title: Lymphangiogenesis in myocardial remodelling after infarction.
abstract: OBJECTIVE
  The lymphatic system is involved in fluid homeostasis of the cardiac interstitium, but lymphangiogenesis in myocardial remodelling has not previously been examined histopathologically. The aim was to investigate by D2-40 immunohistochemistry the sequential changes in lymphatic distribution in the process of myocardial remodelling after myocardial infarction (MI).
  
  
  RESULTS
  Myocardial tissues in various phases of healing after MI were obtained from 40 autopsied hearts. D2-40+ lymphatic vessel density (LD) and CD34+ blood vessel density (BD) in the lesion were determined. BD decreased with advance of myocardial necrosis, subsequently increased at the early stage of granulation and thereafter decreased with the progression of scar formation. In contrast, lymphatic vessels were not detected in lesions with coagulation necrosis, and newly formed lymphatics first appeared in the early stages of granulation. A subsequent increase in LD was demonstrated in the late stages of granulation, and lymphatics remained up to the scar phase. Vascular endothelial growth factor-C was consistently expressed in viable cardiomyocytes around the lesion in all of these stages.
  
  
  CONCLUSIONS
  In myocardial remodelling after MI, lymphangiogenesis lags behind blood vessel angiogenesis; newly formed lymphatics may be involved mainly in the maturation of fibrosis and scar formation through the drainage of excessive proteins and fluid.
authors.affiliation: Department of Pathology, Toho University School of Medicine, Tokyo, Japan. yukio@med.toho-u.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Ishikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Akishima-Fukasawa
authors.forename: K
authors.initials: K
authors.lastname: Ito
authors.forename: Y
authors.initials: Y
authors.lastname: Akasaka
authors.forename: M
authors.initials: M
authors.lastname: Tanaka
authors.forename: R
authors.initials: R
authors.lastname: Shimokawa
authors.forename: M
authors.initials: M
authors.lastname: Kimura-Matsumoto
authors.forename: H
authors.initials: H
authors.lastname: Morita
authors.forename: S
authors.initials: S
authors.lastname: Sato
authors.forename: I
authors.initials: I
authors.lastname: Kamata
authors.forename: T
authors.initials: T
authors.lastname: Ishii
mesh_terms: D000199:Actins / Q000032:analysis; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000911:Antibodies, Monoclonal / Q000032:analysis / Q000276:immunology; D058846:Antibodies, Monoclonal, Murine-Derived; D015703:Antigens, CD / Q000032:analysis; D018952:Antigens, CD34 / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001344:Autopsy; D001808:Blood Vessels / Q000737:chemistry / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D042583:Lymphangiogenesis; D042601:Lymphatic Vessels / Q000737:chemistry / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009130:Muscle, Smooth / Q000737:chemistry; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000737:chemistry / Q000473:pathology*; D012720:Severity of Illness Index; D042582:Vascular Endothelial Growth Factor C / Q000032:analysis; D020257:Ventricular Remodeling; D000097382:CD68 Molecule
chemical_list: D000199:Actins; D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D015703:Antigens, CD; D018952:Antigens, CD34; D015214:Antigens, Differentiation, Myelomonocytic; D042582:Vascular Endothelial Growth Factor C; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C500987:monoclonal antibody D2-40