• J Wohlschlaeger, N Kawaguchi, B Levkau, C Schmid, H H Scheld, and H A Baba.
• Institut für Pathologie, Universität Essen-Duisburg, Hufelandstrasse 55, 45122 Essen, Deutschland.
• Verh Dtsch Ges Pathol. 2004 Jan 1; 88: 113-21.

AbstractLeft ventricular assist devices (LVAD) are used to "bridge" patients with end-stage heart failure until transplantation of a donor heart can be performed ("bridge to transplantation"). However, LVAD support sporadically results in improved cardiac function, and heart transplantation is not necessary even after removal of LVAD in a subset of patients ("bridge to recovery"). Additionally, LVAD appears to be an optional treatment alternative to heart transplantation in patients with contraindication for organ replacement ("destination therapy"). The underlying process has descriptively been termed "reverse remodeling". The molecular basis remains incompletely understood at present, however, some mechanisms have been identified in the past. Alterations of several molecular pathways are involved in the development of chronic heart failure. Some of the pathways appear to be reversible and have been shown to be regulated by LVAD treatment. LVAD lead to lowered cardiac pressure and volume overload followed by decreased ventricular wall tension, reduction of cardiomyocyte hypertrophy, improved coronary perfusion and a decrease of chronic ischemia in the myocardium. Improved coronary flow and myocardial perfusion as well as decreased ventricular wall tension may serve as a possible explanation for changes of the molecular systems involved in the development of chronic cardiac insuffiency. This review focuses on the roles of apoptosis, heme-oxygenase-1 (HO-1), Metallothionein (MT) and the transcription factor NFkkappaB in chronic heart failure after mechanical circulatory support.

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