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Marc Badoz - One of the best experts on this subject based on the ideXlab platform.
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High Risk of Sustained Ventricular Arrhythmia Recurrence After Acute Myocarditis
Journal of Clinical Medicine, 2020Co-Authors: Laurent Rosier, Amir Zouaghi, Valentin Barré, Raphaël Martins, Vincent Probst, Eloi Marijon, Nicolas Sadoul, Samuel Chauveau, Antoine Da Costa, Marc BadozAbstract:Acute Myocarditis is associated with cardiac arrhythmia in 25% of cases; a third of these arrhythmias are ventricular tachycardia (VT) or ventricular fibrillation (VF). The implantation of a cardiac defibrillator (ICD) following sustained ventricular arrhythmia remains controversial in these patients. We sought to assess the risk of major arrhythmic ventricular events (MAEs) over time in patients implanted with an ICD following sustained VT/VF in the acute phase of Myocarditis compared to those implanted for VT/VF occurring on Myocarditis sequelae. Our retrospective observational study included patients implanted with an ICD following VT/VF during acute Myocarditis or VT/VF on Myocarditis sequelae, from 2007 to 2017, in 15 French university hospitals. Over a median follow-up period of 3 years, MAE occurred in 11 (39%) patients of the acute Myocarditis group and 24 (60%) patients of the Myocarditis sequelae group. Kaplan-Meier MAE rate estimates at one and three years of follow-up were 19% and 45% in the acute group, and 43% and 64% in the sequelae group. Patients who experienced sustained ventricular arrhythmias during acute Myocarditis had a very high risk of VT/VF recurrence during follow-up. These results show that the risk of MAE recurrence remains high after resolution of the acute episode.
Kenneth L. Baughman - One of the best experts on this subject based on the ideXlab platform.
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Clinical management of acute Myocarditis and cardiomyopathy
Inflammatory Cardiomyopathy (DCMi), 2010Co-Authors: Kenneth L. BaughmanAbstract:Several forms of acute Myocarditis may present as new onset cardiomyopathy and congestive heart failure. These include Myocarditis characterized as fulminant, giant cell, chronic acute, eosinophilic (particularly necrotizing eosinophilic Myocarditis), peripartum, Lyme, small pox vaccine related, HIV-related, and acute myocardial infarction caused by Myocarditis with coronary arteritis. Treatment of each of these disorders is dependent upon considering the diagnosis, performing endomyocardial biopsy for histologic confirmation, and use of immune modulating or immunosuppressive therapy in appropriate candidates. Some forms of acute Myocarditis may resolve spontaneously without any treatment including fulminant Myocarditis, peripartum, and small pox vaccine related Myocarditis. Others require immune modulating therapy including giant cell Myocarditis, and eosinophilic Myocarditis; while others require specific treatment for the infectious or autoimmune pathogen responsible including eosinophilic Myocarditis, Lyme Myocarditis, and HIV-related. We currently have the technology which may allow us to determine if the 50% of patients with “idiopathic” cardiomyopathy in fact have a viral or post viral autoimmune related compromise of cardiac function.
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Mortality in primary and secondary Myocarditis.
American Heart Journal, 2004Co-Authors: Todd Pulerwitz, G. Michael Felker, Kenneth L. Baughman, Joshua M. Hare, Thomas P. Cappola, Edward K. KasperAbstract:Abstract Background Lymphocytic Myocarditis presents as a primary disorder or in association with a systemic disease. Whether primary and secondary Myocarditis have the same prognosis is unknown. Methods Patients (n = 171) referred to the Johns Hopkins Cardiomyopathy service from 1984 to 1998 with newly diagnosed cardiomyopathy were observed for an average of 5.9 years after an original diagnosis of biopsy-proven Myocarditis or until reaching the end point of death. Giant-cell Myocarditis was excluded from this study. Myocarditis was classified as secondary when a systemic disease was present at the time of presentation; otherwise, Myocarditis was classified as primary. Survival rates among patients with primary and secondary Myocarditis were compared with Kaplan-Meier analysis and Cox proportional hazard models incorporating clinical variables, including baseline hemodynamics and treatment with immunosuppressive therapy. Results The mortality rate associated with secondary Myocarditis varied substantially depending on the underlying systemic disorder. Peripartum Myocarditis, when compared with idiopathic Myocarditis, had a reduced mortality rate (relative hazard, 0.23 [0.06–0.98]; P P = .55). In contrast, human immunodeficiency virus Myocarditis had a particularly poor prognosis (relative hazard, 6.70 [3.51–12.79]; P P = .19). For both primary and secondary Myocarditis, advanced age and pulmonary hypertension were important clinical predictors of death. Conclusions The prognosis of patients with secondary Myocarditis, when compared with patients with idiopathic Myocarditis, seems most affected by the primary disease process.
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Long-term outcome of fulminant Myocarditis as compared with acute (nonfulminant) Myocarditis.
New England Journal of Medicine, 2000Co-Authors: Robert E. Mccarthy, John Boehmer, Ralph H. Hruban, Grover M. Hutchins, Edward K. Kasper, Joshua M. Hare, Kenneth L. BaughmanAbstract:Background Lymphocytic Myocarditis causes left ventricular dysfunction that may be persistent or reversible. There are no clinical criteria that predict which patients will recover ventricular function and which cases will progress to dilated cardiomyopathy. We hypothesized that patients with fulminant Myocarditis may have a better long-term prognosis than those with acute (nonfulminant) Myocarditis. Methods We identified 147 patients considered to have Myocarditis according to the findings on endomyocardial biopsy and the Dallas histopathological criteria. Fulminant Myocarditis was diagnosed on the basis of clinical features at presentation, including the presence of severe hemodynamic compromise, rapid onset of symptoms, and fever. Patients with acute Myocarditis did not have these features. The incidence of the end point of this study, death or heart transplantation, was ascertained by contact with the patient or the patient's family or by a search of the National Death Index. The average period of fol...
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Echocardiographic findings in Fulminant and acute Myocarditis
Journal of the American College of Cardiology, 2000Co-Authors: G. Michael Felker, John Boehmer, Ralph H. Hruban, Grover M. Hutchins, Edward K. Kasper, Kenneth L. Baughman, Joshua M. HareAbstract:Abstract OBJECTIVES We sought to use echocardiography to assess the presentation and potential for recovery of left ventricular (LV) function of patients with fulminant Myocarditis compared with those with acute Myocarditis. BACKGROUND The clinical course of patients with Myocarditis remains poorly defined. We have previously proposed a classification that provides prognostic information in Myocarditis patients. Fulminant Myocarditis causes a distinct onset of illness and severe hemodynamic compromise, whereas acute Myocarditis has an indistinct presentation, less severe hemodynamic compromise and a greater likelihood of progression to dilated cardiomyopathy. METHODS Echocardiography was performed at presentation and at six months to test the hypothesis that fulminant (n = 11) or acute (n = 43) Myocarditis could be distinguished morphologically. RESULTS Patients with both fulminant (fractional shortening 19 ± 4%) and acute Myocarditis (17 ± 7%) had LV systolic dysfunction. Patients with fulminant Myocarditis had near normal LV diastolic dimensions (5.3 ± 0.9 cm) but increased septal thickness (1.2 ± 0.2 cm) at presentation, while those with acute Myocarditis had increased diastolic dimensions (6.1 ± 0.8 cm, p CONCLUSIONS Fulminant Myocarditis is distinguishable from acute Myocarditis by echocardiography. Patients with fulminant Myocarditis exhibit a substantial improvement in ventricular function at six months compared with those with acute Myocarditis. Echocardiography has value in classifying patients with Myocarditis and may provide prognostic information.
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Clinicopathoiogic description of Myocarditis
Journal of the American College of Cardiology, 1991Co-Authors: Eric B. Lieberman, Grover M. Hutchins, Noel R. Rose, Ahvie Herskowitz, Kenneth L. BaughmanAbstract:Histologic evidence of Myocarditis was demonstrated in 35 of 348 patients submitted to endomyocardial biopsy over 5 years. Analysis of the histologic findings and clinical course of these patients resulted in a new clinicopathologic classification of Myocarditis in which four distinct subgroups are identified. Patients with fulminant Myocarditis become acutely ill after a distinct viral prodrome, have severe cardiovascular compromise, multiple foci of active Myocarditis by histologic study and ventricular dysfunction that either resolves spontaneously or results in death. Patients with acute, chronic active and chronic persistent Myocarditis have a less distinct onset of illness. Patients with acute Myocarditis present with established ventricular dysfunction and may respond to immunosuppressive therapy or their condition may progress to dilated cardiomyopathy. Those with chronic active Myocarditis initially respond to immunosuppressive therapy, but they have clinical and histologic relapses and develop ventricular dysfunction associated with chronic inflammatory changes including giant cells on histologic study. Chronic persistent Myocarditis is characterized by a persistent histologic infiltrate, often with foci of myocyte necrosis but without ventricular dysfunction despite other cardiovascular symptoms such as chest pain or palpitation.
Heinz-peter Schultheiss - One of the best experts on this subject based on the ideXlab platform.
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Cardiac Autoantibodies in Viral Myocarditis
Heart Failure Clinics, 2005Co-Authors: Andrea Dörner, Angela Kallwellis-opara, Matthias Pauschinger, Uwe Kühl, Heinz-peter SchultheissAbstract:An episode of acute Myocarditis can initiate heart damage that partly results in dilated cardiomyopathy (DCM). Most clinical cases of Myocarditis in humans are suspected to be of viral etiology. Viruses such as coxsackievirus, influenza, cytomegalovirus, echovirus, adenovirus, and parvovirus have been detected in heart tissue of patients who have Myocarditis and DCM and cause myocardial inflammation (see article by Bowles and colleagues elsewhere in this issue) [1]. Piconaviruses, especially Group B coxsackieviruses, are the best analyzed agents in viral forms of Myocarditis. Despite the strong association between virus infection and Myocarditis, clinical and experimental data support immune and autoimmune mechanisms as playing major roles in the pathogenesis of Myocarditis and DCM. The mechanism by which an acute viral infection or chronic viral persistence can induce autoimmunity is under discussion. Molecular mimicry has been suggested as one mechanism to explain chronic Myocarditis in the postinfectious period following induction of acute Myocarditis by coxsackievirus B3 (CVB3) [2,3]. Several cellular antigens have been identified as probable targets in virus-induced Myocarditis and DCM (Table 1) [4–7]. In several cases, viral antigen
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cardiac troponin t in patients with clinically suspected Myocarditis
Journal of the American College of Cardiology, 1997Co-Authors: Bernward Lauer, Matthias Pauschinger, Uwe Kühl, Christoph Niederau, Mira Schannwell, Bodo Eckhard Strauer, Heinz-peter SchultheissAbstract:Objectives. The present study investigated whether myocyte injury can be assessed sensitively by measurement of serum levels of cardiac troponin T (cTnT) in patients with clinically suspected Myocarditis and whether cTnT levels may predict the results of histologic and immunohistologic analysis of endomyocardial biopsy specimens. Background. Conventionally used laboratory variables often fail to show myocyte injury in patients with clinically suspected Myocarditis, possibly because of a low extent of myocardial injury in these patients. Sensitive variables for myocyte injury have not yet been investigated. Methods. Eighty patients with clinically suspected Myocarditis were screened for creatine kinase (CK) activity, MB isoform of CK (CK-MB) activity and cTnT. Endomyocardial biopsy specimens were examined histologically and immunohistologically. Results. cTnT was elevated in 28 of 80 patients with clinically suspected Myocarditis, CK in 4 and CK-MB in 1. Histologic analysis alone of the endomyocardial biopsy specimen revealed evidence of Myocarditis in only five patients, all with elevated cTnT levels. Twenty-three of 28 patients with elevated cTnT levels had histologically negative findings for Myocarditis. Additional immunohistologic analysis revealed evidence of Myocarditis in 26 (93%) of 28 patients with elevated cTnT levels and in 23 (44%) of 52 patients with normal cTnT levels. Mean cTnT levels were higher in patients with Myocarditis proved histologically or immunohistologically, or both, than in patients without Myocarditis (0.59 ± 1.68 vs. 0.04 ± 0.05, p < 0.001). Conclusions. Measurement of serum levels of cTnT provides evidence of myocyte injury in patients with clinically suspected Myocarditis more sensitively than does conventional determination of cardiac enzyme levels. Myocardial cell damage may be present even in the absence of histologic signs of Myocarditis. Additional immunohistologic analysis often shows lymphocytic infiltrates in these patients. Elevated levels of cTnT are highly predictive for Myocarditis in this group.
Juan Alejos - One of the best experts on this subject based on the ideXlab platform.
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An Approach to the Treatment of Pediatric Myocarditis
Pediatric Drugs, 2002Co-Authors: Daniel Levi, Juan AlejosAbstract:The newest treatment strategies for pediatric Myocarditis have evolved from an understanding of the pathophysiology of myocyte damage. Although the initial stages of viral Myocarditis apparently result from the direct cytopathic effects on the atrial and ventricular myocardium, later stages of progressive decompensation result from immune-mediated myocyte destruction common to many forms of Myocarditis. Despite advances in the understanding of the role of genetics, immunologic mechanisms, and infectious causes of Myocarditis, supportive therapy continues to remain the cornerstone of treatment. Presently, therapies include supportive management with anticongestive agents, antiviral medications, and therapies that attempt to interrupt the immunologic cascade. Clinical studies have yet to provide convincing evidence that the use of immunosuppressants and γ-globulin favorably alters the outcome for pediatric patients with acute Myocarditis. Ventricular assist devices and heart transplantation remain as treatment options for all pediatric patients with severe Myocarditis resistant to all other therapies. Although this review will focus on viral Myocarditis, the supportive strategies and surgical treatment options apply to most forms of cardiomyopathy.
Laurent Rosier - One of the best experts on this subject based on the ideXlab platform.
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High Risk of Sustained Ventricular Arrhythmia Recurrence After Acute Myocarditis
Journal of Clinical Medicine, 2020Co-Authors: Laurent Rosier, Amir Zouaghi, Valentin Barré, Raphaël Martins, Vincent Probst, Eloi Marijon, Nicolas Sadoul, Samuel Chauveau, Antoine Da Costa, Marc BadozAbstract:Acute Myocarditis is associated with cardiac arrhythmia in 25% of cases; a third of these arrhythmias are ventricular tachycardia (VT) or ventricular fibrillation (VF). The implantation of a cardiac defibrillator (ICD) following sustained ventricular arrhythmia remains controversial in these patients. We sought to assess the risk of major arrhythmic ventricular events (MAEs) over time in patients implanted with an ICD following sustained VT/VF in the acute phase of Myocarditis compared to those implanted for VT/VF occurring on Myocarditis sequelae. Our retrospective observational study included patients implanted with an ICD following VT/VF during acute Myocarditis or VT/VF on Myocarditis sequelae, from 2007 to 2017, in 15 French university hospitals. Over a median follow-up period of 3 years, MAE occurred in 11 (39%) patients of the acute Myocarditis group and 24 (60%) patients of the Myocarditis sequelae group. Kaplan-Meier MAE rate estimates at one and three years of follow-up were 19% and 45% in the acute group, and 43% and 64% in the sequelae group. Patients who experienced sustained ventricular arrhythmias during acute Myocarditis had a very high risk of VT/VF recurrence during follow-up. These results show that the risk of MAE recurrence remains high after resolution of the acute episode.
