MYOCARDITIS WITH OUTCOME IN DILATED CARDIOMYOPATHY COMPLICATED BY REFRACTORY HEART FAILURE AND REQUIRING HEART TRANSPLANTATION
Л. А. БалыковаI. V. LeontyevaN. N. UrzyaevaN. V. SchekinaYu. A. PetrushkinaN. V. IvyanskayaV. M. Soloviev
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The article describes the clinical case of subacute myocarditis in a child with an outcome in dilated cardiomyopathy, complicated with congestive heart failure. Difficulties in diagnosing the disease that manifested with cardiac arrhythmia are discussed. The main signs suggesting postmiocardic cardiomyopathy included a reduced deflection voltage and frequent ventricular extrasystoles with episodes of the ventricular tachycardia in the onset of the disease, left ventricular dilatation, a significant decrease in ejection fraction, increased activity of natriuretic peptide, findings of perfusion scintigraphy and magnetic resonance imaging. Medical therapy and implantation of a cardioverter defibrillator were ineffective. The child repeatedly suffered from syncopal conditions with circulatory arrest, which required resuscitation. Due to the ineffectiveness of drug therapy conducted in the leading federal centres, considering cardiac transplantation abroad was recommended.Keywords:
Dilated Cardiomyopathy
Dilated Cardiomyopathy
Viral Myocarditis
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Myocarditis and dilated cardiomyopathy (DCM) are common causes of morbidity and mortality in children and adults. Recently, the human coxsackievirus and adenovirus receptor (CAR), a common receptor for coxsackieviruses and adenoviruses, was discovered and its increased expression has been reported in patients with DCM and myocarditis.To measure the expression of CAR in myocardial tissues of patients with DCM and its cellular localization in DCM cases.Formalin-fixed myocardial tissues collected during autopsy from 26 cases of DCM, and 20 cases each of noncardiac disease and cardiac disease other than DCM were included as the test group, and control groups A and B, respectively. Expression of CAR was studied using immunohistochemical staining of myocardial tissue with a CAR-specific rabbit polyclonal antibody. CAR messenger RNA was semiquantified by reverse transcription polymerase chain reaction followed by agarose gel analysis and measurement of band intensity.CAR positivity in DCM cases was found to be 96% (25 of 26) compared with 30% in control group A and 40% in control group B. CAR was found to be expressed in myocytes, endothelial and interstitial cells; however, positivity in myocytes was significantly higher than in other cells in all groups. The site of CAR expression was predominantly the sarcolemma along with cytoplasm in cardiomyocytes.The present study highlighted the increased expression of CAR in DCM cases, with localization in myocytes and endothelial cells.
Coxsackievirus
Dilated Cardiomyopathy
Viral Myocarditis
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Development of ventricular fibrillation or pulseless ventricular tachycardia after an initial rhythm of pulseless electrical activity or asystole is associated with significantly increased cardiac arrest mortality.To examine differences in epinephrine administration during cardiac arrest between patients who had a secondary ventricular fibrillation or ventricular tachycardia develop and patients who did not.Data were collected for 2 groups of patients with in-hospital cardiac arrest and an initial rhythm of pulseless electrical activity or asystole: those who had a secondary ventricular fibrillation or ventricular tachycardia develop (cases) and those who did not (controls). Dosing of epinephrine during cardiac arrest and other variables were compared between cases and controls.Of the 215 patients identified with an initial rhythm of pulseless electrical activity or asystole, 51 (23.7%) had a secondary ventricular fibrillation or ventricular tachycardia develop. Throughout the total duration of arrest, including periods of return of spontaneous circulation, the dosing interval for epinephrine in patients who had a secondary ventricular fibrillation or ventricular tachycardia develop was 1 mg every 3.4 minutes compared with 1 mg every 5 minutes in controls (P= .001). For the total duration of pulselessness, excluding periods of return of spontaneous circulation during the arrest, the dosing interval for epinephrine in patients who had a secondary ventricular fibrillation or ventricular tachycardia develop was 1 mg every 3.1 minutes versus 1 mg every 4.3 minutes in controls (P= .001).More frequent administration of epinephrine during cardiac arrest is associated with development of secondary ventricular fibrillation or ventricular tachycardia.
Asystole
Pulseless electrical activity
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Dilated cardiomyopathy (DCM) is a heterogeneous group of myocardial diseases clinically defined by the presence of left ventricular dilatation and contractile dysfunction. Among various causes of DCM, a progression from viral myocarditis to DCM has long been hypothesized. Supporting this possibility, studies by endomyocardial biopsy, the only method to obtain a definite diagnosis of myocarditis at present, have provided evidence of inflammation in the myocardium in DCM patients. A number of experimental studies have elucidated a cell‐mediated autoimmune mechanism triggered by viral infection in the progression of myocarditis to DCM. In addition, the important role of inflammation in the pathogenesis of heart failure has been recognized, and many terms including myocarditis, inflammatory cardiomyopathy, and inflammatory DCM have been used for myocardial diseases associated with inflammation. This review discusses the pathophysiology of inflammation in the myocardium, and refers to diagnosis and treatment based on these concepts.
Dilated Cardiomyopathy
Viral Myocarditis
Pathogenesis
Pathophysiology
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Myocarditis is an inflammatory heart muscle disease, resulting from various etiologies, both noninfectious and infectious, which may be associated or not with cardiac dysfunction. Its course is unpredictable: it may spontaneously resolve or evolve into dilated cardiomyopathy and heart failure. A possible connection between myocarditis and dilated cardiomyopathy has long been postulated, but the intimate mechanisms linking these two conditions are still poorly understood. Viral myocarditis could induce a dilated cardiomyopathy through viral persistence and/or by triggering an autoimmune process. Understanding the mechanisms underlying the relationship between myocarditis and dilated cardiomyopathy will help in identifying an effective strategy of treatment aimed to stop and prevent cardiac damage. Specifically, we need to (a) evaluate the potential role of autoantibodies in disease prevention and progression, and understand their importance as markers of disease progression; (b) clarify the role of immunoregulation in exacerbating the disease.
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Implantable cardioverter defibrillators (ICD) are usually implanted in patients with malignant ventricular tachyarrhytmias. Aim of this study was to investigate the recurrence of minor ventricular arrhythmias to predict the occurrence of ventricular fibrillation episodes in patients with ICD. The study design was a retrospective analysis of 237 patients, whose ICD was programmed to deliver electrical therapy only for ventricular fibrillation (VF) but not for ventricular tachycardia (VT). We calculated the number, the mean duration and the mean ventricular cycle of the non-sustained ventricular tachyarrhythmias (NST) and of the sustained ventricular tachyarrhythmias (ST). We found that VF patients had a significant higher incidence of ventricular tachycardia compared to the no-VF patients.In addition, the mean VT episodes duration was higher in patients of the VF group than in patients free from ventricular fibrillation and the ventricular cycle length resulted to be significantly shorter in VF patients.
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Myocarditis and dilated cardiomyopathy both commonly present as new unexplained heart failure. This similarity raises the question of the interrelation of these disorders. What proportion of dilated cardiomyopathy begins as myocarditis, what other cardiac insults commonly lead to myocarditis and how often endomyocardial biopsy yields the diagnosis of myocarditis when present, are unknown. Proof that immunosuppressive treatment of myocarditis is beneficial is also lacking.
Dilated Cardiomyopathy
Endomyocardial Biopsy
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Dilated Cardiomyopathy
Histopathology
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Objective To study the relationships between Coxsackie virus B 3 (CVB 3) infection and the etiology of myocarditis and dilated cardiomyopathy. Methods With biotin labeled DNA probe, the in situ RT PCR for detection of CVB 3 RNA in myocardial samples of myocarditis and dilated cardiomyopathy was established. Results Positive signals were obtained in the 7 out of 16 myocardial biopsy samples from patients with post myocarditis and 5 out of 14 from patients with dilated cardiomyopathy. The patients' diagnoses were all confirmed by the pathological and clinical examinations. No positive signals were detected in the 16 normal myocardial biopsy samples. Conclusion CVB 3 RNA′s existing in some of myocardial tissues of myocarditis and dilated cardiomyopathy showed that there was a link between CVB 3 infection and the etiology of myocarditis and dilated cardiomyopathy.
Dilated Cardiomyopathy
Etiology
Viral Myocarditis
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The implications of ventricular fibrillation induced during elect rophysiologic testing are unclear. To determine the profile of patients in whom this arrhythmia occurs and to determine whether it has any prognostic value, follow‐up data were obtained on all patients in whom this arrhythmia was in duced in our laboratory during a ventricular stimulation protocol over an 18‐month period. Of 836 patients tested, 29 (27 men and 2 women) had inducible ventricular fibrillation. Most (52%) had coronary disease and 12 (41%) had suffered a prior myocardial infarction. All but 3 had some form of heart disease. Sixteen (55%) had abnormal left ventricular function. Eleven (38%) presented with spontaneous sustained ventricular tachycardia or ventricular fibrillation. Eight others had a history of nonsustained ventricular tachycardia.Follow‐up was obtained for a mean of 12 months. In spite of therapy, 2 patients died an arrhythmic death, 1 was resuscitated from ventricular fibrillation, 1 had spontaneous sustained ventricular tachycardia, 4 had inducible sustained ventricular tachycardia, 2 continued to have inducible ventricular fibrillation at second study, and 1 had recurrent syncope. Five patients had ventricular fibrillation induced on multiple occasions. Ventricular fibrillation induced during electraphysiologic study was found primarily in patients with structural heart disease and appeared reasonably reproducible. When reproducible, ventricular fibrillation appears to indicate a poor prognosis rather than an aspecific finding. The clinical profile of our poor prognosis group includes a history of prior ventricular tachycardia or ventricular fibrillation and the presence of coronary artery disease.
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