Key Words: Editorials heart-assist device heart failure ventricles
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
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