Left ventricular assist devices and the failing heart: a bridge to recovery, a permanent assist device, or a bridge too far?

The field of cardiac mechanical assist devices has achieved a number of striking technical breakthroughs over the past 40 years.1 Emblematic of the type of important technical accomplishments that have been achieved in this field has been the development of the portable, battery-driven left ventricular assist device (LVAD) for patients with intractable cardiac failure. Although LVADs have been used primarily as a “bridge to transplantation,” a number of centers have now begun to implant LVADs as an alternative to transplantation.2 Indeed, as the technology in this field improves, it is entirely conceivable that LVADs will evolve into small, unobtrusive devices that will run on small, portable, long-lasting battery supplies that will not require external connection to the outside. This, in turn, will allow LVADs to serve as a very reliable alternative to transplantation for many patients with advanced heart failure who cannot receive transplants or who cannot be weaned from LVAD support. Thus far, the clinical experience with LVADs as a bridge to transplantation has consistently shown dramatic improvements in cardiac output3 4 and New York Heart Association functional class.4 5 Importantly, these clinical changes have been attended by concomitant decreases in levels of neurohormones6 7 and cytokines,8 suggesting that LVAD support may alter the heart failure “milieu.” In an effort to explain these salutary changes in clinical status, investigators have turned to more basic studies and begun to examine myocardial ultrastructure before and after LVAD implantation. These latter studies have shown decreased myocyte necrosis9 10 and apoptosis,11 decreased myocytolysis,3 and improved myocyte contractility.12 The beneficial changes in the biology of the failing myocardium after LVAD support have also been …