Gene expression profile of the recovering human heart

Heart failure is a disease of increasing prevalence and poor prognosis. Current data indicate that 5-year survival following the diagnosis of heart failure is 50%, and patients with end-stage disease face a 1-year survival rate of 50%. Recent predictions suggest that heart failure will become the leading cause of all disability by 2020. For patients with refractory end-stage heart failure, there are few options for effective treatment. Although cardiac transplantation provides the best therapeutic outcome for end-stage HF, substantial limitations of this surgical intervention include an extremely limited supply of acceptable donor hearts, having reached a plateau of less than 3000 per year worldwide. Left ventricular assist device (LVAD) support of end-stage heart failure patients was originally approved as a bridge to cardiac transplant, and recent reports suggest improved outcomes in transplant recipients supported by LVAD in comparison with those treated with chronic inotropes.1 Improved morbidity and mortality were found in the REMATCH trial of long-term LVAD support compared with optimized medical management in severe HF patients ineligible for transplant, leading to the approval of LVAD as destination therapy. Unloading the left ventricle in end-stage heart failure patients with LVAD support can lead to partial normalization of myocardial structure and function, termed reverse remodelling. Reverse remodelling has been associated with changes in gene expression following LVAD support2–6 or pharmacological therapy.7 In select patients, LVAD support in conjunction with pharmacological therapy may result in sufficient reverse remodelling to allow explant of the device. LVAD-associated reverse remodelling provides the unique opportunity to obtain myocardial tissue in humans in end-stage heart failure at the time … *Corresponding author. Tel: +1 585 273 1094; fax: +1 585 276 1914. E-mail address : burns_blaxall{at}urmc.rochester.edu