Heart failure is a major problem in the patient with congenital heart disease. Normally interpreted as a sequela of surgical interventions or abnormal preoperative loading conditions, there is increasing evidence that congenital heart malformations and abnormal ventricular function can have the same underlying genetic cause. With the changing demographic characteristics and increasing complexity of care for patients with congenital heart disease, it can be anticipated that heart failure will be a rapidly growing concern in our field. In this article, we aim to give an overview of recent findings from mouse and human models that highlight shared pathways for the regulation of cardiac development and contractility, and their importance for medical care in the near future.
Copyright © 2013 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.