Ventricular unloading, tissue angiotensin II, matrix modulation, and function during left ventricular assist device support.

eart failure (HF) has become the major epidemic of the ew millennium, and use of the left ventricular (LV) assist evice (LVAD) for mechanical support in end-stage HF is ncreasing. Introduced as an alternative to heart transplanation, LVADs were approved by the Food and Drug dministration a decade ago to provide a bridge to translantation in the moribund end-stage HF patient waiting or a donor heart. However, LVAD is now becoming a ife-saving treatment option for patients with severe HF efractory to optimal medical therapy that includes reninngiotensin-aldosterone system (RAAS) inhibitors, betadrenergic blockers, inotropes, and diuretics. The EMATCH (Randomized Evaluation of Mechanical Asistance for the treatment of Congestive Heart Failure) trial