Abstract
Background: Myocarditis can manifest with lone ventricular tachyarrhythmias (LVT). Elective inflammation of conduction tissue (CT) is supposed but unproved. Methods: Forty-two of 420 patients with biopsy proven myocarditis presented with LVT. Twelve of them included CT sections in endomyocardial biopsies. Real-time polymerase chain reaction (PCR) for viral genomes, immunohistochemistry for viral antigens and Toll like receptor 4 (TLR4) were performed. Twelve myocarditis patients with infarct-like or cardiomyopathic phenotype and CT included in tissue section were used as controls. Results: Four of the 12 patients presented non-sustained ventricular tachycardia (nsVT), six with sustained ventricular tachycardia (sVT), two with ventricular fibrillation. CT was inflamed in all LVT patients and not in controls (p < 0.001). PCR was positive for influenza-A virus in two, herpes simplex virus type 2 (HSV2) in one and adenovirus in one with positive CT immunostaining for viral antigens. In eight patients, negative PCR and TLR4 overexpression suggested an immune-mediated pathway. Patients with influenza-A myocarditis and CT infection responded to oseltamivir, those with HSV2 (Herpes Virus 2) and adenovirus infection died. The eight patients with immune-mediated myocarditis were treated with steroids and azathioprine. Seven of them had no more VT(ventricular tachyarrhythmias)during six-month follow-up. Conclusions: Arrhythmic phenotype of myocarditis is associated with CT inflammation/infection. Molecular characterization of CT damage may lead to pharmacologic control of arrhythmias in 75% of cases.
Highlights
Myocarditis can manifest with a variety of symptoms that can be incorporated into three major phenotypes: infarct-like, cardiomyopathic and arrhythmic type [1]
Functional and morphological data were analyzed according to the Lake Louise criteria [2] for which cardiac magnetic resonance (CMR) diagnosis of myocarditis is suggested by the presence of at least two of the following criteria, including early enhancement, edema on T2-weighted/Short Tau Inversion Recovery (STIR) sequences, and late gadolinium enhancement (LGE) in a nonischemic pattern
CMR was performed in 11 of 12 patients, because the patient with herpes simplex virus type 2 (HSV2)-related myocarditis promptly died of ventricular fibrillation
Summary
Myocarditis can manifest with a variety of symptoms that can be incorporated into three major phenotypes: infarct-like, cardiomyopathic and arrhythmic type [1]. Cardiomyopathic phenotype has a more subtle course with progressive dilatation and dysfunction that looks like a dilated cardiomyopathy and where CMR sensitivity based on Lake Louise criteria [2] is reduced to 57% [3]. In this instance an endomyocardial biopsy is recommended to confirm the diagnosis and establish the most appropriate (anti-viral or immunosuppressive) therapy. Twelve myocarditis patients with infarct-like or cardiomyopathic phenotype and CT included in tissue section were used as controls. Molecular characterization of CT damage may lead to pharmacologic control of arrhythmias in 75% of cases
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