Detail

Keywords

Cardiac surgery; Cardioplegic Solutions; Hypertrophy, Left Ventricular; Ischemic Preconditioning, Myocardial; Mitral Valve Insufficiency; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion

Research group(s)

• Vienna Working Heart Research Group
  Members:
  Bruno Podesser

Research interests

My main research focus is understanding myocardial ischemia/reperfusion (I/R) and the consequences of this clinically relevant phenomenon. I/R is not only responsibel for the majority of death in the developed world but also part of every operation in cardiac surgery. Understanding the underlying mechanisms can lead to possible clinically relevant therapeutic options such as the development of new cardioplegic solutions, new non-invasive protective techniques such as remote conditioning, etc. Additioanlly we have focused on the effects of pressure and volume overlaod in cardiac remodeling with particular interest on a matricellular protein- Tenascin C

Techniques, methods & infrastructure

Our experimental techniques include in vivo models of myocardial infarction in mouse, rat and pig both in acute and chronic state leading to volume overload and progressive heart failure. Similarly, a pressure overload model in mice (aortic transverse constriction) is available to study left ventricular hypertrophy and failure. In addition, a large animal model of functional and primary mitral valve insufficiancy is used to test and develop new interventional and surgical techniques. Our ex vivo models are an isolated heart and a myograph both used to describe cardiac and vascular function. Besides a broad spectrum of biochemical, cell biological, and imaging techniques are used. The latter include echo/ultrasound, PET-CT and MRI in collaboration with the preclinical imaging laboratory. 

Selected publications

1. Aass, T. et al., 2017. Myocardial energy metabolism and ultrastructure with polarizing and depolarizing cardioplegia in a porcine model . European Journal of Cardio-Thoracic Surgery, 52(1), pp.180-188. Available at: http://dx.doi.org/10.1093/ejcts/ezx035.
2. Taggart, D.P. et al., 2016. Randomized Trial of Bilateral versus Single Internal-Thoracic-Artery Grafts. New England Journal of Medicine, 375(26), pp.2540-2549. Available at: http://dx.doi.org/10.1056/NEJMoa1610021.
3. Trescher, K. et al., 2014. The nitric oxide donor, S-nitroso human serum albumin, as an adjunct to HTK-N cardioplegia improves protection during cardioplegic arrest after myocardial infarction in rats. Interactive CardioVascular and Thoracic Surgery, 20(3), pp.387-394. Available at: http://dx.doi.org/10.1093/icvts/ivu383.
4. Trescher, K. et al., 2014. The nitric oxide donor, S-nitroso human serum albumin, as an adjunct to HTK-N cardioplegia improves protection during cardioplegic arrest after myocardial infarction in rats. Interactive CardioVascular and Thoracic Surgery, 20(3), pp.387-394. Available at: http://dx.doi.org/10.1093/icvts/ivu383.
5. Pomper, G. et al., 2010. Introducing a mouse model of brain death. Journal of Neuroscience Methods, 192(1), pp.70-74. Available at: http://dx.doi.org/10.1016/j.jneumeth.2010.07.019.