PMID- 15457156
OWN - NLM
STAT- MEDLINE
DCOM- 20041126
LR  - 20071114
IS  - 0022-5223 (Print)
IS  - 0022-5223 (Linking)
VI  - 128
IP  - 4
DP  - 2004 Oct
TI  - Clinical pulmonary autograft valves: pathologic evidence of adaptive remodeling 
      in the aortic site.
PG  - 552-61
AB  - OBJECTIVE: We studied the pathologic features, cellular phenotypes, and matrix 
      remodeling of clinical pulmonary-to-aortic valve transplants functioning up to 6 
      years. METHODS: Nine autografts and associated vascular walls early (2-10 weeks) 
      and late (3-6 years) postoperatively were examined by using routine morphologic 
      methods and immunohistochemistry. In 4 cases autograft and homograft cusps were 
      obtained from the same patients. RESULTS: Autografts had near-normal trilaminar 
      cuspal structure and collagen architecture and viable valvular interstitial and 
      endothelial cells throughout the time course. In contrast, cusps of homografts 
      used to replace the pulmonary valves in the same patients were devitalized. In 
      early autograft explants, 19.3% +/- 2.4% of cuspal interstitial cells were 
      myofibroblasts expressing alpha-actin. In contrast, myofibroblasts comprised only 
      6.0% +/- 1.1% of cells in late explants and 2.5% +/- 0.4% and 4.6% +/- 0.8% of 
      cells in normal pulmonary and aortic valves, respectively (P <.05). In early 
      autografts only 12.0% +/- 4.6% of endothelial cells expressed the systemic 
      arterial endothelial cell marker EphrinB2, whereas later explants had 85.6% +/- 
      5.4% of endothelial cells expressing EphrinB2 (P <.05). In early autografts 43.8% 
      +/- 8.8% of interstitial cells expressed metalloproteinase 13, whereas late 
      autografts had 11.4% +/- 2.7% of interstitial cells expressing matrix 
      metalloproteinase 13 (P <.05). Collagen content in autografts was comparable with 
      that of normal valves and was higher than that seen in homograft valves (P 
      <.005). However, autograft walls were damaged, with granulation tissue (early) 
      and scarring, with focal loss of normal smooth muscle cells, elastin, and 
      collagen (late). CONCLUSIONS: The structure of pulmonary valves transplanted to 
      the systemic circulation evolved toward that of normal aortic valves. Key 
      processes in this remodeling included onset of a systemic endothelial cell 
      phenotype and reversible plasticity of fibroblast-like valvular interstitial 
      cells to myofibroblasts.
FAU - Rabkin-Aikawa, Elena
AU  - Rabkin-Aikawa E
AD  - Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, 
      Boston, MA 02115, USA.
FAU - Aikawa, Masanori
AU  - Aikawa M
FAU - Farber, Mark
AU  - Farber M
FAU - Kratz, Johannes R
AU  - Kratz JR
FAU - Garcia-Cardena, Guillermo
AU  - Garcia-Cardena G
FAU - Kouchoukos, Nicholas T
AU  - Kouchoukos NT
FAU - Mitchell, Max B
AU  - Mitchell MB
FAU - Jonas, Richard A
AU  - Jonas RA
FAU - Schoen, Frederick J
AU  - Schoen FJ
LA  - eng
GR  - P01 HL-48743/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Thorac Cardiovasc Surg
JT  - The Journal of thoracic and cardiovascular surgery
JID - 0376343
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Ephrin-B2)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Animals
MH  - Antibodies, Monoclonal
MH  - Aortic Valve/physiopathology/*surgery
MH  - Child
MH  - Cricetinae
MH  - Ephrin-B2/immunology
MH  - Extracellular Matrix/physiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Pulmonary Valve/physiopathology/*transplantation
MH  - Time Factors
MH  - Transplantation, Autologous
MH  - Transplantation, Homologous
EDAT- 2004/10/01 05:00
MHDA- 2004/12/16 09:00
CRDT- 2004/10/01 05:00
PHST- 2004/10/01 05:00 [pubmed]
PHST- 2004/12/16 09:00 [medline]
PHST- 2004/10/01 05:00 [entrez]
AID - S0022522304006415 [pii]
AID - 10.1016/j.jtcvs.2004.04.016 [doi]
PST - ppublish
SO  - J Thorac Cardiovasc Surg. 2004 Oct;128(4):552-61. doi: 
      10.1016/j.jtcvs.2004.04.016.