European Heart Journal Advance Access published online on November 18, 2005
European Heart Journal, doi:10.1093/eurheartj/ehi659
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1 DHZB, Augustenburger Platz 1, 13353 Berlin, Germany; Center for Cardiovascular Research Charité, University-Medicine Berlin, Hessische Str 3-4, 10115 Berlin, Germany
* To whom correspondence should be addressed. Aims The sympathetic nervous system plays a central role in cardiac growth but its overstimulation is associated with increased mortality in patients with chronic heart failure. Pre-synaptic Methods and results We genotyped and phenotyped 345 patients presenting with DCM in the heart transplant unit of the German Heart Institute, starting in 1994. Patients were treated according to guidelines (99% ACEI, 76% Conclusion
Received May 17, 2005
Revised October 19, 2005
Accepted October 27, 2005
Clinical research
Vera Regitz-Zagrosek 1 *,
Berthold Hocher 2,
Martin Bettmann 3,
Marc Brede 4,
Kerstin Hadamek 4,
Carolin Gerstner 4,
Hans Brendan Lehmkuhl 3,
Roland Hetzer 3,
and
Lutz Hein 4
2C-Adrenoceptor polymorphism is associated with improved event-free survival in patients with dilated cardiomyopathy
2 Center for Cardiovascular Research Charité, University-Medicine Berlin, Hessische Str 3-4, 10115 Berlin, Germany; Division of Nephrology, Inselspital, University of Berne, CH-3008 Berne, Switzerland
3 DHZB, Augustenburger Platz 1, 13353 Berlin, Germany
4 Institute of Pharmacology and Toxicology, University of Freiburg, Germany
Vera Regitz-Zagrosek, E-mail: vrz{at}dhzb.de
Abstract 
2-adrenoceptors are essential feedback regulators to control the release of norepinephrine from sympathetic nerves. In this study we tested whether a deletion polymorphism in the human 2C-adrenoceptor gene (2CDel322-325) affects progression of heart failure in patients with dilated cardiomyopathy (DCM).
-blockers) and were followed until December 2002 or until a first event [death, heart transplantation, or implantation of a left ventricular assist device (LVAD) for a life-threatening condition] occurred. Mean follow-up time was 249 weeks (4.9 years) in event-free patients and 104 weeks (2 years) in patients with events. During follow-up, 51% of the patients exhibited an event: death (18%), implantation of LVAD as bridging for transplantation (7%), or heart transplantation (25%). By Kaplan-Meier analysis, DCM patients with the deletion variant Del322-325 in the 2C-adrenoceptor showed significantly decreased event rates (P = 0.0043). Cox regression analysis revealed that the presence of the deletion was associated with reduced death rate (relative risk: 0.129, 95% CI: 0.18-0.9441, P = 0.044) and event rates (relative risk: 0.167, 95% CI: 0.041-0.685, P = 0.012).2C-Adrenoceptor deletion may be a novel, strong, and independent predictor of reduced event rates in DCM patients treated according to guidelines.
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