Subject(s)
Humans , Male , Adult , Shock, Cardiogenic/diagnostic imaging , COVID-19/diagnosis , Myocarditis/diagnostic imaging , Shock, Cardiogenic/drug therapy , Shock, Cardiogenic/virology , Enalapril/administration & dosage , Bisoprolol/administration & dosage , COVID-19/complications , Heart Failure/drug therapy , Heart Failure/virology , Heart Failure/diagnostic imaging , Myocarditis/drug therapy , Myocarditis/virologyABSTRACT
ABSTRACT A male patient with flu-like symptoms and tomography and laboratory diagnosis of severe acute respiratory syndrome. He developed acute cardiac dysfunction during admission and was submitted to a cardiac magnetic resonance imaging examination, which confirmed acute myocarditis, indicating cardiac involvement by coronavirus disease 2019. A review and discussion about coronavirus disease 2019-related cardiac manifestations are reported, focusing on the imaging findings to make diagnosis.
RESUMO Paciente do sexo masculino apresentando síndrome gripal aguda com diagnóstico tomográfico e laboratorial de infecção por síndrome respiratória aguda grave. Evoluiu com disfunção cardíaca aguda durante a internação, motivo pelo qual foi submetido à ressonância magnética cardíaca, que confirmou miocardite aguda, indicando acometimento cardíaco por COVID-19. Foram realizadas revisão e discussão sobre o acometimento cardíaco na COVID-19, com ênfase nos aspectos por imagem para o diagnóstico.
Subject(s)
Humans , Male , Pneumonia, Viral/complications , Coronavirus Infections/complications , Myocarditis/virology , Pneumonia, Viral/diagnosis , Magnetic Resonance Imaging , Coronavirus Infections/diagnosis , Pandemics , Betacoronavirus , SARS-CoV-2 , COVID-19 , Myocarditis/diagnostic imagingABSTRACT
Objective: This study aimed to investigate whether interleukin-28A (IL-28A) plays a role in murine myocarditis induced by coxsackievirus B3 (CVB3), and to explore its possible mechanism involved. Methods: Male BALB/c mice both infected and not infected by CVB3 were randomly divided into four groups (n = 40), untreated or treated with different doses of IL-28A for 4 days, and then sacrificed on days 4 and 7 post-infection. The heart samples were collected for histopathologic examination. Cardiac viral load was determined by a plaque assay. Additionally, immunoblot analysis, TUNEL assay, and immunohistochemistry were performed to examine the expression of signal transducer, activator of transcription 1 and 2 (STAT1 and STAT2), CVB3-induced apoptosis and the expression of Bcl-2, BAX and Caspase-3. Results: Compared to uninfected mice, the CVB3 infected mice exhibited higher mortality rate (p < 0.001), apparent inflammation and myocardial lesion (p < 0.01), and higher cardiac viral load (p < 0.01). After CVB3 infection, IL-28A treated mice presented no death (p < 0.001), reduced inflammation and myocardial lesion (p < 0.01), and lower viral load (p < 0.01) compared to untreated mice. Besides, treatment with IL-28A markedly increased the expressions of STAT1 and STAT2, and inhibited CVB3-induced apoptosis in myocardial cells with increased ratio of Bcl-2/BAX. Conclusion: The antiviral and myocyte protective effects of IL-28A in CVB3-inducedmyocarditis are regulated by STAT1 and STAT2. .
Subject(s)
Animals , Male , Mice , Antiviral Agents/therapeutic use , Coxsackievirus Infections , Interleukins/metabolism , Myocarditis/virology , Apoptosis , /immunology , /metabolism , Coxsackievirus Infections/drug therapy , Coxsackievirus Infections/immunology , Coxsackievirus Infections/metabolism , Immunoblotting , Immunohistochemistry , In Situ Nick-End Labeling , Interleukins/immunology , Mice, Inbred BALB C , Myocarditis/immunology , Myocarditis/metabolism , /immunology , /metabolism , STAT1 Transcription Factor/immunology , STAT1 Transcription Factor/metabolism , /immunology , /metabolism , Viral Load , /immunology , /metabolismABSTRACT
Caso de miocardite fulminante associada ao vírus influenza H1N1, em que foi descrita a evolução clínica do paciente e enfatizada a importância do ecocardiograma à beira do leito como auxílio no diagnóstico precoce e manejo de crianças com disfunção miocárdica grave, além de terem sido discutidos aspectos relevantes relacionados à terapêutica e ao prognóstico da miocardite fulminante. Trata-se de paciente do sexo feminino, 4 anos e 8 meses, previamente hígida, com história de quadro gripal há 2 semanas. Admitida no pronto-socorro com sinais de instabilidade hemodinâmica, necessitando de suporte ventilatório e drogas vasoativas. Exames laboratoriais, radiografia de tórax e ecocardiograma sugestivos de miocardite. Pesquisa positiva para H1N1 em secreção de nasofaringe. Evoluiu com choque cardiogênico refratário a despeito das medidas clínicas, indo a óbito em 48 horas após admissão na unidade de terapia intensiva. O vírus influenza H1N1 é agente etiológico associado a quadros de miocardite aguda, porém poucos são os casos relatados de miocardite fulminante pelo vírus H1N1. A identificação de sinais e sintomas sugestivos de evolução fulminante deve ser imediata e o ecocardiograma à beira do leito é uma ferramenta útil para detecção precoce de disfunção miocárdica e orientação terapêutica. O uso de terapia imunossupressora, em casos de miocardite fulminante de etiologia viral, é controverso, bem como o de terapia antiviral, de tal forma que o tratamento baseia-se em suporte hemodinâmico e ventilatório. O uso de suporte hemodinâmico, por meio de oxigenação por membrana extracorpórea, aparece como terapia promissora.
A case of fulminant myocarditis associated with the H1N1 influenza virus. This case report describes the patient's clinical course and emphasizes the importance of bedside echocardiography as an aid in the early diagnosis and management of children with severe myocardial dysfunction. It also discusses aspects relevant to the treatment and prognosis of fulminant myocarditis. The patient was a female, 4 years and 8 months old, previously healthy and with a history of flu symptoms in the past two weeks. The patient was admitted to the emergency room with signs of hemodynamic instability, requiring ventilatory support and vasoactive drugs. The laboratory tests, chest X-ray and echocardiogram suggested the presence of myocarditis. The test for H1N1 in nasopharyngeal secretions was positive. The patient evolved to refractory cardiogenic shock despite the clinical measures applied and died 48 hours after admission to the intensive care unit. The H1N1 influenza virus is an etiological agent associated with acute myocarditis, but there are few reported cases of fulminant myocarditis caused by the H1N1 virus. The identification of signs and symptoms suggestive of fulminant progression should be immediate, and bedside echocardiography is a useful tool for the early detection of myocardial dysfunction and for therapeutic guidance. The use of immunosuppressive therapy and antiviral therapy in acute myocarditis of viral etiology is controversial; hence, the treatment is based on hemodynamic and ventilatory support. The use of hemodynamic support by extracorporeal membrane oxygenation emerges as a promising treatment.
Subject(s)
Child, Preschool , Female , Humans , Influenza A Virus, H1N1 Subtype/isolation & purification , Influenza, Human/complications , Myocarditis/virology , Influenza, Human/virologyABSTRACT
OBJECTIVE@#To discuss the myocardial expression of Spry1 and MAPK proteins of viral myocarditis (VMC), to reveal its mechanism of sudden death, and to provide guides for forensic identification of sudden cardiac death.@*METHODS@#Thirty Balb/c male mice were randomly divided into VMC group and control group, inoculated intraperitoneally with Coxsackievirus B3 and Eagel's solution, respectively. After the mice were sacrificed, the cardiac tissues of the mice were taken to proceed regular pathological examination. The changes of Spry1 protein, Spry1 mRNA and MAPK protein were detected by immunohistochemistry, Western blotting and real-time PCR.@*RESULTS@#Under light microscope, the pathologic changes included myocardial interstitial edema, inflammatory cells infiltration, myocardial necrosis, and focal and patchy necrosis of myocardial fiber in VMC group. The expression of Spry1 protein in VMC group was lower than that in control group (P < 0.05). There was slightly decreased expression of Spry1 of the mRNA level in VMC group (P > 0.05). But the MAPK protein expression in VMC group was higher than that in control group (P < 0.05).@*CONCLUSION@#The pathway of MAPK/ERK involving Spry1 protein accelerates the expression of collagen, which may contribute to arrhythmia, heart failure and even sudden cardiac death.
Subject(s)
Animals , Male , Mice , Adaptor Proteins, Signal Transducing/metabolism , Coxsackievirus Infections/pathology , Death, Sudden, Cardiac/pathology , Disease Models, Animal , Immunohistochemistry , Membrane Proteins/metabolism , Mice, Inbred BALB C , Mitogen-Activated Protein Kinases/metabolism , Myocarditis/virology , Myocardium/pathology , Phosphoproteins/metabolism , RNA, Messenger/metabolism , Random Allocation , Real-Time Polymerase Chain ReactionABSTRACT
OBJECTIVE@#To observe the expression and distribution of vascular cell adhesion molecule-1 (VCAM-1) and caspase-3 in myocardium of persons who died from viral myocarditis and to explore its pathogenesis and death mechanism.@*METHODS@#Twenty cases died from viral myocarditis were selected as the experimental group. Ten cases died from traumatic shock and massive hemorrhage shock after traffic accidents were selected as the control group. The sections of myocardium were stained by immunohistochemistry for VCAM-1 and caspase-3, and observed under microscope. The positive expressions of VCAM-1 and caspase-3 of the two groups were compared with each other by image analysis and statistical analysis.@*RESULTS@#(1) The vascular endothelial cells expressed VCAM-1 with dark-brown colors in the experimental group, and weak expression was observed in the control group. The average optical density in the experimental group was higher than that in the control group (P < 0.05). (2) The caspase-3 positive cells were mostly inflammatory cells around the myocardial vessels with brown-red granules in the experimental group. The positive cell number in the experimental group was higher than that in the control group (P < 0.05).@*CONCLUSION@#VCAM-1 may play an important role in the inflammatory cells exudation caused by viral myocarditis, and may provide the reference for diagnosis of viral myocarditis in forensic pathology. However, the myocardial apoptosis mediated by caspase-3 doesn't affect the lethal mechanism in the late stage of viral myocarditis.
Subject(s)
Adolescent , Adult , Child , Female , Humans , Male , Middle Aged , Young Adult , Caspase 3/metabolism , Death, Sudden, Cardiac/etiology , Forensic Pathology , Immunohistochemistry , Myocarditis/virology , Myocardium/pathology , Myocytes, Cardiac/pathology , Shock, Traumatic/pathology , Vascular Cell Adhesion Molecule-1/metabolismABSTRACT
Introduction: During the winter of 2009, some patients infected with Influenza virus H1N1 presented a severe disease. Some isolated reports of myocarditis were described. Objective: To describe severe cases of H1N1 with myocardial involvement. Patients and Methods: Chart review of children between 0-15 y.o. diagnosed as presenting Influenza A H1N1 through Polimerase Chain Reaction, who were admitted to the PICU at Hospital Roberto del Río and Clínica Dávila between June and July of 2009. Myocardial involvement was considered positive if the clinical picture showed such signs, and/or there was an altered echocardiogram. Results: Twenty one patients were hospitalized with the diagnosis of severe Infection by Influenza A H1N1 (+), of which 8 patients (38 percent) presented myocardial involvement. All required mechanical ventilation. Echocardiogram performed in the first 24 hours post admission showed shortening of the left ventricle on average 21,8 percent, with a range of 19 to 38 percent. In 7 patients (87.5 percent) a systodyastolic dysfunction was shown. Myocardial involvement lasted from 2 to 10 days (median 4). One patient died. Conclusions: Involvement of myocardium is frequent in this series. It must be sought to treat it adequately.
Introducción: Durante el invierno 2009 algunos paciente con infección por virus Influenza A H1N1, evolucionaron en forma grave. Se han descrito reportes aislados de miocarditis secundaria a Influenza A H1N1. Objetivo: Descripción de los casos graves de H1N1 que presentaron compromiso miocárdico. Material y Métodos: Revisión de los casos diagnosticados como Influenza A H1N1 por Reacción Polimerasa en Cadena, en niños entre 0-15 años, hospitalizados en la Unidad de Paciente Crítico del Hospital Roberto del Río y de Clínica Dávila, durante el período Junio - Julio del 2009. Se consideró criterio de compromiso miocárdico el cuadro clínico y/o una ecocardiografía alterada. Resultados: : 21 pacientes fueron hospitalizados con diagnóstico de infección grave por Influenza A H1N1 (+), de éstos 8 pacientes ( 38 por ciento) presentaron compromiso miocárdico. Todos requirieron ventilación mecánica. La ecocardiografia en las primeras 24 horas postingreso, evidenció una fracción de acortamiento del ventrículo izquierdo promedio de 21,8 por ciento, con un rango de 19 a 38 por ciento. En 7 pacientes (87.5 por ciento) se constató una disfunción sistodiastólica. La duración promedio del compromiso miocárdico osciló entre 2 a 10 días ( mediana 4).Hubo 1 fallecido en esta serie. Conclusiones: La frecuencia de compromiso miocárdico en esta serie es importante, debiendo buscarse dirigidamente para adecuar plan terapéutico.
Subject(s)
Humans , Male , Adolescent , Female , Infant , Child, Preschool , Child , Echocardiography , Influenza, Human/complications , Myocarditis/physiopathology , Myocarditis/virology , Ventricular Dysfunction, Left/physiopathology , Hypertension, Pulmonary , Influenza A Virus, H1N1 Subtype , Myocarditis , Retrospective Studies , Stroke Volume/physiologyABSTRACT
Presentamos el caso de una paciente joven que presentó choque cardiogénico por virus Coxsakie B6. La paciente acudió a una clínica particular con un cuadro clínico compatible con gastroenterocolitis aguda a la que después de una hora de estar recibiendo hidratación y manejo del cuadro diagnosticado, se agregó hipotensión que llegó al estado de choque, hipoxemia severa y compromiso pulmonar bilateral intersticial por lo que ingresó a Unidad de Cuidados Intensivos, donde recibió manejo de soporte. Debido al cuadro clínico y elevación de enzimas cardiacas se sospechó de compromiso cardiaco, la ecocardiografía evidenció cambios sugerentes de miocarditis. La evolución fue favorable y se le pudo dar de alta después de una semana. El diagnóstico etiológico del cuadro se hizo en el seguimiento, presentando serología con elevación de títulos para virus Coxsakie B6.
We present the case of a young woman who suffered cardiogenic due to by Coxsackie virus B6. The patient attended a private clinic with an acute gastroenteritis and after one hour of receiving hydratation,she developed hypotension and shock, severe hypoxemia and bilateral lung infiltrate. The patient entered the Intensive Care Unit, where she received hemodynamic support. Due to the clinical picture and cardiac enzymes increase, a cardiac failure was suspected and the echocardiographic findings suggested "myocarditis". The evolution was successful and Coxsackie B6 virus infection diagnosis was made during the follow up by increase of the levels of antibodies for virus Coxsackie B6.
Subject(s)
Adolescent , Female , Humans , Coxsackievirus Infections , Enterovirus B, Human , Gastroenteritis/virology , Myocarditis/virology , Acute Disease , Coxsackievirus Infections/diagnosis , Gastroenteritis/diagnosis , Myocarditis/diagnosisABSTRACT
The 2009 Pandemic Novel Influenza A [H1N1] resulted in mild disease mostly but severe cases and death were associated with pneumonia, respiratory failure and multi-organ failure. We present a case of severe disease with acute heart failure and arrhythmia due to fulminant myocarditis in a 50-year old obese man with diabetes mellitus.
La nueva gripe A [H1N1] pandémica resultó ser una enfermedad leve en su mayor parte, pero se produjeron casos graves y muertes asociadas con neumonía, insuficiencia respiratoria y fallo multiorgánico. Presentamos un caso de enfermedad severa con insuficiencia cardíaca aguda y arritmia debido a miocarditis fulminante en un hombre obeso de 50 años de edad con diabetes mellitus.
Subject(s)
Humans , Male , Middle Aged , Influenza A Virus, H1N1 Subtype , Influenza, Human/complications , Myocarditis/diagnosis , Abdomen, Acute , Influenza, Human/virology , Myocarditis/virologyABSTRACT
OBJECTIVE: Cytomegalovirus (CMV) systemic disease and myocarditis in healthy persons is infrequently reported in the literature, although in increasing numbers in recent years. The importance of the recognition of the syndrome that usually has an initial picture of a mononucleosis like infection in an otherwise healthy person, is the available therapeutic agent, ganciclovir, that can cure the infectious disease. METHODS: We analyzed the clinical result of pulsotherapy with steroids in a patient with CMV myocarditis after 7 days of etiological treatment, with ganciclovir, intravenous vasodilators, and the conventional treatment for congestive heart failure. RESULTS: The clinical condition of the patient improved accordingly to the better function of the left ventricle, and the ganciclovir was kept for 21 days, most of it in an out patient basis. The patient was dismissed from the hospital, with normal myocardial function. CONCLUSION: Potentially curable forms of myocarditis, like M pneumoniae and CMV, for example, can have an initial disproportionate aggression to the myocardium, by the acute inflammatory reaction, that can by itself make worse the damage to the LV function. In our opinion, the blockade of this process by pulsotherapy with steroids can help in the treatment of these patients. We understand that the different scenario of immunosuppressive treatments for the possible auto immunity of the more chronic forms of the presumably post viral cardiomyopathy has been in dispute in the literature, and has stolen the focus from the truly acute cases.
OBJETIVO: Doença sistêmica por citomegalovírus (CMV) com miocardite em pessoas saudáveis é raramente referida na literatura, apesar de em maior número em anos recentes. A importância do reconhecimento da síndrome, que usualmente tem um quadro inicial "mononucleosis like" em uma pessoa sadia é a disponibilidade do agente terapêutico ganciclovir, que pode curar a infecção. MÉTODOS: Nós analisamos o resultado da pulsoterapia com esteróides em um paciente com miocardite por CMV, após 7 dias de tratamento etiológico com ganciclovir, vasodilatadores intravenosos e o tratamento convencional para insuficiência cardíaca congestiva. RESULTADOS: A condição clínica do paciente melhorou com a melhor função do ventrículo esquerdo e o ganciclovir foi mantido por 21 dias após alta hospitalar.A função miocárdica retornou ao normal. CONCLUSÃO: Formas curáveis de miocardites como M pneumonia e CMV, por exemplo, podem ter uma agressão grave ao miocárdio por uma ação inflamatória que pode piorar a função cardíaca. Em nossa opinião, o bloqueio deste processo pela pulsoterapia com esteróides pode auxiliar no tratamento destes pacientes. Entendemos que existe um cenário diferente de tratamento com imunossupressores para possível agressão auto-imune das formas mais crônicas de cardiomiopatias dilatadas e isso está em disputa na literatura, talvez mudando o foco dos casos realmente agudos.
Subject(s)
Adult , Humans , Male , Cytomegalovirus Infections/drug therapy , Myocarditis/drug therapy , Shock, Cardiogenic/drug therapy , Anti-Bacterial Agents/therapeutic use , Antihypertensive Agents/therapeutic use , Antiviral Agents/therapeutic use , Ganciclovir/therapeutic use , Glucocorticoids/therapeutic use , Injections, Intravenous , Myocarditis/virology , Prednisone/therapeutic use , Shock, Cardiogenic/etiology , Teicoplanin/therapeutic useABSTRACT
OBJECTIVE@#In order to improve accuracy and reliability of forensic diagnosis of sudden cardiac death, pathogenesis and relationship between the viral myocarditis (VMC) and dilated cardiomyopathy (DCM) were investigated.@*METHODS@#Improved immunohistochemical technique was used to detect the expression of the CAR in myocardium samples, including 22 deceased with VMC, 20 deceased with DCM and 16 control deceased.@*RESULTS@#The brown staining on the cell membrane of myocardium showed positive result. There was a prominent CAR expression in VMC group and DCM group, which were statistically significant difference compared with control group (P < 0.05).@*CONCLUSION@#The CAR expression showed significantly higher in VMC and DCM groups. The viral infection can result in myocardial necrosis and impaired cardiac functions. These abnormalities can trigger a cascade of events that contributed to the progress of VMC to DCM.
Subject(s)
Female , Humans , Male , Cardiomyopathy, Dilated/pathology , Case-Control Studies , Coxsackie and Adenovirus Receptor-Like Membrane Protein , Coxsackievirus Infections/complications , Death, Sudden, Cardiac , Forensic Pathology , Immunohistochemistry , Myocarditis/virology , Myocardium/pathology , Receptors, Virus/metabolism , Staining and LabelingSubject(s)
Adult , Humans , Male , Influenza A Virus, H1N1 Subtype , Influenza, Human/virology , Myocarditis/virology , Acute DiseaseABSTRACT
OBJECTIVE@#To explore the expression and significance of monocyte chemoattractant protein-1 (MCP-1) in myocardium in sudden death caused by viral myocarditis (VMC).@*METHODS@#To investigate the expression of MCP-1 in VMC sudden death group and control group using improved immunohistochemical technique and to compare the difference of the expression of MCP-1 between two groups with statistical method.@*RESULTS@#In VMC sudden death group, MCP-1 was positively expressed in 17 of 20 cases. While only 4 of the 20 cases in the control group showed a mildly positive expression sparsely in myocardium, and the rest cases were completely negative. The rate of positive expression of MCP-1 in VMC group was obviously higher than that of the control group (P<0.01).@*CONCLUSION@#The expression of MCP-1 detected by immunohistochemistry provides an objective morphologic evidence for the diagnosis of VMC sudden death in forensic pathology.
Subject(s)
Adolescent , Adult , Aged , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Young Adult , Autopsy , Case-Control Studies , Chemokine CCL2/metabolism , Death, Sudden, Cardiac , Forensic Pathology , Immunohistochemistry , Myocarditis/virology , Myocardium/pathology , Staining and LabelingABSTRACT
OBJECTIVE@#To study the pathogenesis of viral myocarditis (VMC) and dilated cardiomyopathy (DCM) and their relationship.@*METHODS@#Sixty samples including 20 VMC, 20 DCM and 20 controls were collected. The expression of Fas protein in myocardium of each group was detected by modified immunohistochemistry with unequivocal brown staining in the myocardial membrane scored as positive, and the results of positive reaction were analyzed by Ridit test.@*RESULTS@#Fas protein expression increased obviously in VMC and DCM groups as compared with that of the control group. The difference of positive results between each group analyzed by Ridit test was statistically significant (P<0.005). Statistically significant differences were found between VMC and control groups as well as between DCM and control groups (P<0.05), but not between VMC and DCM groups (P>0.05) by multiple comparison Ridit test.@*CONCLUSION@#The expression of Fas protein is significantly higher in the VMC and DCM groups than in that of the control group. These results suggest that both the VMC and DCM may share a similar pathogenesis, which most likely involves cell apoptosis.
Subject(s)
Female , Humans , Male , Apoptosis/physiology , Cardiomyopathy, Dilated/pathology , Case-Control Studies , Forensic Pathology , Myocarditis/virology , fas Receptor/metabolismABSTRACT
OBJECTIVE@#To explore etiology and pathogenesis of viral myocarditis (VMC) and dilated cardiomyopathy (DCM).@*METHODS@#The expression of Coxsackie B virus and adenovirus receptors (CAR) were detected with modified immunohistochemical (IHC) technique in myocardium of left ventricle, right ventricle, interventricular septum, and septal papillary muscle from 28 patients with viral myocarditis, 31 patients with dilated cardiomyopathy and 17 control patients (including normal, hypertension heart disease, myocardial infarction and coronary atherosclerotic heart disease).@*RESULTS@#The brown staining on the cell membrane of myocardium represents positive result. 100% (28 of 28) of VMC patients (IHC surface integral: 4.3975 +/- 0.0365) and 84% (26 of 31) of DCM patients (4.2064 +/- 0.052 6) had prevalent CAR expression compared to 0% (0 of 19) control patients (0.073 1 +/- 0.0362). There were statistically significant differences between VMC/DCM and control patients (P < 0.05).@*CONCLUSION@#The prevalence of CAR expression was significantly higher in VMC and DCM patients (100% and 84% vs. 0% in control). In contrast, there was no difference found between VMC and DCM patients. These results suggest that both VMC and DCM involve viral etiology and could share a similar pathogenesis.
Subject(s)
Female , Humans , Male , Adenovirus Infections, Human/complications , Cardiomyopathy, Dilated/virology , Case-Control Studies , Coxsackie and Adenovirus Receptor-Like Membrane Protein , Coxsackievirus Infections/complications , Death, Sudden, Cardiac , Immunohistochemistry , Myocarditis/virology , Myocardium/pathology , Receptors, Virus/metabolismABSTRACT
OBJECTIVE@#To study the value of Fibronectin(Fn) immunohistochemical staining for diagnosing slight viral myocarditis.@*METHODS@#The heart samples of human with myocarditis were studied by using LSAB immunohistochemical staining with anti-fibronectin antibody.@*RESULTS@#Dense deposition was found in the myocardium of human with myocarditis. Some Fn-positive cardiomyocytes were observed.@*CONCLUSION@#Slight degeneration of cardiomyocytes could be identified by Fn-LSAB immunohistochemical staining and Fn-deposition is one of the reliable marks for inflammation in the myocardium.