Materiały źródłowe

• #1 Myocarditis: Etiology, Pathogenesis, and Their Implications in Clinical Practice

  https://pmc.ncbi.nlm.nih.gov/articles/PMC10295542/

  Myocarditis is an inflammatory disease of the myocardium caused by infectious or non-infectious agents. It can lead to serious short-term and long-term sequalae, such as sudden cardiac death or dilated cardiomyopathy. […] As it stands, the pathogenesis and etiology of myocarditis is only partially understood. Moreover, the impact of certain clinical features on risk assessment, patient outcomes and treatment options is not entirely clear. […] The understanding of myocarditis has greatly improved in recent years, but many questions still remain to be answered. […] The therapeutic significance and prognostic utility of etiopathogenesis, patients genetic background and mechanisms participating in the immune response are still not entirely understood. […] In this review, we summarize available evidence regarding the etiopathogenesis of myocarditis, as well as discuss how it impacts patient management and outcomes.

• #2 Myocarditis: Etiology, Pathogenesis, and Their Implications in Clinical Practice

  https://www.mdpi.com/2079-7737/12/6/874?type=check_update&version=1

  Myocarditis is an inflammatory disease of the myocardium caused by infectious or non-infectious agents. It can lead to serious short-term and long-term sequalae, such as sudden cardiac death or dilated cardiomyopathy. […] As it stands, the pathogenesis and etiology of myocarditis is only partially understood. Moreover, the impact of certain clinical features on risk assessment, patient outcomes and treatment options is not entirely clear. Such data, however, are essential in order to personalize patient care and implement novel therapeutic strategies. In this review, we discuss the possible etiologies of myocarditis, outline the key processes governing its pathogenesis and summarize best available evidence regarding patient outcomes and state-of-the-art therapeutic approaches. […] The etiopathogenesis of myocarditis is complex as it is caused by a variety of infectious (i.e., viruses, bacteria, fungi, parasites) and non-infectious (i.e., organ-specific or systemic immune-mediated disease, drugs, vaccines, toxins) factors.

• #2 Myocarditis: Etiology, Pathogenesis, and Their Implications in Clinical Practice

  https://www.mdpi.com/2079-7737/12/6/874?type=check_update&version=1

  The understanding of myocarditis has greatly improved in recent years, but many questions still remain to be answered. As it stands, it is unclear why some patients progress to DCM, while others spontaneously recover. The therapeutic significance and prognostic utility of etiopathogenesis, patients’ genetic background and mechanisms participating in the immune response are still not entirely understood. […] In this review, we summarize available evidence regarding the etiopathogenesis of myocarditis, as well as discuss how it impacts patient management and outcomes.

• #3 Republished: Pathogenesis and diagnosis of myocarditis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5813801/

  Acute myocarditis is an inflammatory disease of the heart muscle that may progress to dilated cardiomyopathy and chronic heart failure. […] A number of factors including the sex hormone testosterone, components of innate immunity, and profibrotic cytokines have been identified in animal models as important pathogenic mechanisms that increase inflammation and susceptibility to chronic dilated cardiomyopathy. […] Most of the information about the pathogenesis of myocarditis and DCM comes from animal models rather than human studies. […] In animal models, the progression from acute myocarditis to chronic DCM can be simplified to a three-stage process: phase 1, cardiac injury and activation of the innate immune response; phase 2, acute myocarditis involving components of the innate and acquired immune response; and phase 3 recovery in resistant individuals versus progression to DCM in susceptible individuals.

• #4 Myocarditis – Wikipedia

  https://en.wikipedia.org/wiki/Myocarditis

  Most forms of myocarditis involve the infiltration of heart tissues by one or two types of pro-inflammatory blood cells, lymphocytes and macrophages plus two respective descendants of these cells, NK cells and macrophages. […] The pathophysiology of viral myocarditis is not well understood, but it is believed to involve cardiotropic viruses (viruses with a high affinity for the heart muscle) gaining entry to cardiac muscle cells, usually via binding to a transmembrane receptor. […] Over approximately the next 17 days the virus replicates and causes inflammation leadings to necrosis and apoptosis of cardiac muscle cells (myocytes) and activation of the innate immune system. […] Over the next 14 weeks, viral replication continues with subsequent activation of the acquired immune system leading to T cell infiltration and the formation of antibodies, including possibly auto-antibodies.

• #5 Infectious factors in myocarditis: a comprehensive review of common and rare pathogens | The Egyptian Heart Journal | Full Text

  https://tehj.springeropen.com/articles/10.1186/s43044-024-00493-3

  Myocarditis is a significant health threat today, with infectious agents being the most common cause. Accurate diagnosis of the etiology of infectious myocarditis is crucial for effective treatment. […] Myocarditis can be caused by a multitude of infectious agents (Fig. 1), such as viruses, prokaryotes, parasites, and fungi, as well as by noninfectious triggers including drugs, toxins, and hypersensitivity reactions. Among these drivers, viral infection has been proved to be the most prevalent contributor to myocarditis. […] The pathogenesis of viral myocarditis includes direct injury by viral infection and consequent damage secondary to the hosts immune response. Viruses commonly invade cardiomyocytes through specific receptors and co-receptors to utilize substances from the reservoir cell for their own biosynthesis and replication, which leads to metabolic disruption and even death of the host cell.

• #6 Clozapine-Induced Myocarditis

  https://www.uspharmacist.com/article/clozapineinduced-myocarditis

  The mechanisms behind CIM are not completely understood, but a widely accepted theory is that a directly cardiotoxic metabolite of clozapine forms via altered metabolism and damages myocardial tissue. […] Further exacerbating myocardial injury is the increased blood concentration of catecholamines resulting from clozapine’s inhibition of the norepinephrine transporter. […] Additionally, a type 1 immunoglobulin E-mediated hypersensitivity reaction is responsible for the release of proinflammatory cytokines and inflammatory infiltrates in the heart.

• #7 Myocarditis – Wikipedia

  https://en.wikipedia.org/wiki/Myocarditis

  Over the next few months to years, this process either resolves and concludes with viral clearance or it may progress to cause permanent heart damage such as dilated cardiomyopathy, ventricular dysfunction or other cardiomyopathies. […] The mechanism by which coxsackie B viruses (CBVs) trigger inflammation is believed to be through the recognition of CBV virions by Toll-like receptors. […] The binding of many types of coronaviruses, including the SARS-CoV-2 virus, through ACE2 receptors present in heart muscle may be responsible for direct viral injury leading to myocarditis. […] Hyperactive immune responses in COVID-19 patients may lead to the initiation of the cytokine storm. […] In addition to direct cardiac myocyte (heart muscle cell) damage due to SARS-CoV-2 viral infiltration and inflammation, there are other suspected mechanisms that COVID-19 may indirectly cause myocarditis.

• #8 Republished: Pathogenesis and diagnosis of myocarditis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5813801/

  A number of factors including sex hormones, particularly testosterone, components of innate immunity, and profibrotic cytokines have been identified in animal models as important pathogenic mechanisms that increase inflammation and susceptibility to chronic DCM. […] The incidence and severity of myocarditis and DCM is greater in men than women. […] Studies in animal models of myocarditis show that testosterone drives the inflammation and remodelling that allows progression to DCM. […] Infection is a major source of cardiac injury that activates innate immune mechanisms like Toll-like receptor (TLR) 2 and TLR4 on mast cells and macrophages. […] Innate immunity is a dominant feature during acute myocarditis, where TLR2 and TLR4 levels remain elevated in the heart and induce proinflammatory cytokines like tumour necrosis factor (TNF) and interleukin 1 (IL1).

• #9 Republished: Pathogenesis and diagnosis of myocarditis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5813801/

  A characteristic of the early innate immune response in mice that are susceptible to develop DCM (ie, BALB/c and A/J) is elevated levels of the proinflammatory cytokines TNF and IL1 in the spleen and heart, and higher expression of TLR2 and TLR4 on innate immune cells like mast cells and macrophages. […] TLR2 and TLR4 signalling increase TNF concentrations, and TLR2 acts synergistically with TLR4 to increase IL1 concentrations. […] Cardiac TLR4 mRNA expression has been found to be higher in patients with myocarditis than controls, and to correlate with viral RNA values in the heart. […] Myocarditis patients with active viral replication had higher concentrations of TLR4 that was associated with lower systolic function. […] Mice with defective TLR4 signalling have reduced acute experimental and viral myocarditis and reduced viral replication in the heart, indicating that TLR4 increases susceptibility to infection.

• #10 Republished: Pathogenesis and diagnosis of myocarditis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5813801/

  Thus, data so far suggest that viral specific TLRs like TLR3 and TLR9 reduce acute myocarditis, while TLR2 and TLR4, which increase viral replication and the immune response to infection and damaged self, increase disease. […] Susceptibility in model systems to an elevated innate immune response is dependent on at least two factors: (1) male sex (eg, testosterone); and (2) genetic background (ie, T helper (Th)2 responding BALB/c mice). […] Similar to findings in clinical biopsies of myocarditis patients, the primary infiltrate found in mouse models of acute myocarditis consists of macrophages and neutrophils with lower levels of T cells, B cells, mast cells, and dendritic cells. […] IL1 and IL17 are known to induce cardiac remodelling that leads to fibrosis, DCM, and heart failure following acute myocarditis in mice.

• #11 Spatiotemporal transcriptomics elucidates the pathogenesis of fulminant viral myocarditis | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-025-02143-9

  During the course of the disease, there is a significant inflammatory infiltration in the heart and a drastic increase in a variety of immune cells, especially pro-inflammatory macrophages and T cells. […] The intricate network of immune and cardiac cells, coupled with the cellular, spatial, and dynamic heterogeneity of FM, complicates efforts to elucidate its molecular pathogenesis. […] Our data illuminated the tropism of the virus in cardiac cells, the sequential activation of cardiac structural and immune cells, cell type-specific immune responses, and the transcriptional profiles of cell types involved in circulating immune cell recruitment and inflammatory cytokine production. […] We demonstrated the potent immunomodulatory effects of intravenous immunoglobulin (IVIG), which significantly improved cardiac function in FM patients during clinical treatment.

• #12 Myocarditis pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Myocarditis_pathophysiology

  After the host immune system eliminates the viral genomes from the body, the immune system may remains activated in patients who develop myocarditis. This leads to the development of an autoimmune reaction where T-cells and cytokines target the host tissue such as the myocardium which causes further myocyte damage. […] Cytokines, which are produced in reaction to infection and cell death, are a leading cause of dilated cardiomyopathy. […] Matrix metalloproteinases, such as gelatinase, collagenases, and elastases may also be activated by cytokines during the autoimmune phase. […] Protease produced by coxsackie virus can modify the sarcoglycan complex in myocytes leading to ventricular dilation. […] Eosinophilic infiltration in myocardium lead to release of eosinophilic proteins which increase cellular membrane permeability which in turn leads to cell death. […] The pathogenesis of this hypersensitivity reaction include either an immediate reaction which involves the degranulation of mast cells and basophils mediated by IgE, or a delayed reaction involving the activation of helper T-cells and interleukin-5.

• #13 Myocarditis: Background, Etiology, Pathophysiology

  https://emedicine.medscape.com/article/156330-overview

  Both the innate and adaptive immune systems are dysregulated. The transition from an acute inflammatory response to chronic autoimmune myocarditis often involves molecular mimicry, in which viral antigens resemble self-antigens in the heart (such as myosin), leading to an autoimmune attack against cardiac tissues. […] The persistence of inflammation leads to fibroblast activation, which results in the deposition of collagen and formation of scar tissue within the myocardium. This fibrosis disrupts normal electrical conduction, increases the risk of arrhythmias, and contributes to a stiffer, less compliant myocardium. Over time, the heart undergoes structural remodeling, with LV dilatation and wall thinning. This remodeling compromises systolic and diastolic function, creating a chronic, progressive form of cardiomyopathy.

• #14 Spatiotemporal transcriptomics elucidates the pathogenesis of fulminant viral myocarditis | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-025-02143-9

  Fulminant myocarditis (FM) is a severe inflammatory condition of the myocardium that often results in sudden death, particularly in young individuals. […] Our findings reveal that mesothelial cells play a critical role in the early stage of myocarditis by acting as primary targets for CVB3 infection. This triggers the activation of macrophages, initiating a cascade of inflammation. […] We also identified Cd8+ effector T cells as key mediators of cardiomyocyte injury. These cells release cytotoxic molecules, particularly IFN-, which modulates the expression of Spi1, a factor implicated in exacerbating cardiomyocyte death and amplifying disease progression. […] The pathogenesis of FM involves both direct viral-mediated damage and immune-mediated injury, often referred to as an inflammatory storm.

• #15 Q&A: What Causes Rare Instances of Myocarditis After mRNA COVID-19 Vaccines? < Yale School of Medicine

  https://medicine.yale.edu/news-article/qanda-what-causes-rare-instances-of-myocarditis-after-mrna-covid-19-vaccines/

  its possible testosterone may be involved in vaccine-related myocarditis, but we dont have any proof of it. […] One speculation is based on our thinking about the different organ systems. In our analyses, some of the cells associated with inflammation have signatures consistent with immune molecules that can recognize what we call stress ligands on tissue cells. […] So vaccines, unfortunately, in a subset of people, are causing some inflammation and other adverse events. […] a study from Canada that showed that spacing apart the first and second dose does seem to reduce the risk for developing myocarditis. […] myocarditis after vaccination for the most part appears to be transient, and these patients recover. In comparison, getting COVID could lead to more severe, more prolonged myocarditis.

• #16 Republished: Pathogenesis and diagnosis of myocarditis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5813801/

  Several weeks later in susceptible strains of mice (ie, BALB/c males) a low level inflammation re-emerges that is associated with myocyte necrosis, fibrosis, and DCM. […] TNF and IL1 are elevated in the heart during acute myocarditis in mice and humans and are known to induce myocyte hypertrophy, contractile dysfunction, and myocyte apoptosis, and contribute to extracellular matrix remodellinga step critical in the progression from myocarditis to DCM. […] Profibrotic cytokines like TNF, IL1, IL4, IL17, and transforming growth factor 1 (TGF1) are believed to initiate remodelling during acute myocarditis that results in the appearance of cardiac fibrosis/scar tissue several weeks or months later.

• #17

  https://ucardioj.com.ua/index.php/UJC/article/view/216

  Diagnosis and prognosis of myocarditis course remain one of the most complex and unsolved problems of contemporary cardiology, not only in Ukraine but also in the developed countries of the world. […] In the pathogenesis of impaired cardiac function and its dilation in both acute and chronic stages of myocarditis, the primary role played by immunopathological reactions manifested by autoimmunization and hyperreactivity against the structural elements of the heart muscle. […] The pathogenetic mechanisms of viral myocarditis are based on a complex of factors direct cytotoxic effect of virus on cardiomyocytes, activation of apoptotic processes, as well as reactions of primary and secondary immunity, microvascular lesion, remodeling of the contractile apparatus of the heart muscle. […] The main proinflammatory cytokines produced by immune cells in the inflammation zone are: -interferon, tumor necrosis factor-, interleukin (IL) 1, IL-2, IL-6, IL-17A, IL-23.

• #18

  https://ucardioj.com.ua/index.php/UJC/article/view/216

  Another mechanism of myocardial contraction is associated with the activation of immunopathological responses of the humoral type with the synthesis of cardiospecific antibodies, in particular to the 1-adrenoceptor, cardiac myosin, actin, laminin, vimentin and other structures of the heart muscle. […] A significant role in the pathogenesis of myocarditis is now given to stimulation of Toll-like receptors of type 2 and type 4 and activation of matrix metalloproteinases, which has a direct relationship with the production of proinflammatory cytokines. […] Promising to clarify some of the pathogenetic mechanisms of inflammatory heart damage is currently considered the study of different microRNAs types. […] Currently, the world cardiology community recognizes the relevance of further study of the various mechanisms of myocarditis pathways in order to identify those pathogenetic links, the impact of which can reduce the pathological effect of inflammatory cardiac damage and the severity of the disease and improve prognosis for patients with myocarditis.

• #19

  https://ucardioj.com.ua/index.php/UJC/article/view/216?articlesBySameAuthorPage=2

  Diagnosis and prognosis of myocarditis course remain one of the most complex and unsolved problems of contemporary cardiology, not only in Ukraine but also in the developed countries of the world. […] In the pathogenesis of impaired cardiac function and its dilation in both acute and chronic stages of myocarditis, the primary role played by immunopathological reactions manifested by autoimmunization and hyperreactivity against the structural elements of the heart muscle. […] The pathogenetic mechanisms of viral myocarditis are based on a complex of factors direct cytotoxic effect of virus on cardiomyocytes, activation of apoptotic processes, as well as reactions of primary and secondary immunity, microvascular lesion, remodeling of the contractile apparatus of the heart muscle. […] Another mechanism of myocardial contraction is associated with the activation of immunopathological responses of the humoral type with the synthesis of cardiospecific antibodies, in particular to the 1-adrenoceptor, cardiac myosin, actin, laminin, vimentin and other structures of the heart muscle.

• #20 Cardiac antigen identified as mechanism for heart complication with immunotherapy-related myocarditis | DAIC

  https://www.dicardiology.com/content/cardiac-antigen-identified-mechanism-heart-complication-immunotherapy-related-myocarditis

  Myocarditis is a complication that can occur in cancer patients treated with immune checkpoint inhibitors. […] Now, researchers from Vanderbilt-Ingram Cancer Center have identified the mechanism for the deadly heart inflammation. […] The researchers discovered that T-cells recognizing the cardiac antigen -myosin are the mechanism for this complication, setting the framework to identify biomarkers so at-risk patients can be recognized and medical strategies developed for them to tolerate the immunotherapy. […] The study is the first to identify the role of -myosin in the mechanism of heart complications from immune checkpoint inhibitors. […] Our data show that -myosin is a disease-relevant autoantigen in patients with immunotherapy-related myocarditis. […] While autoreactive T cells are the presumed mechanism for many toxicities to immunotherapies, tracing the condition back to a specific T cell receptor (often unique to each patient) and antigen source (drawing from tens- to hundreds- of thousands of potential antigens in the human body) is a daunting task.

• #21 Myocarditis: Etiology, Pathogenesis, and Their Implications in Clinical Practice

  https://pmc.ncbi.nlm.nih.gov/articles/PMC10295542/

  The pathogenesis of Chagas disease has been extensively studied in animal models and clinical observation. […] The exact mechanisms behind myocardial injury induced by other viruses are not well understood. […] Immune-mediated myocardial injury is suspected to play a major role in the progression of myocarditis. […] The presence of viruses may be cleared from the myocardium, which influences therapeutic approaches available to patients, as treatments for autoimmune myocarditis become an option. […] However, routine use of intravenous immunoglobulin (IVIG) is also not supported by robust evidence, as the results of available meta-analyses are conflicting. […] Immunosuppressive therapy should be modulated on the histological type of myocarditis. […] The utility of anti-heart antibody detection in patients remains unclear. […] The mechanisms responsible for myocardial injury in COVID-19-associated myocarditis are unclear and require further research.

• #22 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-is-Myocarditis.aspx

  Three essential pathways have been implicated in the pathogenesis of myocarditis. Direct myocardial invasion by cardiotropic viruses or other causes of the disease swiftly progresses to the second phase of immunologic activation. The activation of CD4+ T helper cells induces clonal expansion of B cells, resulting in additional myocytolysis, further local inflammation, as well as the production of circulating anti-heart antibodies.

• #23 Pathogenesis of Myocarditis and Inflammatory Dilated Cardiomyopathy: the Sign of Four

  https://jscholarship.library.jhu.edu/items/7038ff39-4717-46df-b480-27299754a9f4

  Myocarditis and inflammatory dilated cardiomyopathy (DCMi) are major causes of heart failure in individuals below the age of 40. In the work presented in this dissertation, using a model of mouse experimental autoimmune myocarditis (EAM) and DCMi, the roles of four pathogenic factors: CD4+ T lymphocytes, interleukin 23 (IL-23), interleukin 17A (IL-17A), and granulocyte macrophage colony-stimulating factor (GM-CSF), are investigated. […] With transgenic IL-23a-/- and IL-17ra-/- mice, we demonstrate that IL-23 drives the pathogenicity of CD4+ T cells and maintains their IL-17A production. IL-17A induces chemokine production by cardiac fibroblasts, resulting in an infiltrate rich in neutrophils and Ly6Chi MO/Ms in the heart, which aggravate disease and lead to worse prognosis. Furthermore, IL-17A directs monocytic infiltrates into an even more inflammatory phenotype by inducing GM-CSF production from cardiac fibroblasts. Taken together, this IL-23 CD4+ T lymphocytes IL-17A GM-CSF axis provides a novel target for the treatment of DCMi and related inflammatory cardiac diseases.

• #24 Myocarditis: Background, Etiology, Pathophysiology

  https://emedicine.medscape.com/article/156330-overview

  In myocarditis related to coronavirus disease 2019 (COVID-19), cardiac inflammation is generally due to direct cardiac invasion with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or a result of the intense cytokine storm that often arises during the course of the disease. […] The pathophysiology of myocarditis involves a complex interplay of immunologic, genetic, and environmental factors that drive myocardial inflammation and the subsequent progression to chronic cardiomyopathy. […] Viral infections are among the most common triggers of myocarditis, with viruses like coxsackievirus, adenovirus, parvovirus B19, and others directly infecting cardiac myocytes. […] The initial viral invasion of heart cells typically elicits an innate immune response, including activation of toll-like receptors (TLRs) on cardiac cells. This response leads to the release of proinflammatory cytokines (eg, TNF-, IL-1, IL-6) and chemokines, which recruit immune cells to the site of infection. If the virus is not efficiently cleared, the ongoing immune response can progress from an acute to a chronic inflammatory phase, often marked by T-cell activation, antibody production, and, in some cases, an autoimmunity-driven attack against cardiac cells.

• #25 COVID-19 and myocarditis: a review of literature | The Egyptian Heart Journal | Full Text

  https://tehj.springeropen.com/articles/10.1186/s43044-022-00260-2

  An alternative way SARS-CoV-2 can cause myocardial damage is via the infection of endothelial cells in the heart. This theory is supported by the discovery of SARS-CoV-2 in endothelial cells of numerous organs, including the heart, under histology. […] Systemic inflammation may also play a role in the development of COVID-19 myocarditis. IL-6 is a cytokine implicated in the pathophysiology of myocarditis, recruiting inflammatory cells to the myocardium. IL-6 is also a primary mediator of the cytokine storm, a life-threatening condition seen in some patients who have developed COVID-19, which is characterized by extreme increases in pro-inflammatory cytokines and an uncontrolled immune response. […] The possible pathophysiology of COVID-19 myocarditis is outlined in Fig. 1.

• #26 Q&A: What Causes Rare Instances of Myocarditis After mRNA COVID-19 Vaccines? < Yale School of Medicine

  https://medicine.yale.edu/news-article/qanda-what-causes-rare-instances-of-myocarditis-after-mrna-covid-19-vaccines/

  Myocarditis is inflammation of the heart muscle. It occurs most commonly after an infection but can also be triggered by other things. […] One is autoimmune myocarditis, which is when the immune cells start to attack our own host cells. This can be serious, because once you generate autoimmune responses, its difficult to revert back to baseline. Our second hypothesis was myocarditis caused by hypersensitivity. This is an allergic response that some people experience after drug toxicity that is demarcated by these cell types known as eosinophils. […] the third hypothesis is the one that we found to be most likely, which is inflammation-related myocarditis. This is immune cell mediated. We found that activated immune cells like cytotoxic killer cells and myeloid cells are elevated in these patients, which appears to suggest that mRNA vaccine-associated myocarditis is the most consistent with being inflammatory cell-mediated.

• #27 Q&A: What Causes Rare Instances of Myocarditis After mRNA COVID-19 Vaccines? < Yale School of Medicine

  https://medicine.yale.edu/news-article/qanda-what-causes-rare-instances-of-myocarditis-after-mrna-covid-19-vaccines/

  Autoimmune-related myocarditis is more difficult to treat. It would be more chronic, because once you trigger an autoimmune response, its very difficult to shut it down. […] inflammation-induced myocarditis is more transientwe actually found that inflammation as well as the immune cell types go back to normal after patients recover. […] Something empirically that our clinical colleagues have found is that treatments like NSAIDs or steroidstemporary measures that can calm the inflammation back downcan help these young patients bounce back quickly. […] if you space the dosing of the mRNA vaccines far enough apart, you might allow time for the waning of the inflammatory response and reduce the risk of myocarditis. […] Studies have also shown that the severity of disease and length of recovery are greater in myocarditis post-COVID, in contrast to this transient experience of inflammation after vaccination.

• #28 International team discovers potential mechanism in the development of myocarditis after SARS-CoV-2 vaccination

  https://medicalxpress.com/news/2022-09-international-team-potential-mechanism-myocarditis.html

  A multidisciplinary, international team formed around Drs Lorenz Thurner and Jochen Pfeifer (both University Hospital Homburg/Saar, Germany) as well as Dr. Christoph Kessel (University Children’s Hospital, Münster, Germany) and Prof. Karin Klingel (University Hospital Tübingen, Germany) provides new observations in the context of myocarditis after SARS-CoV-2 vaccination, pinpointing a potential role of autoantibodies towards IL-1Ra in the pathophysiology. […] In particular, in male adolescents and young men with histologically confirmed myocarditis, autoantibodies against a key endogenous anti-inflammatory agent called interleukin-1 receptor antagonist were detected. […] The interleukin-1 receptor antagonist (IL-1-Ra) is one such natural antagonist that can block the docking site for IL-1 on the cell surface and thus shuts down the signaling pathway.

• #29 SciELO Brazil – Pathogenesis of chronic Chagas’ myocarditis Pathogenesis of chronic Chagas’ myocarditis

  https://www.scielo.br/j/spmj/a/B3YKP4jxpwvnfQHy6nqLHzF/?lang=en

  The pathogenesis of chronic Chagas’ myocarditis is still not completely understood. Several theories have been advanced: 1) direct tissue destruction by Trypanosoma cruzi; 2) neurogenic theory; 3) anti-heart immune reactions; and 4) microvascular disease. […] We believe that the development of myocarditis is related to progressive and additive focal cellular necrosis, and associated reactive and reparative myocardial fibrosis and surrounding myocyte hypertrophy. These processes may be initiated and perpetuated by anti immune factors and alterations in the myocardial microcirculation. […] The destruction of the ganglion cells of the heart may be involved in the patho-clinical evolution of chronic Chagas’ cardiopathy. […] The Chronic Chagas’ Myocarditis Pathogenesis is, however, not completely understood. Several different types of treatment have been proposed.

• #30 SciELO Brazil – Pathogenesis of chronic Chagas’ myocarditis Pathogenesis of chronic Chagas’ myocarditis

  https://www.scielo.br/j/spmj/a/B3YKP4jxpwvnfQHy6nqLHzF/?lang=en

  The action of self immune mechanisms has been held to be the main cause of chronic Chagas’ myocarditis. […] These findings allow us to conclude that self immunity is the principle mechanism implied in the rejection of transplanted syngenic cardiac tissue in the ear of chronically T. cruzi infected mice. The similarity of the lesions to those observed in humans suggests that self immunity is involved in human Chagas’ myocarditis pathogenesis. […] It has been recently been claimed that microvascular abnormalities play a significant part in the pathogenesis of chronic Chagas’ cardiopathy. […] The proposed physiopathogenic mechanism would imply future therapeutic strategy for treating chronic Chagas’ patients, enhancing medical care and treatment and, hopefully, improving prognosis.

• #31 Myocarditis and inflammatory cardiomyopathy in 2021: an update – Polish Archives of Internal Medicine

  https://www.mp.pl/paim/issue/article/16010

  Genetic predisposition (in both human leukocyte antigenrelated and unrelated forms) may play a role in the pathogenesis of myocarditis and its progression to postinflammatory cardiomyopathy (Figure 1).1,12,13 […] Regardless of its etiology, myocardial injury initiates an inflammatory cascade that, based on experimental animal models, evolves into 3 phases. […] A specific infectious or noninfectious cause alters the myocyte membrane and triggers an immune response, ranging from transient / mild to fulminant / severe, which consists of predominant macrophage and lymphocyte infiltration of myocardial tissue. This may be associated with an increased production of immune mediators and cytokines leading to inflammatory changes (edema, hyperemia, necrosis with or without fibrosis) in myocardial tissue.

• #32

  https://ucardioj.com.ua/index.php/UJC/article/view/216?articlesBySameAuthorPage=2

  A significant role in the pathogenesis of myocarditis is now given to stimulation of Toll-like receptors of type 2 and type 4 and activation of matrix metalloproteinases, which has a direct relationship with the production of proinflammatory cytokines. […] Promising to clarify some of the pathogenetic mechanisms of inflammatory heart damage is currently considered the study of different microRNAs types. […] Currently, the world cardiology community recognizes the relevance of further study of the various mechanisms of myocarditis pathways in order to identify those pathogenetic links, the impact of which can reduce the pathological effect of inflammatory cardiac damage and the severity of the disease and improve prognosis for patients with myocarditis.

• #33 Myocarditis and inflammatory cardiomyopathy: current evidence and future directions | Nature Reviews Cardiology

  https://www.nature.com/articles/s41569-020-00435-x

  Inflammatory cardiomyopathy, characterized by inflammatory cell infiltration into the myocardium and a high risk of deteriorating cardiac function, has a heterogeneous aetiology. […] The role of specific viruses, immune cells and autoimmunity in the pathogenesis of myocarditis and inflammatory cardiomyopathy is still incompletely understood, and advanced animal and cell models are required for future research. […] Advanced animal models that take into account immune experience and exposure to environmental factors and in vitro models with immune cell interactions are needed to facilitate better clinical translation of the findings. […] The current knowledge and open questions regarding the cardiovascular effects associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are also discussed.

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