For the science hotline, a number of late braking presentations were selected based on their outstanding quality. They covered new approaches to three central areas of clinical problems:
- Insufficient growth of collateral vessels under ischaemic conditions
- Insufficient supply of adequate pluripotent cells for tissue repair
- Insufficient understanding of mechanisms of arrhythmia.
In the first group, there were two presentations by K. Troidl (Bad Nauheim, Germany), ‘Intra-collateral adenoviral gene transfer of actin binding Rho activating protein (ABRA) improves collateral conductance’ and by A. Limbourg (Hannover, Germany) ‘The Notch ligand, Delta like 1 (Dll 1), determines adult phenotype and regulates postnatal arteriogenesis in response to ischaemia’.
Troidl showed that the crucial effect of shear stress on the development of collateral vessels can be simulated by local expression of a signalling protein, ABRA. This finding could support the development of treatment options aiming at increasing collateral growth, both in cardiac and peripheral conditions of arterial narrowing.
The relevance of mechanisms active during the embryonic development for arteriogenesis was investigated by Limbourg and coworkers. They could demonstrate that Dll1 is specifically relevant for the regulation of arterial reactions to ischaemic challenges also in the adult.
The following three, ‘The murine abdominal adipose stromal cell compartment supports the differentiation into endothelial, but not into haematopoietic progenitor cells’ by R. Madona (Houston, USA), ‘Cardiac cell generation from mouse adult spermatogonial stem cells’ by G Hasenfuss (Goettingen, Germany) and ‘Human cardiac stem cells are involved in pathological processes’ by AP Beltrami (Udine, Italy), investigated possible novel sources of stem cells. The testes sources include the adipose tissue, the male testis and the heart itself. While both adipose derived and spermatogonial cells seem to have a large therapeutic potential, the use of autologous cardiac precursor cells from the patient is overshadowed by the finding that these cells exhibit reduced regenerative potential as compared to controls derived from healthy subjects.
In the last presentation ‘Focal and reentrant mechanism of ventricular arrhythmias in a knock-in mouse model of catecholaminergic polymorphic ventricular tachycardia’, M. Cerrone (Syracuse, USA) presented a mouse model mimicking polymorphic ventricular tachycardia.
This model could be used to achieve a better understanding of the pathophysiology and treatment of such conditions.