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This article is part of the supplement: 4th International Conference of cGMP Generators, Effectors and Therapeutic Implications

Open Access Poster presentation

Phosphodiesterase-5 inhibition delays cardiac dilation and improves myocardial function in a rat model of heart failure due to chronic volume overload

Sivakkanan Loganathan1*, Tamás Radovits12, Kristóf Hirschberg12, Sevil Korkmaz1, Matthias Karck1 and Gábor Szabó1

Author Affiliations

1 Department of Cardiac Surgery, University of Heidelberg, 2. OG. INF 326. 69120 Heidelberg, Germany

2 Heart Center, Semmelweis University, Városmajor u. 68. 1122 Budapest, Hungary

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BMC Pharmacology 2009, 9(Suppl 1):P41  doi:10.1186/1471-2210-9-S1-P41

The electronic version of this article is the complete one and can be found online at:

Published:11 August 2009

© 2009 Loganathan et al; licensee BioMed Central Ltd.


Chronic volume overload caused by insufficient cardiac valves is a well known pathomechanism to the development and progress of cardiac dilation. Recent studies suggest that PDE-5-inhibitors may have positive inotrope and cardioprotective effects. Nevertheless the long-term outcome of PDE-5 treatment in heart failure remains unknown. In this study we investigated the effects of chronic vardenafil treatment on myocardial dysfunction in rats developing heart failure on account of a surgically induced AV-shunt.

Materials and methods

In young male Sprague-Dawley rats heart failure was developed during a 3 months period after surgically inducing an AV-shunt between the inferior caval vein and abdominal aorta. In the treatment group vardenafil (10 mg/kg/d) was applied orally for 3 months. Control animals received vehicle instead. After the treatment left ventricular pressure-volume relations were measured using a microtip Millar conductance catheter. Baseline hemodynamic parameters and indexes of contractility were calculated.


Treatment with vardenafil resulted in a significant increase in load independent indexes of contractility and efficiency (ESPVR: 1.07 ± 0.14 vs. 1.67 ± 0.12 mmHg/μl*; efficiency: 45.0 ± 6.0 vs. 65.0 ± 5.0%*; PRSW: 65.40 ± 15.58 vs. 81.07 ± 13.72 mmHg, dPdt/EDV: 45.11 ± 9.57 vs. 48.74 ± 14.51 mmHg; control vs. treatment; *p < 0.05). Furthermore a reduced left ventricular dilatation and increased ejection fraction has been proven (EDV: 295.89 ± 53.55 vs. 257.91 ± 45.77 μl; EF: 50.99 ± 3.54 vs. 56.45 ± 4.00%; control vs. treatment).


Our current result further support the concept that chronic downregulation of intracellular cGMP signalling may play an important role in the development of ventricular dilation and myocardial dysfunction induced by chronical volume overload. Therefore PDE-5-inhibition could represent a novel therapeutic approach in the treatment of heart failure.