INVITED COMMENTARY Can Bridge to Recovery Help to Reveal the Secrets of the Failing Heart? Michael Ibrahim & Cesare Terracciano & Magdi H. Yacoub Published online: 18 May 2012 # Springer Science+Business Media, LLC 2012 Abstract Despite several decades of research and clinical experience, the basic mechanisms of the failing heart remain largely a secret. While pharmacological therapy can induce limited reverse remodeling, left ventricular assist device (LVAD) therapy offers the opportunity to induce significant improvements to the structure and function of the heart, with major clinical implications. LVAD therapy also provides significant insight into which changes have an impact on function and which do not, and could therefore reveal some of the secrets of the failing heart. In addition, LVAD-induced mechanical unloading may unlock further myocardial prop- erties hitherto unknown such as the proliferation of the stem cell compartment. It may also serve as an important platform for emerging therapies such as gene and cell therapies. In this review, we highlight the most recent novel discoveries related to LVAD therapy and bridge to recovery (BTR). Discovering the integrated network of events that underlies BTR could unravel the secrets of the failing heart. Keywords LVAD . Recovery . Heart failure . Bridge to recovery Introduction Heart failure (HF) is a disease of massive proportions with approximately 800,000 patients in the United Kingdom alone, and HF carries a quality of life and survival worse than most common cancers [1, 2]. Despite major research efforts, its basic mechanisms remain largely unknown. A major reason for this is the difficulty in determining which changes are primary and which are secondary. The understanding of the mechanisms of HF has changed tremendously over the last five decades, which is reflected in the changes to its treatment. The most fundamental change has been a shift from treating symptoms to attempt- ing to improve prognosis. In the 1950s, the clinical syn- drome of HF was thought to be a disease of renal insufficiency and treatment was aimed at improving symp- toms using digitalis (to enhance cardiac contractility, and improve symptoms by reducing breathlessness), diuretics (to reduce the circulating volume and reduce peripheral and pulmonary edema), and prolonged bed rest. In the 1960s to 1980s, focus shifted to thinking of HF as a cardio- vascular disease, based on pathological preload, afterload, and contractility. Treatment was still aimed at relieving symptoms, using vasodilators (to reduce pre- and afterload) and inotropes. In the 1980s and to the current era, HF includes a neuroendocrine disorder, and the move toward evidence-based medicine shifted attention toward prognosis. Angiotensin-converting enzyme inhibitors (ACEIs), β- adrenergic blockers, and training became the mainstay of treatment for prognostic benefit. Thus, in 50 years, treatment has changed from positive inotropes to nega- tive inotropes, from rest to training, and from vasodila- tors to ACEIs. Today the mainstay of therapy is ACEIs, diuretics, and β-adrenergic blockers [3]. The current understanding of remodeling as a central driver of HF pathophysiology can be seen as a network of interacting changes. While many of the therapies available have some influence on these changes, left ventricular assist device (LVAD) therapy offers the most comprehensive strategy for the reversal of remodeling and the induction of cardiac recovery in some patients. M. Ibrahim : C. Terracciano : M. H. Yacoub (*) Harefield Heart Science Centre, National Heart and Lung Institute, Imperial College London, Harefield Hospital, London UB9 6JH, UK e-mail: m.yacoub@imperial.ac.uk Curr Cardiol Rep (2012) 14:392–396 DOI 10.1007/s11886-012-0282-x