Silent Myocarditis Research Articles

COVID-19-induced silent myocarditis and newly developed hypertension in a 3-year-old boy

BackgroundCOVID-19 myocarditis occurs in 7–28% of patients admitted in the hospital with or without multisystem inflammatory syndrome. It may present as fulminant myocarditis. Dilated cardiomyopathy as a sequela of COVID-19 myocarditis has been reported in the pediatric population. However, to date, no case of silent COVID-19 myocarditis progressing to dilated cardiomyopathy has been reported in children. Furthermore, although newly developed hypertension as a sequela of COVID-19 infection has been reported in adults, there is no report of newly developed COVID-induced hypertension in children. We report a 3-year-old boy with silent COVID-19 myocarditis progressing to dilated cardiomyopathy and newly developed systemic hypertension.Case presentationA 3-year-old boy was referred to the emergency department because of respiratory distress. The parents gave a history of SARS-CoV-2 infection in the child 5 months ago that was manifested as fever and cough, for which he was treated as an outpatient. Echocardiographic examination revealed a severe decrease in left ventricular systolic function in favor of dilated cardiomyopathy. Cardiac magnetic resonance imaging established the diagnosis of myocarditis. The patient left ventricular systolic function did not improve after 2 weeks of intravenous inotropic support. Therefore, the child was transferred to another tertiary center with extracorporeal membrane oxygenation and pediatric cardiac transplantation facilities.ConclusionsCOVID-19 can induce silent myocarditis with progression to dilated cardiomyopathy and newly developed systemic hypertension. Thus, a thorough examination of the heart and measurement of blood pressure are mandatory in every child with COVID-19 infection. Cardiac MR is an indispensable tool in the diagnosis, follow-up, and prognostication of COVID-19 myocarditis. Moreover, four-chamber speckle tracking strain imaging showed apical rocking in all the four heart chambers in this child with opposite direction in the failed left ventricle compared with other cardiac chambers. Lastly, the presence of septal flash on M-mode echocardiography, apical rocking and prestretch–rebound stretch patterns on longitudinal strain imaging of the failed left ventricle in this child may be of predictive value for response to cardiac resynchronization therapy.

Myasthenia Cardiomyopathy Silent Myocarditis Unveiled by Cardiovascular Magnetic Resonance

In myastheniagravis (MG) patients, heart muscle is one of the autoimmune targets. The presentation of cardiac involvement with MG varies and may include myocarditis. Beyond comprehensive left ventricular volume and ejection fraction quantification, cardiovascular magnetic resonance (CMR) provides incomparable non-invasive tissue characterisation. Hence, CMR in MG may allow early detection of subclinical myocarditis or evaluation of remote myocardial damage by late gadolinium enhancement technique.We present the first case of cardiac involvement of immune-mediated myocarditis imaged by CMR in MG.

Cardiovascular magnetic resonance detects silent heart disease missed by echocardiography in systemic lupus erythematosus.

Background Accurate diagnosis of cardiovascular involvement in systemic lupus erythematosus (SLE) remains challenging, due to limitations of echocardiography. We hypothesized that cardiovascular magnetic resonance can detect cardiac lesions missed by echocardiography in SLE patients with atypical symptoms. Aim To use cardiovascular magnetic resonance in SLE patients with atypical symptoms and investigate the possibility of silent heart disease, missed by echocardiography. Patients/methods From 2005 to 2015, 80 SLE patients with atypical cardiac symptoms/signs (fatigue, mild shortness of breath, early repolarization and sinus tachycardia) aged 37 ± 6 years (72 women/8 men), with normal echocardiography, were evaluated using a 1.5 T system. Left and right ventricular ejection fractions, T2 ratio (oedema imaging) and late gadolinium enhancement (fibrosis imaging) were assessed. Acute and chronic lesions were defined as late gadolinium enhancement-positive plus T2>2 and T2<2, respectively. Lesions were characterized according to late gadolinium enhancement patterns as: diffuse subendocardial, subepicardial and subendocardial/transmural, due to vasculitis, myocarditis and myocardial infarction, respectively. Results Abnormal cardiovascular magnetic resonance findings were identified in 22/80 (27.5%) of SLE patients with normal echocardiography, including 4/22 with recent silent myocarditis, 5/22 with past myocarditis (subepicardial scar in inferolateral wall), 9/22 with past myocardial infarction (six inferior and three anterior subendocardial infarction) and 4/22 with diffuse subendocardial fibrosis due to vasculitis. No correlation between cardiovascular magnetic resonance findings and inflammatory indices was identified. Conclusions Cardiovascular magnetic resonance in SLE patients with atypical cardiac symptoms/signs and normal echocardiography can assess occult cardiac lesions including myocarditis, myocardial infarction and vasculitis that may influence both rheumatic and cardiac treatment.

Silent myocarditis in systemic sclerosis detected by cardiovascular magnetic resonance using Lake Louise criteria

BackgroundSystemic sclerosis (SSc) is an autoimmune disease characterized by microvascular abnormalities, inflammation and fibrosis. We hypothesized that myocarditis may be diagnosed in asymptomatic SSc, undergoing routine cardio-vascular magnetic resonance (CMR) for fibrosis assessment, using the Lake Louise criteria: T2 ratio, early (EGE) and late gadolinium enhanced (LGE) images.MethodsEighty-two asymptomatic SSc, diagnosed according to American College of Rheumatology criteria, aged 43 ± 5 yrs., 62 with diffuse (dSSc) and 20 with localized (lSSc) systemic sclerosis were evaluated by CMR, performed at 1.5 T scanner, according to Lake Louise criteria.ResultsCMR documented normal biventricular function in all SSc. However, 7/62 (11.2%) with dSSc and 2/20 (10%) with lSSc, had CMR signs of myocarditis according to Lake Louise criteria, without any clinical cardiac symptom. In these 9 patients, T2 ratio, EGE ratio and LGE (positive in all 9 SSc) were 2.8 ± 0.5%, 8 ± 3% and 5 ± 3% of LV mass, respectively. No correlation between CMR and blood inflammatory indices (C-reactive protein and erythrocyte sedimentation rate), cardiac troponin T, disease characteristics or type of SSc was identified. A repeat CMR at 6 months, after treatment with prednisone and azathioprine, showed normalisation of the acute inflammation CMR indices.ConclusionsSilent myocarditis may be diagnosed using the Lake Louise paper criteria in SSc patients without cardiac symptoms, has no correlation with blood inflammatory indices, cardiac troponin or disease characteristics. CMR is a promising tool to diagnose silent myocarditis in SSc and monitor the response to immunosuppressive treatment.

Abstract 13292: Bradycardia as a Manifestation of Chikungunya Myocarditis. A New Threat to America

Background: Chikungunya fever is an arthropod-borne disease that has caused millions of infections globally. Local transmission has been reported in the United States. There are very few published reports concerning the cardiac complications in general and bradycardia in particular. Objective: To investigate the occurrence of myocarditis and bradycardia in patients with Chikungunya fever. Methods: Prospective multicenter observational studio of 287 patients with a chikungunya infection during a Venezuelan outbreak. Clinical evaluation, X Ray, ECG, Echocardiogram, Holter, laboratory including virological evaluation, cardiac biomarkers, and cardiac MRI procedures were performed. Results: Of the 287 patients examined, 117 were male with a mean age of 59 ± 8; 277 patients presented with fever and polyarthralgia and 91 developed palpitations. Arrhythmias occurred in 45% of cases; they included bradiarrhytmias (33%), atrial and ventricular ectopic beats and tachyarrhythmia’s in which atrial fibrillation was observed in 19 cases. There were also ectopic atrial tachycardia and non-sustained ventricular tachycardia, conduction disturbances and 3 cases of sudden death. Conclusion: Physicians should be aware of the possibility of manifest or silent myocarditis in almost half of patients with Chikungunya disease. In a proper epidemiological context, the triad of fever, polyarthralgia and new arrhythmia, including bradiarrhytmias suggests Chikungunya myocarditis.

Abstract 12496: A New Arrhythmic Threat to America. Chikungunya Myocarditis

Background: The mosquito-borne Chikungunya virus infection is one of the most important emerging virus diseases globally. Local transmission has been found in the United States. There are very few published reports concerning the cardiac complications in general and less of arrhythmias in particular. Chikungunya can be fatal: there have been sudden deaths reports . Objective: To investigate arrhythmic complications of Chikungunya myocarditis. Methods: Prospective multicenter observational study of 280 patients with a Chikunguya infection from a Venezuelan Outbreak. Clinical evaluation, ECG, laboratory including virological evaluation and cardiac biomarkers, Echocardiogram, Holter and cardiac MRI procedures were carried out. Results: Of the 280 patients examined, 113 patients were male, with a mean age of 59 ± 9; 270 patients presented with fever and polyarthralgia and 85 developed palpitations. Arrhythmias occured in 45% of cases; they included bradyarrhythmias (33%), atrial and ventricular ectopic beats and tachyarrhythmias in which atrial fibrillation was observed in 19 cases. There were also ectopic atrial tachycardia and non sustained ventricular tachycardia, conduction disturbances and 3 cases of sudden death. Conclusion: Physicians should know that almost half of the Chikungunya patients will develop arrhythmias and manifest or silent myocarditis. In the proper epidemiological context, the triad of fever, polyarthralgia and new arrhythmia including bradiarrhythmias suggest Chikungunya Myocarditis.

Silent myocarditis in myasthenia gravis. Role of cardiovascular magnetic resonance imaging

Silent myocarditis in myasthenia gravis. Role of cardiovascular magnetic resonance imaging

Subepicardial delayed gadolinium enhancement in asymptomatic athletes: let sleeping dogs lie?

BackgroundSubepicardial delayed gadolinium enhancement (DGE) patches without underlying cardiomyopathy is poorly understood. It is often reported as the result of prior silent myocarditis. Its prognostic relevance in asymptomatic athletes is...

Corticosteroid therapy for ventricular tachycardia in children with silent lymphocytic myocarditis

Objective: The objective of our study was to describe the efficacy of cortico steroids for ventricular tachycardia in four children with structurally normal hearts in whom endomyocardial biopsy revealed histologic changes of lymphocytic myocarditis. Patients: The four patients had unexplained ventricular tachycardia. Three dysrhythmias were sustained, and one was inducible by exercise. Patient ages ranged from 4 months to 12 years. Three of the four patients had no symptoms. In two of them, ventricular tachycardia was identified by mass screening for heart disease. Two patients received oral steroids and two received pulse steroid therapy. Results: In all four patients, significant underlying diseases were not found by noninvasive evaluation. Right ventricular endomyocardial biopsy revealed abnormal histologic findings of chronic lymphocytic myocarditis in all patients. Steroid therapy was effective in all four patients, two of whom received methylprednisolone pulse therapy. Conclusions: We conclude that unexplained ventricular tachycardia may be the only manifestation of clinically silent myocarditis. Steroid therapy should therefore be considered if conventional antiarrhythmic medication is not effective and histologic findings confirm the presence of lymphocytic myocarditis. (J P EDIATR 1995;126:304-8)

Animal model of silent myocarditis in athymic mice.

To clarify the role of the immune system in the development of myocarditis, BALB/c-nu/nu mice (group 1), BALB/c-nu/+ mice (group 2), BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice (group 3), and BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice treated with rat anti-Thy-1.2 monoclonal antibody with complement (group 4) were inoculated with encephalomyocarditis virus. There were no significant differences in the incidence of myocarditis among the four groups. Virus titrations of the heart and serum neutralising antibody titres in the four groups did not show any significant differences. Fifty two per cent (26/50) of group 2 and 43% (20/46) of group 3 died on days 9-15, when congestive heart failure developed. Only 9% (5/54) of group 1 and 8% (1/12) of group 4, however, died on days 9-15. Pathological examination confirmed congestive heart failure in groups 2 and 3 but not in groups 1 and 4. Dilatation of the ventricular cavities, pleural effusion, ascites, and congestion of the lungs and liver were present in groups 2 and 3 but not in groups 1 and 4. Cellular infiltration and myocardial necrosis were severe in groups 2 and 3 but minimal in groups 1 and 4. Thus the severity of myocarditis may be regulated by T cells. So-called silent myocarditis seen in clinical settings may be similar to myocarditis in BALB/c-nu/nu mice.

Immunologic behavior of lymphocytes in experimental viral myocarditis: significance of T lymphocytes in the severity of myocarditis and silent myocarditis in BALB/c-nu/nu mice.

To clarify the immune mechanism in myocarditis, we examined by immunofluorescence techniques the serial changes in percentages of T and B lymphocytes in the heart, spleen, and peripheral blood of DBA/2 mice inoculated with encephalomyocarditis (EMC) virus (experiment I). B cells were demonstrated by staining with fluorescein isothiocyanate (FITC)-labeled rabbit antimouse immunoglobulin (Ig). T cells were demonstrated with rat anti-Thy1.2 monoclonal antibody plus FITC-labeled antimouse Ig. There was a marked decrease in T cells in peripheral blood and a moderate decrease in the cells in the spleen on day 14. There were no significant changes in B cells in peripheral blood or spleen throughout the entire period and T cells accounted for approximately 80% of the cells in the myocardium on days 7 and 14. To confirm the involvement of T cells in the development of myocarditis, we also carried out studies in which BALB/c-nu/nu mice (group 1, n = 58), BALB/c-nu/+ mice (group 2, n = 54), and BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice (group 3, n = 50) were inoculated with EMC virus (experiment II). Four mice from each of the three groups were killed on day 6 for virologic studies. In experiment II, there were no significant differences in the incidence of myocarditis among the three groups. Virus titrations of the heart and serum neutralizing antibody titers did not show any significant differences between the three groups on days 6 and 16.(ABSTRACT TRUNCATED AT 250 WORDS)