Morphology of transmyocardial laser revascularisation. [19]

Details

Serval ID
serval:BIB_12205
Type
Inproceedings: an article in a conference proceedings.
Publication sub-type
Abstract (Abstract): shot summary in a article that contain essentials elements presented during a scientific conference, lecture or from a poster.
Collection
Publications
Institution
Title
Morphology of transmyocardial laser revascularisation. [19]
Title of the conference
34th Congress of the European Society for Surgical Research
Author(s)
Mueller X., Tevaearai H., Genton C., von Segesser L.
ISBN
1421-9921
Publication state
Published
Issued date
1999
Volume
31
Series
European Surgical Research
Pages
10
Language
english
Notes
Introduction: Transmyocardial Laser Revascularisation (TMLR) has emerged as a therapeutic modality for angina refractory to conventional therapy. Initially, blood flowing from the ventricular cavity through the patent channels was thought to be the underlying mechanism. This study analyses longterm morphology of the laser channels in the pig. Methods: Fifteen pigs were randomised either to ligation of marginal arteries (n D 5), or TMLR of the left lateral wall (n D 5), or a control group (n D 5). Animals were sacrificed after 28 days. The channel regions were sliced perpendicularly to the channels. A computed morphometrical analysis was performed for the surface areas of the channels and for their vascular density, expressed as number of vascular structures per mm2 (_1 SD). Results: Macroscopically, all the endocardial openings of the channels were occluded. Histologically the channels showed a central area of necrosis (5 _ 1%) surrounded by scar tissue (95 _ 1%). There was no central lumen. Vascular density of scar tissue was significantly larger than that of myocardial infarction alone: 49:6 _ 12:8/mm2 vs 25:5 _ 8:6/mm2 (p < 0:0001). The area immediately adjacent to the channels exhibited a density of 6:3 _ 1:7/mm2 which was similar to that of normal myocardial tissue (5:2 _ 1:9/mm2). Discussion and Conclusion: Laser channels are occluded by scar tissue with a vascular density larger than that of myocardial infarction alone. Thus channel patency is unlikely to be the explanation for clinical improvement. However neovascularisation is a potential mechanism requiring further evaluation.
Create date
19/11/2007 12:03
Last modification date
20/08/2019 12:39
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