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The membranous ventriculo-atrial defect can be recognized echocardiographically on the basis of dilation of the right atrium in the setting of an unusually high Doppler echocardiogram gradient compared to the ventricular septal defect with shunting only at ventricular level. Since all patients in our series were symptomatic, we recommend surgical closure of all these defects.

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Background-Whether ventricular remodeling from hypertrophic cardiomyopathy (HCM), systemic hypertension, or other pathologies arises through a common signaling pathway or through independent molecular mechanisms is unknown. Conclusions-The uniform hypertrophic response to increased ventricular load in wild-type and ␣MHC403/ϩ mice indicates independent cardiac remodeling pathways and predicts that coexistent hypertension and HCM should not profoundly exacerbate cardiac hypertrophy. In contrast, sarcomere mutation and cyclosporin A-mediated calcineurin inhibition stimulate a shared hypertrophic signaling pathway. Defining distinct signaling pathways that trigger myocyte growth should help to tailor therapies for cardiac hypertrophy.

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