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Review
. 2016 Nov 8;3(4):31.
doi: 10.3390/jcdd3040031.

Myocarditis in Paediatric Patients: Unveiling the Progression to Dilated Cardiomyopathy and Heart Failure

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Free PMC article
Review

Myocarditis in Paediatric Patients: Unveiling the Progression to Dilated Cardiomyopathy and Heart Failure

Inês Teixeira Farinha et al. J Cardiovasc Dev Dis. .
Free PMC article

Abstract

Myocarditis is a challenging and potentially life-threatening disease associated with high morbidity in some paediatric patients, due to its ability to present as an acute and fulminant disease and to ultimately progress to dilated cardiomyopathy. It has been described as an inflammatory disease of the myocardium caused by diverse aetiologies. Viral infection is the most frequent cause of myocarditis in developed countries, but bacterial and protozoal infections or drug hypersensitivity may also be causative agents. The prompt diagnosis in paediatric patients is difficult, as the spectrum of clinical manifestation can range from no myocardial dysfunction to sudden cardiac death. Recent studies on myocarditis pathogenesis have revealed a triphasic nature of this disease, which influences the diagnostic and therapeutic strategies to adopt in each patient. Endomyocardial biopsy remains the gold standard for diagnosing myocarditis, and several non-invasive diagnostic tools can be used to support the diagnosis. Intravenous immunoglobulin has become part of routine practice in the treatment of myocarditis in paediatric patients at many centres, but its true effect on the cardiac function has been the target of many studies. The aim of this review is to approach the recently discovered facets of paediatric myocarditis regarding its progression to dilated cardiomyopathy.

Keywords: dilated cardiomyopathy; heart failure; inflammation; myocarditis; viral myocarditis.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Myocarditis: A triphasic disease. In recent years, myocarditis has been set in a framework of three successive and distinct phases with undefined borders. For each phase, average duration (regarding the case of coxsackievirus-mediated myocarditis), characteristics and physiopathological intervenients are indicated. CD, cluster of differentiation; Th1, T helper 1; Th17, T helper 17; Treg, regulatory T.
Figure 2
Figure 2
A 15-year-old boy with Epstein–Barr virus myocarditis: (a) a short-axis T2-weighted image demonstrating focal myocardial oedema (red arrows); and (b) a short-axis T1-weighted late gadolinium enhancement image (red arrows). RV, right ventricle; LV, left ventricle.
Figure 3
Figure 3
ECG of a 14-year-old girl with familial DCM showing sinus tachycardia, right axis deviation and nonspecific ST-wave changes.
Figure 4
Figure 4
Four-chamber apical view echocardiogram of an 11-month-old boy with DCM. RA, right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle.

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