in Acute Phase: Core Treatments
15.2 Mechanical Circulation Support
15.3 Immunomodulation Therapy
15.4 Administration of Neuraminidase Inhibitors and Antiviral Drugs
15.5 Assessment of Treatment Effects
15.6 Auxiliary Care
References
16: Prevention and Treatment of Arrhythmias Complicated by Fulminant Myocarditis
16.1 Prediction and Prevention of Lethal Arrhythmias
16.1.1 Hypotension
16.1.2 Usage of Catecholamines
16.1.3 Long-Term Usage of α-Receptor Agonists
16.1.4 Sustained Shock
16.1.5 Prolonged QRS Interval
16.1.6 Female Patients
16.1.7 Hypokalemia
16.1.8 Hypoxemia
16.2 Treatments to Bradyarrhythmia
16.2.1 Drug Treatment
16.2.2 Temporary Pacemaker
16.3 Tachycardia
16.3.1 Electrolytes Management
16.3.2 Monitor the QTc Interval
16.3.3 Anti-arrhythmia Drugs
16.3.4 Electrical Cardioversion
16.3.5 Electrical Storms
16.3.6 Traditional Chinese Medicine
References
17: Prevention and Treatment of Disseminated Intravascular Coagulation in Fulminant Myocarditis
17.1 Etiology of DIC Secondary to Fulminant Myocarditis
17.2 Pathogenesis of DIC Secondary to Fulminant Myocarditis
17.2.1 Activation of the Coagulation System
17.2.2 Fibrinolysis Dysfunction
17.3 Factors Affecting the Occurrence and Development of DIC
17.3.1 Impaired Function of the Monocyte-Macrophage System
17.3.2 Severe Liver Dysfunction
17.3.3 Hypercoagulative State of the Blood
17.3.4 Microcirculation Disturbance
17.4 Main Clinical Manifestations of DIC Secondary to Fulminant Myocarditis
17.5 Treatment of DIC Secondary to Fulminant Myocarditis
References
18: Rehabilitation Treatment for Myocarditis
18.1 Overview
18.2 Cardiac Rehabilitation
18.2.1 Cardiac Assessment
18.3 Five Prescriptions for Cardiac Rehabilitation
References
19: Follow-Up and Long-Term Prognosis of Myocarditis and Fulminant Myocarditis
19.1 Histopathological Type and Prognosis
19.2 Clinical Manifestations and Prognosis
19.3 Clinical Treatment and Prognosis
19.4 Follow-Up of Fulminant Myocarditis Patients
References
20: Clinical Nursing for Patients with Fulminant Myocarditis
20.1 Basic Nursing
20.1.1 Pressure Ulcer Prevention
20.1.2 Keeping Warm
20.1.3 Continuous Monitoring
20.2 Nursing of Life-Support Devices
20.2.1 ECMO
20.2.1.1 Catheter Care
20.2.1.2 The Monitoring of ECMO Patients
Speed and Flow Rate
Oxygenation Monitor
Gas Management
Pressure Monitor
Temperature Management
Volume Management
Anticoagulation Monitor
Indicators for Weaning ECMO [11–13]
20.2.2 IABP
20.2.2.1 Effective Trigger
20.2.2.2 Continuous Observation
20.2.2.3 Catheter Care
20.2.2.4 Surveil Anticoagulant
20.2.2.5 Indicators for Weaning IABP [17, 18]
20.2.2.6 Care After Weaning IABP
20.2.3 Care for Temporary Pacemaker
20.2.4 Care for Invasive Ventilator
20.2.4.1 Respirator-Assisted Ventilation
20.2.4.2 Tracheal Cannula
20.2.4.3 Mechanical Ventilation
20.2.4.4 Respiratory Tract Nursing
20.2.5 CRRT Nursing
20.2.5.1 CRRT Mode [42]
20.2.5.2 Vascular Access
20.2.5.3 Parameters Setting
20.2.5.4 Anticoagulation for CRRT
20.2.5.5 Commencing Treatment
20.2.5.6 Volume Management
20.2.5.7 Disconnection
20.2.5.8 Supplement
20.3 Nursing of Drug Therapy
20.4 Nursing of Complications
20.5 Rest and Nutrition
20.6 Psychological Nursing
References
21: Introduction of Clinical Courses of Typical Cases of Fulminant Myocarditis (Including Six Cases)
21.1 Typical Case 1
21.1.1 Clinical Features
21.1.1.1 Chief Complaint
21.1.1.2 Present Medical Information
21.1.1.3 Medical History
21.1.1.4 Physical Examination
21.1.2 Diagnosis
21.1.3 Physical Examination and Tests
21.1.3.1 Day 1 of Admission
Bedside Echocardiography
Laboratory Tests
Treatments and Course After Admission
21.1.3.2 Day 2 of Admission
Bedside Ultrasound Examination
21.1.3.3 Day 3 of Admission (Fig. 21.6)
21.1.3.4 Days 4–7 of Admission
21.1.4 Variation Trend of the Main Indicators During Admission
21.1.5 Case Review
21.2 Typical Case 2
21.2.1 The Clinical Features
21.2.1.1 Chief Complaint
21.2.1.2 Present Medical History
21.2.1.3 Past Medical History
21.2.1.4 Physical Examination
Laboratory Tests
21.2.2 Diagnosis
21.2.3 Treatment
21.2.3.1 Bedside Echocardiography
21.2.3.2 Day 2 After Admission
21.2.3.3 Physical Examination
Laboratory Tests
Bedside Echocardiography (10 a.m., Feb 7, 2019)
21.2.3.4 3–5 Days After Admission
21.2.3.5 Holter 1 Week After Admission
21.2.4 Variation Trend of Main Biomarkers and Cardiac Function During Treatments (Figs. 21.14, 21.15, and 21.16)
21.2.5 Comments
21.3 Typical Case 3
21.3.1 Clinical Features
21.3.1.1 Chief Complaint
21.3.1.2 Present Medical History
21.3.1.3 Past Medical History
21.3.1.4 Physical Examination
21.3.1.5 Examination and Laboratory Tests
21.3.2 Diagnosis
21.3.3 Treatment
21.3.3.1 Day 1
21.3.3.2 Bedside Echocardiography
21.3.3.3 2 Days After Admission
21.3.3.4 Days 3–5
21.3.3.5 6 Days After Admission: Before Discharge
21.3.4 Variation Trend of Primary Indicators During Admission
21.3.5 Comments
21.4 Typical Case 4
21.4.1 Comments
21.5 Typical Case 5
21.5.1 The Clinical Features
21.5.1.1 Chief Complaint
21.5.1.2 Present Medical History
21.5.1.3 Past Medical History
21.5.1.4 Physical Examination
21.5.1.5 Examination (Fig. 21.22)
21.5.2 Diagnosis
21.5.3 Treatment
21.5.3.1 Day 1 After Admission
Bedside Echocardiography
21.5.3.2 On the Second Day of Hospital
Ambulatory ECG
21.5.3.3 The Third Day of Admission
21.5.3.4 Day 4–7 of Admission
21.5.3.5 Day 8 of Admission
21.5.3.6 Echocardiography Diagnosis After 1 Week: Reduced Left Ventricular Systolic Function
21.5.3.7 The Ninth Day of Admission
21.5.3.8 On the Tenth Day of Admission
21.5.4 Variation Trend of Main Indicators During Admission
21.5.5 Comments
21.6 Typical Case 6
21.6.1 Comments
Appendix A: Chinese Expert Consensus Statement on the Nursing Strategies of Adult Fulminant Myocarditis
Consensus
Formulation
Application Scope
Clinical Evaluation and Treatments
Definition
Etiology
Symptoms
Treatments
Symptomatic and Supportive Treatment
Anti-viral and Immunomodulating Therapy
Mechanical Circulatory Support
Contents of the Consensus
Early Assessment and Dynamic Monitoring
Intravenous Treatment and Medication Nursing
Intravenous Treatment
Medication Nursing
Life Support Nursing
Application Time
Circulatory Support Nursing
Respiratory Support Care
Continuous Renal Replacement Therapy (CRRT) Care
Catheter Management
Anticoagulation Management
Common Complications Prevention and Care
Arrhythmia
Hemorrhage and Thrombosis Care
Infection
Hemolysis
Lower Extremity Arterial Ischemia
Brain Injury
Rehabilitation Strategy
Exercise Rehabilitation
Nutrition Rehabilitation
Psychological Rehabilitation
Health Instruction and Follow-Up
Professional Team Management
Appendix B: Actively Promote and Apply the China’s Regimen for Treatments of Fulminant Myocarditis to Save More Lives
Diagnosis and Treatment Status at Home and Abroad
Core Content of the Chinese Regimen
Features of the Chinese Regimen