title: Ultrastructural and immunohistochemical analysis of early myocardial changes following transmyocardial laser revascularization.
abstract: OBJECTIVE
  Transmyocardial laser revascularization (TMR) has demonstrated significant relief in patients presenting with refractory angina. However, the mechanism by which TMR improves clinical symptoms is unclear. This study analyzes the early immunohistochemical and ultrastructural features of the human myocardium following TMR.
  
  
  METHODS
  Specimens of myocardium that contained laser channels were removed in toto at autopsy from three male patients, ages 41, 57, and 65 (mean age 55.8) who had died 1 to 11 days (mean 6.8) following laser revascularization. Consecutive parallel sections of specimens were stained with cell-type specific antibodies to CD3 (to identify T-lymphocytes), CD68 (macrophages), Factor VIII (endothelial cells), and myosin (myocytes). Additionally, adjacent areas of myocardium that contained laser channels were processed and analyzed by transmission electron microscopy.
  
  
  RESULTS
  The internal lining surface of laser channels was composed of vacuolized and condensed myocardial debris. No obvious connections were noted between laser channels and the ventricular cavity. No endothelialization of channels was observed, whereas the adjacent noninjured myocardium demonstrated microvessels lined by well-preserved endothelial cells. The laser channels were surrounded by zones of necrotic cardiomyocytes.
  
  
  CONCLUSIONS
  Our observations suggest that laser channels are not lined by endothelial cells during the early stages following TMR. Mechanisms other than direct myocardial perfusion from the ventricular cavity by patent endothelialized channels may explain the immediate relief from angina provided by TMR.
authors.affiliation: Surgical Professorial Unit, St. Vincent's Hospital, Sydney, Australia.
authors.forename: S M
authors.initials: SM
authors.lastname: Cherian
authors.forename: Y V
authors.initials: YV
authors.lastname: Bobryshev
authors.forename: H
authors.initials: H
authors.lastname: Liang
authors.forename: N M
authors.initials: NM
authors.lastname: Sankar
authors.forename: S J
authors.initials: SJ
authors.lastname: Inder
authors.forename: A Y
authors.initials: AY
authors.lastname: Wang
authors.forename: R S
authors.initials: RS
authors.lastname: Lord
authors.forename: K M
authors.initials: KM
authors.lastname: Cherian
mesh_terms: D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000378:metabolism / Q000401:mortality / Q000601:surgery*; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D017252:CD3 Complex / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D005169:Factor VIII / Q000378:metabolism; D006801:Humans; D053685:Laser Therapy; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D009204:Myocardial Revascularization; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology / Q000648:ultrastructure*; D009218:Myosins / Q000378:metabolism; D009336:Necrosis; D013997:Time Factors; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; D005169:Factor VIII; D009218:Myosins; C067980:CD68 antigen, human; D000097382:CD68 Molecule