Interferon-β treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunction

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Abstract

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 × 106 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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Kühl, U., Pauschinger, M., Schwimmbeck, P. L., Seeberg, B., Lober, C., Noutsias, M., … Schultheiss, H. P. (2003). Interferon-β treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunction. Circulation, 107(22), 2793–2798. https://doi.org/10.1161/01.CIR.0000072766.67150.51

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