title: [Histomorphology after transmyocardial laser revascularization].
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 Freshly clotted material had been replaced by a granular tissue of variable density.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.
authors.affiliation: Deutsches Herzzentrum Berlin, Charité Berlin.
authors.forename: T
authors.initials: T
authors.lastname: Krabatsch
authors.forename: F
authors.initials: F
authors.lastname: Schäper
authors.forename: L
authors.initials: L
authors.lastname: Tambeur
authors.forename: C
authors.initials: C
authors.lastname: Leder
authors.forename: U
authors.initials: U
authors.lastname: Thalmann
authors.forename: R
authors.initials: R
authors.lastname: Hetzer
mesh_terms: D000368:Aged; D003326:Coronary Circulation / Q000502:physiology*; D003327:Coronary Disease / Q000473:pathology / Q000601:surgery*; D003331:Coronary Vessels / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D053685:Laser Therapy / Q000295:instrumentation*; D008297:Male; D008875:Middle Aged; D009204:Myocardial Revascularization / Q000295:instrumentation*; D009206:Myocardium / Q000473:pathology*; D018919:Neovascularization, Physiologic / Q000502:physiology; D016896:Treatment Outcome