Ventricular remodeling and survival are more favorable for myocarditis than for idiopathic dilated cardiomyopathy in childhood: an outcomes study from the Pediatric Cardiomyopathy Registry

Foerster, S. R.; Canter, C. E.; Cinar, A.; Sleeper, L. A.; Webber, S. A.; Pahl, E.; Kantor, P. F.; Alvarez, J. A.; Colan, S. D.; Jefferies, J. L.; Lamour, J. M.; Margossian, R.; Messere, J. E.; Rusconi, P. G.; Shaddy, R. E.; Towbin, J. A.; Wilkinson, J. D.; Lipshultz, S. E.

Circ Heart Fail. 2010 Sep 14; 3(6):689-97


BACKGROUND: Myocarditis is a cause of a new-onset dilated cardiomyopathy phenotype in children, with small studies reporting high rates of recovery of left ventricular (LV) function. METHODS AND RESULTS: The presenting characteristics and outcomes of children with myocarditis diagnosed clinically and with biopsy confirmation (n=119) or with probable myocarditis diagnosed clinically or by biopsy alone (n=253) were compared with children with idiopathic dilated cardiomyopathy (n=1123). Characteristics at presentation were assessed as possible predictors of outcomes. The distributions of time to death, transplantation, and echocardiographic normalization in the biopsy-confirmed myocarditis and probable myocarditis groups did not differ (P>/=0.5), but both groups differed significantly from the idiopathic dilated cardiomyopathy group (all P2 (hazard ratio, 0.36; 95% confidence interval, 0.22 to 0.58; P<0.001) and greater septal wall thickness (hazard ratio, 1.16; 95% confidence interval, 1.01 to 1.34; P=0.04). CONCLUSIONS: Children with biopsy-confirmed or probable myocarditis had similar proportions of death, transplantation, and echocardiographic normalization 3 years after presentation and better outcomes than those of children with idiopathic dilated cardiomyopathy. In children with myocarditis who had impaired LV ejection at presentation, rates of echocardiographic normalization were greater in those without LV dilation and in those with greater septal wall thickness at presentation. Clinical Trial Registration- URL: Unique identifier: NCT00005391.

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