Only transient increase of vascular growth factors and microvascular density after percutaneous myocardial laser.

Abstract

OBJECTIVE We tested the hypothesis that percutaneous myocardial laser may stimulate microvascular growth in areas surrounding the laser channels. METHODS We conducted a study of 24 domestic pigs, which underwent percutaneous myocardial laser to left ventricular myocardium using holmium:YAG laser. The pigs were sacrificed in groups of four after one day, 3-4 days, one week, three weeks and six weeks. Frozen sections from both normal and treated myocardium were prepared for immunofluorescence microscopy and stained with antibodies against von Willebrand factor, vascular endothelial growth factor (VEGF) and Extra Domain-A cellular fibronectin (ED-AcFN). Microvascular density (MVD) and vascular area (VA) were determined in sections stained with antibodies against von Willebrand factor VIII using a digitised image analysis system. When determined in laser treated areas, channel core remnants were excluded from analysis. RESULTS Within the laser channel remnants and in the tissue closely surrounding these, expression of VEGF and ED-AcFN increased significantly after treatment at one, 3-4, and seven days and decreased to normal at three and six weeks. Expression of ED-AcFN was detected adjacent to endothelial cells of microvessels. The original laser channels were rapidly invaded by granulation tissue. There was no sign of recanalization at any stage during the six weeks. Morphometric analysis showed no increase in MVD and VA in the myocardium surrounding the laser channels. CONCLUSION An increase of VEGF and ED-AcFN after myocardial laser is transient and is not associated with increase of MVD or VA in myocardium not involving laser channel remnants.

Cite this paper

@article{Salem2004OnlyTI, title={Only transient increase of vascular growth factors and microvascular density after percutaneous myocardial laser.}, author={Mohamed Abdel Rahman Salem and Svein Rotevatn and Reidar J Pettersen and Karel K-J Kuiper and Thorvald Saetersdal and Jan Erik Nordrehaug}, journal={Coronary artery disease}, year={2004}, volume={15 7}, pages={441-8} }