[Therapeutic perspectives in heart failure]].
Many different diseases may lead to heart failure. Nevertheless, the symptoms and pathophysiological changes in heart failure are uniform as are the basic principles of treatment. Although significant progress has been achieved in understanding the biology of heart failure and the therapeutic options, the quality of life of heart failure patients and their survival are often poor. Since cardiac transplantation as a final therapeutic option is limited by the availability of donor organs, new strategies and technologies need to be explored to treat the failing heart effectively. Approaches to improve the medical therapy of heart failure mainly focus on strategies to escape the vicious circle of decreased contractility and neurohumoral activation. Substances with promising experimental and clinical results include neutral endopeptidase inhibitors, endothelin antagonists or cytokine inhibitors, e.g. TNF antagonists. Mechanical and electrical devices are under development such as left ventricular assist devices (LVADs), biventricular pacemakers and artificial hearts, which may become valuable alternative therapies. Gene therapy approaches aim to improve the vascularization of the heart, the Ca-homeostasis of the myocytes or the survival of cardiac cells in disease. Finally, cellular cardiomyoplasty is a relatively novel approach to replace or support the cardiomyocytes of the diseased heart by implanting new ones. Which cell type under which conditions will turn out to be the most suitable is still unknown and subject to debate. Ongoing clinical studies will only help to demonstrate the safety and feasibility of this technique but not determine its long-term efficacy. It is highly desirable that one of these new therapeutic strategies or a combination of them will have a significant impact on the future management of heart failure. Currently, our main clinical focus must be to treat as many patients as possible with drugs that are known to improve symptoms and survival, like ACE inhibitors, beta-blockers, cardiac glycosides, diuretics and spironolactone.
Müller-Ehmsen
Jochen
J
Klinik III für Innere Medizin der Universität zu Köln. muller.ehmsen@uni-koeln.de
Schwinger
Robert H
RH
D006333:Heart Failure / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D006353:Heart-Assist Devices; D006801:Humans; D015996:Survival Rate