Myocarditis

doi:10.1016/S0140-6736(11)60648-X

The Lancet

Volume 379, Issue 9817, 25 February–2 March 2012, Pages 738-747

https://doi.org/10.1016/S0140-6736(11)60648-X Get rights and content

Summary

Myocarditis is an underdiagnosed cause of acute heart failure, sudden death, and chronic dilated cardiomyopathy. In developed countries, viral infections commonly cause myocarditis; however, in the developing world, rheumatic carditis, Trypanosoma cruzi, and bacterial infections such as diphtheria still contribute to the global burden of the disease. The short-term prognosis of acute myocarditis is usually good, but varies widely by cause. Those patients who initially recover might develop recurrent dilated cardiomyopathy and heart failure, sometimes years later. Because myocarditis presents with non-specific symptoms including chest pain, dyspnoea, and palpitations, it often mimics more common disorders such as coronary artery disease. In some patients, cardiac MRI and endomyocardial biopsy can help identify myocarditis, predict risk of cardiovascular events, and guide treatment. Finding effective therapies has been challenging because the pathogenesis of chronic dilated cardiomyopathy after viral myocarditis is complex and determined by host and viral genetics as well as environmental factors. Findings from recent clinical trials suggest that some patients with chronic inflammatory cardiomyopathy have a progressive clinical course despite standard medical care and might improve with a short course of immunosuppression.

Introduction

Myocarditis refers to the clinical and histological manifestations of a broad range of pathological immune processes in the heart. Alterations in the number and function of lymphocyte subsets and macrophages and antibody-mediated injury are typically found in patients with acute and chronic myocarditis. The immune reaction in the heart causes structural and functional abnormalities in cardiomyocytes, which in turn leads to regional or global contractile impairment, chamber stiffening, or conduction system disease. Patients with acute myocarditis often present with non-specific symptoms of chest pain, dyspnoea, or palpitations; however, sometimes acute viral myocarditis can cause cardiac damage without symptoms, and the risk of chronic dilated cardiomyopathy (DCM) in this setting is uncertain. Immune-mediated cardiac injury and dysfunction can also occur in chronic myocarditis.

Section snippets

Classification

Myocarditis can be classified by cause, histology, immunohistology, and clinicopathological and clinical criteria (panel, figure 1). From each categorisation, the treating clinician should consider what information will provide unique prognostic and therapeutic information in a given clinical scenario. For example, assessment of left ventricular function in acute myocarditis is useful because more severe ventricular dysfunction is associated with greater risk of death or need for heart

Cause

Myocarditis can result from a wide spectrum of infectious pathogens, including viruses, bacteria, chlamydia, rickettsia, fungi, and protozoans, as well as toxic and hypersensitivity reactions. Viruses are the infectious pathogens most frequently implicated in reports of acute myocarditis. In the 1950s and 1960s, experimental and later seroepidemiological studies linked enteroviruses, particularly group B Coxsackie viruses, to myocarditis.29, 30 In the 1980s, molecular techniques, including PCR,

Pathogenesis

Myocarditis results from the interaction of an external environmental trigger with the host's immune system. The availability of murine enteroviral models of myocarditis has facilitated much of our understanding of the disorder.56, 57 From the pathophysiological point of view, the disease can be conceptually divided into three phases: (1) acute viral, (2) subacute immune, and (3) chronic myopathic.

Diagnosis

When myocarditis is suspected, more common causes of cardiovascular disease, such as atherosclerotic and valvular heart disease, should be excluded according to present American Heart Association (AHA), American College of Cardiology Foundation (ACCF), European Society of Cardiology (ESC), and Heart Failure Society of America (HFSA) guidelines.65, 66, 67

In patients with clinically suspected acute myocarditis, confirmatory testing usually begins with serum biomarkers. Troponin 1 was raised in

Possible subclinical acute myocarditis

The optimum management strategy for patients who have a rise in troponin concentrations or ECG changes suggestive of myocarditis or myopericarditis without cardiovascular symptoms is not known. These patients are often encountered during a medical assessment for non-cardiovascular disorders such as a flu-like illness. The short-term prognosis of possible subclinical acute myocarditis is good, but the long-term consequences are unknown. If ventricular function is normal, a reasonable therapeutic

Summary

The aim of this Seminar was to provide a clinical classification and guidelines for the assessment and treatment of suspected myocarditis in medical environments and epidemiological research where biopsy is unfeasible at present. We have emphasised the strengths and limitations of non-invasive methods such as echocardiography and cardiac MRI. Recently, several clinical scenarios in which EMB results added unique prognostic data or guide therapy have been defined. Therefore, we recommend that

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Elucidation for the pharmacological effects and mechanism of Shen Bai formula in treating myocardial injury based on energy metabolism and serum metabolomic approaches
2024, Journal of Ethnopharmacology
Shen Bai formula (SBF) is a proven effective traditional Chinese medicine for treating viral myocarditis (VMC) sequelae in clinic, and myocardial injury is the pathological basis of VMC sequelae. However, the pharmacological action and mechanism of SBF have not been systematically elucidated.
In present research, the doxorubicin-induced myocardial injury rat model was used to evaluate the efficacy of SBF, and energy metabolism and metabolomics approaches were applied to elucidate the effects of SBF on myocardial injury.
Through energy metabolism measurement system and UPLC-Q-TOF-MS/MS oriented blood metabolomics, directly reflected the therapeutic effect of SBF at a macro level, and identified biomarkers of myocardial injury in microcosmic, revealing its metabolomic mechanism.
Results showed that SBF significantly improved the electrocardiogram (ECG), heart rate (HR), extent of myocardial tissue lesion, and ratio of heart and spleen. In addition, the serum levels of AST, CK, LDH, α-HBDH, cTnI, BNP, and MDA decreased, whereas SOD and ATP activity and content increased. Moreover, SBF increased locomotor activity and basic daily metabolism in rats with myocardial injury, restoring their usual level of energy metabolism. A total of 45 potential metabolomic biomarkers were identified. Among them, 44 biomarkers were significantly recalled by SBF, including representative biomarkers arachidonic acid (AA), 12-HETE, prostaglandin J₂ (PGJ₂), 15-deoxy-Δ-12,14-PGJ₂, 15-keto-PGE₂, 15(S)-HPETE, 15(S)-HETE, 8,11,14-eicosatrienoic acid and 9(S)-HODE, which involved AA metabolism, biosynthesis of unsaturated fatty acids and linoleic acid metabolism.
We successfully replicated a myocardial injury rat model with the intraperitoneal injection of doxorubicin, and elucidated the mechanism of SBF in treating myocardial injury. This key mechanism may be achieved by targeting action on COX, Alox, CYP, and 15-PGDH to increase or decrease the level of myocardial injury biomarker, and then emphatically interven in AA metabolism, biosynthesis of unsaturated fatty acids and linoleic acid metabolism, and participate in regulating purine metabolism, sphingolipid metabolism, primary bile acid biosynthesis, and steroid hormone synthesis.
Blood transcriptome analysis uncovered COVID-19–myocarditis crosstalk
2024, Microbial Pathogenesis
The condition of COVID-19-related myocarditis has emerged as a prominent contributor to COVID-19 mortality. As the epidemic persists, its incidence continues to rise. Despite ongoing efforts, the elucidation of COVID-19-related myocarditis underlying molecular mechanisms still requires further investigation.
Hub genes for COVID-19-related myocarditis were screened by integrating gene expression profile analysis via differential expression in COVID-19 (GSE196822) and myocarditis (GSE148153 and GSE147517). After verification with independent datasets (GSE211979, GSE167028, GSE178491 and GSE215865), the hub genes were studied using a range of systems-biology approaches, such as ceRNA, TF-mRNA networks and PPI networks, as well as gene ontology, pathway enrichment, immune infiltration analysis and drug target identification.
TBKBP1 and ERGIC1 were identified as COVID-19-related myocarditis hub genes via integrated bioinformatics analysis. In addition, receiver operating characteristic curves constructed based on the expression levels of TBKBP1 and ERGIC1 could effectively distinguish healthy control individuals from patients with COVID-19. Functional enrichment analysis suggested several enriched biological pathways related to inflammation and immune response. Immune cell changes correlated with TBKBP1 and ERGIC1 levels in patients with COVID-19 or patients with COVID-19 and myocarditis. Tamibarotene, methotrexate and theophylline were identified as a potential drug targeting TBKBP1 and ERGIC1.
TBKBP1 and ERGIC1 were identified as crucial genes in the development of COVID-19-related myocarditis and have demonstrated a strong association with innate antiviral immunity. The present work may be helpful for further investigation of the molecular mechanisms and new therapeutic drug targets correlated with myocarditis in COVID-19.
Paradigm shift in myocarditis treatment
2024, Journal of Cardiology
Although most cases of myocarditis are self-limiting with a gradual improvement in cardiac function, the involvement of myocarditis in sudden cardiac death among children and young adults remains substantial, with rates of 3–17 % and 8.6–12 %, respectively. Moreover, the risk of developing chronic dilated cardiomyopathy ranges from 21 % to 30 % in all cases confirmed by biopsy. Current therapeutic strategies for myocarditis and its complications range from standard supportive care for heart failure and arrhythmias to etiologically oriented, case-based therapeutic options. For example, immunosuppression is indicated only in certain forms of acute myocarditis with clinical or endomyocardial biopsy evidence of immune checkpoint inhibitor-induced myocarditis and autoimmune diseases, including giant cell myocarditis, eosinophilic myocarditis, vasculitis, or cardiac sarcoidosis. However, our views on myocarditis treatment have changed considerably over the past two decades, thanks to the emergence of regenerative cells/tissues as well as drug and gene delivery systems. Cell-based therapies are now growing in popularity in any field of medicine. Studies evaluating the therapeutic efficacy of different stem cells in the treatment of acute myocarditis and its chronic complications have shown that although the experimental characteristics varied from study to study, in general, these strategies reduced inflammation and myocardial fibrosis while preventing myocarditis-induced systolic dysfunction and adverse remodeling in animal models.
Myocarditis: A multi-omics approach
2024, Clinica Chimica Acta
Myocarditis, an inflammatory condition of weakened heart muscles often triggered by a variety of causes, that can result in heart failure and sudden death. Novel ways to enhance our understanding of myocarditis pathogenesis is available through newer modalities (omics). In this review, we examine the roles of various biomolecules and associated functional pathways across genomics, transcriptomics, proteomics, and metabolomics in the pathogenesis of myocarditis. Our analysis further explores the reproducibility and variability intrinsic to omics studies, underscoring the necessity and significance of employing a multi-omics approach to gain profound insights into myocarditis pathogenesis. This integrated strategy not only enhances our understanding of the disease, but also confirms the critical importance of a holistic multi-omics approach in disease analysis.
Sex differences in myocarditis hospitalizations: Rates, outcomes, and hospital characteristics in the National Readmission Database; Impact of sex on myocarditis outcomes
2024, Current Problems in Cardiology
Inflammation of the myocardium, or myocarditis, presents with varied severity, from mild to life-threatening such as cardiogenic shock or ventricular tachycardia storm. Existing data on sex-related differences in its presentation and outcomes are scarce. Using the Nationwide Readmission Database (2016–2019), we identified myocarditis hospitalizations and stratified them according to sex to either males or females. Multivariable regression analyses were used to determine the association between sex and myocarditis outcomes. The primary outcome was in-hospital mortality, and the secondary outcomes included sudden cardiac death (SCD), cardiogenic shock (CS), use of mechanical circulatory support (MCS), and 90-day readmissions. We found a total of 12,997 myocarditis hospitalizations, among which 4,884 (37.6 %) were females. Compared to males, females were older (51 ± 15.6 years vs. 41.9 ± 14.8 in males) and more likely to have connective tissue disease, obesity, and a history of coronary artery disease. No differences were noted between the two groups with regards to in-hospital mortality (adjusted odds ratio [aOR] 1.20; confidence interval [CI] 0.93–1.53; P = 0.16), SCD (aOR:1.18; CI 0.84-1.64; P = 0.34), CS (aOR: 1.01; CI 0.85-1.20;P = 0.87), or use of MCS (aOR: 1.07; CI:0.86–1.34; P = 0.56). In terms of interventional procedures, females had lower rates of coronary angiography (aOR: 0.78; CI 0.70-0.88; P < 0.01), however, similar rates of right heart catheterization (aOR 0.93; CI:0.79–1.09; P = 0.36) and myocardial biopsy (aOR: 1.16; CI:0.83–1.62; P = 0.38) compared to males. Additionally, females had a higher risk of 90-day all-cause readmission (aOR: 1.25; CI: 1.16–1.56; P < 0.01) and myocarditis readmission (aOR:1.58; CI 1.02–2.44; P = 0.04). Specific predictors of readmission included essential hypertension, congestive heart failure, malignancy, and peripheral vascular disease. In conclusion, females admitted with myocarditis tend to have similar in-hospital outcomes with males; however, they are at higher risk of readmission within 90 days from hospitalization. Further studies are needed to identify those at higher risk of readmission.
Fatal ventricular arrhythmias in myocarditis: A review of current indications for defibrillator devices
2024, Journal of Cardiology
Historically, patients with myocarditis were considered for implantable cardioverter defibrillator (ICD) utilization only in the chronic phase of the disease following the development of persistent cardiomyopathy refractory to medical therapy or occurrence of a major ventricular arrhythmic event. However, recent literature has indicated that ventricular arrhythmias are frequently reported even in the acute phase of the disease, challenging the long-standing perception that this disease process was largely reversible. Given this changing environment of information, the latest US and European guidelines were recently updated in 2022 to now consider ICD implantation during the acute phase which has significantly increased the number of individuals eligible for these devices. Additionally, several studies with small subgroups of patients have demonstrated a possible benefit of wearable cardioverter defibrillators (WCDs) in this patient demographic. Assuming that larger studies confirm their utility, it is possible that WCDs can assist in detection of ventricular arrhythmias and selection of high-risk candidates for ICD implantation, while providing temporary protection for a small percentage of patients before the development of a major arrhythmic event. This review ultimately serves as a comprehensive review of the most recent guidelines for defibrillator use in acute and chronic myocarditis.
The latest US and European guidelines support ICD use for myocarditis patients following the development of persistent cardiomyopathy refractory to medical therapy or occurrence of a major ventricular arrhythmic event. Previously, patients in the acute phase were excluded from ICD utilization even after experiencing malignant ventricular tachycardia or ventricular fibrillation due to the long-standing perception that this disease process was largely reversible. However, recent literature has indicated that ventricular arrhythmias are frequently reported even in the acute phase of the disease. Additionally, we found that the myocardial damage that is inflicted persists many years after the initial episode. Given this changing environment of information, guidelines were recently updated in 2022 to now consider ICD implantation during the acute phase which has significantly increased the number of individuals eligible for these devices. We support possible ICD utilization for secondary prevention during the acute phase of myocarditis given the elevated risk of arrhythmia recurrence and the fact that any ventricular arrhythmia can induce sudden cardiac death. Future prospective studies are needed to assess which patients may benefit most from early ICD implantation.
WCDs have improved survival in patient populations at high-risk for sudden cardiac death who are not candidates for ICD implantation. After analyzing several recent studies with small subgroups of patients, WCDs appear to demonstrate similar efficacy for myocarditis patients as well. Assuming that larger studies confirm their utility, we believe that WCDs can assist in detection of ventricular arrhythmias and selection of high-risk candidates for ICD implantation. Furthermore, WCDs have the additional benefit of acting as primary prevention by providing temporary protection for a small percentage of myocarditis patients before they develop a major arrhythmic event.

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SeminarMyocarditis

Summary

Introduction

Section snippets

Classification

Cause

Pathogenesis

Diagnosis

Possible subclinical acute myocarditis

Summary

J Allergy Clin Immunol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

Am Heart J

J Am Coll Cardiol

Int J Cardiol

J Infect

Lancet

Cardiovasc Pathol

Heart Failure Clinics

Am J Cardiol

Cell

J Am Coll Cardiol

J Am Coll Cardiol

Am Heart J

J Am Coll Cardiol

J Heart Lung Transplant

Am J Cardiol

J Am Coll Cardiol

J Thorac Cardiovasc Surg

J Thorac Cardiovasc Surg

J Thorac Cardiovasc Surg

J Heart Lung Transplant

J Am Coll Cardiol

Transcriptomic biomarkers for the accurate diagnosis of myocarditis

Circulation

Viral persistence in the myocardium is associated with progressive cardiac dysfunction

Circulation

The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology

Circulation

Elevated serum myosin light chain I in influenza patients

Intern Med

Myocarditis, pericarditis, and dilated cardiomyopathy after smallpox vaccination among civilians in the United States, January–October 2003

Clin Infect Dis

Long-term outcome of fulminant myocarditis as compared with acute (nonfulminant) myocarditis

N Engl J Med

Clinical and demographic predictors of outcomes in recent onset dilated cardiomyopathy. Results of the IMAC (intervention in myocarditis and acute cardiomyopathy)-2 study

J Am Coll Cardiol

Competing risks for death and cardiac transplantation in children with dilated cardiomyopathy: results from the pediatric cardiomyopathy registry

Circulation

Giant cell myocarditis: natural history and treatment

N Engl J Med

Coronary vasospasm as the underlying cause for chest pain in patients with PVB19 myocarditis

Heart

Parvovirus B19 infection mimicking acute myocardial infarction

Circulation

Medical therapy of pericardial diseases: part I: idiopathic and infectious pericarditis

J Cardiovasc Med (Hagerstown)

Endomyocardial biopsy findings in 50 patients with idiopathic atrioventricular block: presence of myocarditis

Jpn Heart J

Chagas myocarditis and syncope

J Cardiovasc Magn Reson

Lyme carditis in children: presentation, predictive factors, and clinical course

Pediatrics

Cardiac sarcoidosis and giant cell myocarditis as causes of atrioventricular block in young and middle-aged adults

Circ Arrhythm Electrophysiol

A clincal and histopathologic comparison of cardiac sarcoidosis and idiopathic giant cell myocarditis

J Am Coll Cardiol

Randomized, placebo-controlled study for immunosuppressive treatment of inflammatory dilated cardiomyopathy: two-year follow-up results

Circulation

Predictors of outcome in patients with suspected myocarditis

Circulation

Immunosuppressive therapy for active lymphocytic myocarditis: virological and immunologic profile of responders versus nonresponders

Circulation

Randomized study of the efficacy of immunosuppressive therapy in patients with virus-negative inflammatory cardiomyopathy: the TIMIC study

Eur Heart J

Study on microbial persistence in end-stage idiopathic dilated

Clin Infect Dis

Seminar
Myocarditis