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Ann Thorac Surg 2001;72:2050
© 2001 The Society of Thoracic Surgeons
a Ruhr Universität Bochum, Herz- und Diabeteszentrum NRW, Klinik für Thorax- und Kardiovaskularchirurgie, Georgstrasse 11, D-32545 Bad Oeynhausen, Germany
e-mail: rkoerfer{at}hdz-nrw.de
Terminal heart failure has been one of the leading causes of morbidity and mortality in the 20th century and its treatment will certainly be important in the next decades in industrial countries—despite increasing understanding of underlying biological processes.
Since the introduction of ventricular assist devices into clinical practice, different heart centers have published successful weaning of patients from the device without heart transplantation, which implies that transient ventricular assist device (VAD) implantation may be an alternative to heart transplantation. Indeed, years of research has revealed that the heart failure related biochemical phenotype may be improved by mechanical circulatory support in a subset of patients. However, until now it is almost impossible to transfer these data into clinical decisions and to predict sustained cardiac recovery.
In this article Dr Razeghi and colleagues add a further piece to the puzzle of reverse remodeling. They report quantification of TNF
expression at the mRNA level in myocardial samples from transplantation candidates bridged by VADs. Surprisingly they could not find any correlation between the hemodynamic data and regulation of this proinflammatory cytokine. This is in sharp contrast to previously published immunohistological findings, which revealed a dramatic myocardial downregulation of this cytokine in VAD supported hearts on the protein level [1]. TNF has been of special interest in the onset of dilated cardiomyopathy and is certainly an important cytokine involved in the upstream regulation of heart failure associated with remodeling processes, ie, collagene and metalloproteinase dynamics underlined by a recent report on transgenic mice [2]. Therefore the regulation of TNF is certainly more complicated than previously thought.
However, more important for clinical practice may be that the myocardial response to mechanical support is as heterogenous as the cause of heart failure. Unfortunately it is far from clear, whether the successful weaning of patients reported from the Berlin group in 1997 [3] is based on different indications for implantation of VADs or a biological phenomenon [4]. Convincing evidence is lacking to show that the Berlin experience represents a proven therapeutic concept. Thus, four years later we are still searching for reliable markers of sustained cardiac recovery in endstage heart failure patients. To address these conflicting clinical experiences the launched multicenter studies in Europe and the United States will help us decide what is real and what is fiction.
Apart from theoretical scientific considerations the analysis of failing myocardium supported by ventricular assist devices will lead to the development of powerful tools to evaluate innovative therapies such as ie, cell transplantation.
References
Related Article
expression does not correlate with clinical indices of heart failure in patients on left ventricular assist device support
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