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Heart Failure (HF) represents an increasing clinical problem with a reported mortality (for either diastolic or systolic HF) of approximately 60% at 5 years after diagnosis (Shahar et al. 2004). The incidence of end-stage HF has increased four-fold in the last 20 years (Hubler et al. 2003; Terracciano et al. 2010). Symptomatic HF confers a worse prognosis than the majority of cancers, with mortality as high as 45% at one year (Cohn 1996; Jessup and Brozena 2003), and there are currently more than 16 million people in Europe and the United States (US) suffering from this disease. HF is also a major burden in the developing world (Mayosi 2007). Despite substantial medical advances in the treatment of HF, cardiac transplantation (CTx) remains the best long term therapy for patients suffering from endstage disease, with 50 % survival at 10 years post CTx (Hunt, SA et al. 2009a; Trulock et al. 2007). A fixed and inadequate donor organ pool means that CTx is available to only a small proportion of eligible patients. In the US an estimated 100 000 patients are believed to be suitable for CTx (Maybaum et al. 2008), but only 2200 transplants are performed annually (Hunt,SA et al. 2009b). As a consequence the use of LVADs as Bridge-to-Transplantation (BTT) has increased steadily over the last few years and approximately 9000 CTx candidates, i.e. more than a third of all listed candidates in the US, have undergone LVAD implantation since 1999 (Mancini and Lietz 2010). Initially, LVADs were utilised in the acute setting, in the management of post-cardiotomy cardiogenic shock (PCCS), a rare clinical scenario associated with high morbidity and mortality (Mehta et al. 1996). Despite improvements in LVAD technology, and the understanding of PCCS, the use of mechanical unloading (MU) in this acute setting is now minimal, with large studies showing survival of 23-52.4% (Sylvin et al. 2010). The role of LVADs subsequently expanded to incorporate patients with severe drugresistant HF, primarily as a BTT, with subsequent extension of the role to include “destination therapy” (DT) in those patients unsuitable for CTx (Kirklin et al. 2011). In a small minority of patients a third application for chronic LVAD therapy, “Bridge-toRecovery” (BTR) evolved, following the observation that MU appeared to coincide with cellular, molecular, electrophysiological and structural myocardial changes consistent with functional recovery (Altemose et al. 1997; Farrar et al. 2002; Heerdt,PM et al. 2000a; Hetzer et al. 2000; Ogletree-Hughes et al. 2001; Sylvin et al. 2010; Young 2001). Such observations allied with anecdotal examples of cardiac recovery in isolated patients following enforced device removal (mandated by the development of complications) (Frazier 1994; Frazier and

Myocardial Recovery Following Left Ventricular Assist Device Therapy