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[Histomorphology after transmyocardial laser revascularization]
T Krabatsch1, F Schäper, L Tambeur
1Deutsches Herzzentrum Berlin, Charité Berlin.
Insights
Transmyocardial laser revascularization (TMLR) creates channels in the heart. Histological analysis shows these channels close, with cellular activity and new capillary formation, but unlikely to connect to the ventricle lumen.
Area of Science:
- Cardiovascular Surgery
- Histopathology
- Regenerative Medicine
Context:
- Diffuse coronary artery disease (CAD) refractory to conventional therapy poses a significant clinical challenge.
- Transmyocardial laser revascularization (TMLR) is an alternative treatment for patients unsuitable for angioplasty or bypass surgery.
- Understanding the histological changes post-TMLR is crucial for evaluating its efficacy.
Purpose:
- To investigate the histological changes in myocardial tissue following transmyocardial laser revascularization (TMLR).
- To analyze the cellular response and tissue remodeling in TMLR-treated areas.
- To assess the potential for neovascularization within laser-created channels.
Summary:
- Postmortem histological examination of TMLR-treated myocardium revealed recently closed channels with surrounding necrosis within five days.
- Two to three weeks post-TMLR, channels showed granular tissue, significant macrophage and monocyte activity, and fibroblast proliferation indicative of scar formation.
- Evidence of neovascularization, with capillary structures lined by endothelium, was observed within the channels, suggesting potential therapeutic mechanisms.
Impact:
- The findings provide insights into the healing process after TMLR, highlighting tissue remodeling and neovascularization.
- Histological evidence suggests TMLR may promote angiogenesis, potentially improving myocardial perfusion.
- Further research is needed to confirm the long-term patency of these channels and their functional significance in treating ischemic heart disease.
Abstract:
From 11/1994 to 4/1997 we enrolled 140 patients with diffuse CAD refractory to maximum antianginal therapy who are not candidates for PTCA or CABG for transmyocardial laser revascularisation (TMLR). Of these patients aged 63.5 +/- 15 years, 98 had coronary 3-vessel disease, and the average left ventricular ejection fraction was 44%. Eleven out of these 140 patients died from different reasons (pneumonia, myocardial infarction, septicemia). Seven patients who died between the 1st and 20th postoperative day underwent a postmortem examination with histological analysis of the areas treated by TMLR. On the seven investigated ventricles a total of 220 channels were created. The predominant finding in specimens within five days after TMLR was recently closed channels. Furthermore, a zone of necrosis with an average extension of 500 microns on each side of the channel was evident. Many changes were noticeable in specimens from patients who died two or three weeks after TMLR. Freshly clotted material had been replaced by a granular tissue of variable density. High macrophage and monocyte activity was evident. The extent of this cellular activity could be depicted by staining with a special proliferation marker, such as MiB. On the one hand numerous dividing macrophages were observed, on the other, active fibroblasts indicative for the transformation into scar-like tissue. After staining for type-4-collagen, typical for the basal membrane of capillaries, a large number of stained structures was noticeable in the closed channel lumen. Numerous garlandlike structures became visible under higher magnification. By CD 31 incubation, these structures, were found to be lined with endothelium. Further research will be required to indicate whether the laser channels later are partially or completely open, from where the capillaries are supplied, and whether they even connect to the ventricle lumen. But in conclusion, it seems unlikely, that TMLR follows the mechanism of the amphibian heart.