Myocardial enterovirus infection with left ventricular dysfunction: A benign disease compared with idiopathic dilated cardiomyopathy

Figulla, Hans R.; Stille-Siegener, Michael; Mall, Gerhard; Heim, Albert; Kreuzer, H

doi:10.1016/0735-1097(94)00517-t

Cited by 66 publications

(49 citation statements)

References 28 publications

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“…Although efficacy of an immunomodulatory treatment of enteroviral infections was demonstrated in animal myocarditis models, reported applications in humans are anecdotal. 32,33,40,41 Successful treatment of myocarditis with antiviral agents has been reported in case reports. 42 A 6-month treatment with IFN-␣2a in 4 patients with enteroviral infection led to hemodynamic improvement in all patients, but virus was still detected in 2 of 4 patients.…”

Section: Searching For Novel Treatment Strategiesmentioning

confidence: 99%

Interferon-β Treatment Eliminates Cardiotropic Viruses and Improves Left Ventricular Function in Patients With Myocardial Persistence of Viral Genomes and Left Ventricular Dysfunction

et al. 2003

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Background— Viral infections are important causes of myocarditis and may induce cardiac dysfunction and finally lead to dilated cardiomyopathy. We investigated whether interferon (IFN)-β therapy is safe and may achieve virus clearance and prevent deterioration of left ventricular (LV) function in patients with myocardial virus persistence. Methods and Results— In this phase II study, 22 consecutive patients with persistence of LV dysfunction (history of symptoms, 44±27 months) and polymerase chain reaction–proven enteroviral or adenoviral genomes were treated with 18×10 6 IU/week IFN-β (Beneferon) subcutaneously for 24 weeks. Histological and immunohistological analysis of endomyocardial biopsies was used to characterize myocardial inflammation. LV diameters and ejection fraction were assessed by echocardiography and angiography, respectively. During the treatment period, IFN-β was well tolerated by all patients. No patient deteriorated. Clearance of viral genomes was observed in 22 of 22 of patients after antiviral therapy. Virus clearance was paralleled by a significant decrease of LV end diastolic and end systolic diameters, decreasing from 59.7±11.1 to 56.5±10.0 mm ( P <0.001) and 43.2±13.6 to 39.4±12.1 mm ( P <0.001), respectively. LV ejection fraction increased from 44.6±15.5% to 53.1±16.8% ( P <0.001). Conclusions— A 6 months, IFN-β treatment was safe in patients with myocardial enteroviral or adenoviral persistence and LV dysfunction and resulted in elimination of viral genomes (22 of 22 patients) and improved LV function (15 of 22 patients).

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Section: Searching For Novel Treatment Strategiesmentioning

confidence: 99%

Interferon-β Treatment Eliminates Cardiotropic Viruses and Improves Left Ventricular Function in Patients With Myocardial Persistence of Viral Genomes and Left Ventricular Dysfunction

et al. 2003

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“…104 Genomic analysis of biopsy specimens has, to date, provided conflicting prognostic information. An initial singlecenter study of 77 patients by Figulla et al 105 reported a significantly better 4-year transplant-free survival rate for enterovirus-positive (Coxsackie B3 viral genome) patients compared with enterovirus-negative patients (95% versus 55%; PϽ0.05). Furthermore, LVEF increased significantly from 35Ϯ13% to 43Ϯ9% (PϽ0.05) in the virus-positive group but remained unchanged in the virus-negative group (34Ϯ12% to 37Ϯ14%; PϭNS).…”

Section: Natural History Of Myocarditismentioning

confidence: 99%

Myocarditis

2006

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“…To determine the influence of CVB3 infection on cytokine concentrations early after infection, the AUC day [1][2][3][4] values of infected cultures were compared with AUC day 1-4 values of controls, indicating a significant increase of cytokine concentrations (IL-6, Figure 2A, Pϭ0.026, MannWhitney test; IL-8, Figure 2B, PϽ0.001, t test). Moreover, a combined analysis of AUC day 1-4 data (depicted in Figures 2A and 2B) with AUC day 1-4 data from 2 other long-term experiments using different lines of myocardial fibroblasts (raw data not shown) confirmed an early increase of IL-6 concentrations (Pϭ0.0035, t test, nϭ24) and IL8 concentrations (PϽ0.001, t test, nϭ24) after CVB3 infection.…”

Section: Transient Induction Of Il-6 and Il-8 By Cvb3 Infectionmentioning

confidence: 99%

“…1,2 Chronic enterovirus myocarditis may result in congestive heart failure, and the only remedy then may be heart transplantation. 2,3 Recently, rapid diagnosis of myocardial enterovirus infections was achieved by endomyocardial biopsy with subsequent detection of enterovirus RNA. 1,4,5 Despite the progress in diagnosing enterovirus heart disease, its pathogenesis is not yet understood completely.…”

mentioning

confidence: 99%

Transient Induction of Cytokine Production in Human Myocardial Fibroblasts by Coxsackievirus B3

Heim

Zeuke

Weiss

et al. 2000

Circulation Research

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Abstract-Cytokine expression in enterovirus infections of the heart may trigger inflammation and have detrimental effects on myocytes. However, the induction of cytokines in human myocardial cells by cardiotropic enteroviruses, for example, Coxsackievirus B3 (CVB3), was not yet demonstrated. Fibroblasts are the predominant cell type of the myocardial interstitium before inflammatory infiltration develops. Hence, we investigated, by enzyme immunoassays, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and nucleic acid sequence-based amplification (NASBA), whether CVB3 induces cytokine expression in cultured human myocardial fibroblasts. As early as 3 hours after infection, RT-qPCR demonstrated a 2-fold increase of interleukin (IL)-6 and IL-8 mRNA compared with basal transcription, resulting in a significant increase of IL-6 and IL-8 to a median level of 1500 pg/mL (range, 1246 to 1858) and 529 pg/mL (range, 428 to 601) in culture supernatants, respectively. IL-6 and IL-8 expression returned to basal levels within 3 and 5 days, respectively, despite a persistent (carrier-state) CVB3 infection. For comparison, IL-6 and IL-8 were induced in dermal fibroblasts later than 3 days after CVB3 infection. Although the low-level IL-1␣ transcription of myocardial fibroblasts was not significantly increased, IL-1␣ was released from cells to culture supernatants 5 days after infection. Furthermore, a suppression of interferon-␤ transcription was demonstrated up to 24 hours after CVB3 infection of myocardial fibroblasts by highly sensitive NASBA. In conclusion, our results demonstrate a heart-specific pattern of a rapid and transient induction of proinflammatory cytokines after CVB3 infection, whereas the expression of protective interferon-␤ was suppressed by CVB3. (Circ Res. 2000;86:753-759.)

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Myocardial enterovirus infection with left ventricular dysfunction: A benign disease compared with idiopathic dilated cardiomyopathy

Cited by 66 publications

References 28 publications

Interferon-β Treatment Eliminates Cardiotropic Viruses and Improves Left Ventricular Function in Patients With Myocardial Persistence of Viral Genomes and Left Ventricular Dysfunction

Interferon-β Treatment Eliminates Cardiotropic Viruses and Improves Left Ventricular Function in Patients With Myocardial Persistence of Viral Genomes and Left Ventricular Dysfunction

Myocarditis

Transient Induction of Cytokine Production in Human Myocardial Fibroblasts by Coxsackievirus B3

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