High-pressure distention of the saphenous vein during preparation results in increased markers of inflammation: A potential mechanism for graft failure

Maseeha S. Khaleel, Tracy A. Dorheim, Michael J. Duryee, Harold E. Durbin, Walter D. Bussey, Robert P. Garvin, Lynell Warren Klassen, Geoffrey Milton Thiele, Daniel R Anderson

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Background: Coronary artery disease is the single leading cause of death in the United States. Commonly it is treated with coronary bypass grafting using the saphenous vein (SV) or internal mammary artery (IMA) as a conduit. Unfortunately, the SV has much lower patency rates compared with the IMA. Several hypotheses exist as to why occlusion occurs more commonly in SV grafts than in IMA grafts. However detailed studies in this area have been limited. This study investigates the effects of pressure distention on inflammation in SV conduit used in coronary artery bypass grafting (CABG). Methods: Saphenous vein distention pressure was measured intraoperatively during 48 CABG procedures. A segment of SV was excised from the conduit before distention. Because the vein was used for coronary artery grafting, sequential pieces were archived for evaluation. Real-time polymerase chain reaction (RT-PCR) and immunohistochemical analyses were performed to investigate a change in the expression of biomarkers. Results: Upregulation of various biomarkers occurred. These biomarkers included scavenger receptors A and B (SR-A, SR-B), toll-like receptors 2 and 4 (TLR2, TLR4), platelet endothelial cell adhesion molecule (PECAM), vascular cell adhesion molecule (VCAM), and intercellular cell adhesion molecule (ICAM) in segments of SV that were subjected to distention. Immunohistochemical results mirrored RT-PCR findings. A significant correlation was observed between biomarkers and pressure values. Conclusions: These studies demonstrate that markers of inflammation are upregulated in response to SV distention. The data suggest that the pressure used in graft preparation procedures should be regulated to avoid inflammation and its potential to induce graft failure.

Original languageEnglish (US)
Pages (from-to)552-558
Number of pages7
JournalAnnals of Thoracic Surgery
Volume93
Issue number2
DOIs
StatePublished - Feb 1 2012

Fingerprint

Saphenous Vein
Inflammation
Transplants
Pressure
Mammary Arteries
Cell Adhesion Molecules
Biomarkers
Coronary Artery Bypass
Real-Time Polymerase Chain Reaction
Toll-Like Receptor 2
Scavenger Receptors
Toll-Like Receptor 4
Vascular Cell Adhesion Molecule-1
Coronary Artery Disease
Cause of Death
Veins
Coronary Vessels
Up-Regulation
Blood Platelets
Endothelial Cells

Keywords

  • CABG
  • CD
  • ICAM
  • IMA
  • LPS
  • PDGF
  • PECAM
  • SR
  • SV
  • TLR
  • cluster of differentiation
  • coronary artery bypass grafting
  • internal mammary artery
  • intracellular adhesion molecule
  • lipopolysaccharide
  • platelet endothelial cell adhesion molecule
  • platelet-derived growth factor
  • saphenous vein
  • scavenger receptor
  • toll-like receptor

ASJC Scopus subject areas

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

High-pressure distention of the saphenous vein during preparation results in increased markers of inflammation : A potential mechanism for graft failure. / Khaleel, Maseeha S.; Dorheim, Tracy A.; Duryee, Michael J.; Durbin, Harold E.; Bussey, Walter D.; Garvin, Robert P.; Klassen, Lynell Warren; Thiele, Geoffrey Milton; Anderson, Daniel R.

In: Annals of Thoracic Surgery, Vol. 93, No. 2, 01.02.2012, p. 552-558.

Research output: Contribution to journalArticle

Khaleel, Maseeha S. ; Dorheim, Tracy A. ; Duryee, Michael J. ; Durbin, Harold E. ; Bussey, Walter D. ; Garvin, Robert P. ; Klassen, Lynell Warren ; Thiele, Geoffrey Milton ; Anderson, Daniel R. / High-pressure distention of the saphenous vein during preparation results in increased markers of inflammation : A potential mechanism for graft failure. In: Annals of Thoracic Surgery. 2012 ; Vol. 93, No. 2. pp. 552-558.
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abstract = "Background: Coronary artery disease is the single leading cause of death in the United States. Commonly it is treated with coronary bypass grafting using the saphenous vein (SV) or internal mammary artery (IMA) as a conduit. Unfortunately, the SV has much lower patency rates compared with the IMA. Several hypotheses exist as to why occlusion occurs more commonly in SV grafts than in IMA grafts. However detailed studies in this area have been limited. This study investigates the effects of pressure distention on inflammation in SV conduit used in coronary artery bypass grafting (CABG). Methods: Saphenous vein distention pressure was measured intraoperatively during 48 CABG procedures. A segment of SV was excised from the conduit before distention. Because the vein was used for coronary artery grafting, sequential pieces were archived for evaluation. Real-time polymerase chain reaction (RT-PCR) and immunohistochemical analyses were performed to investigate a change in the expression of biomarkers. Results: Upregulation of various biomarkers occurred. These biomarkers included scavenger receptors A and B (SR-A, SR-B), toll-like receptors 2 and 4 (TLR2, TLR4), platelet endothelial cell adhesion molecule (PECAM), vascular cell adhesion molecule (VCAM), and intercellular cell adhesion molecule (ICAM) in segments of SV that were subjected to distention. Immunohistochemical results mirrored RT-PCR findings. A significant correlation was observed between biomarkers and pressure values. Conclusions: These studies demonstrate that markers of inflammation are upregulated in response to SV distention. The data suggest that the pressure used in graft preparation procedures should be regulated to avoid inflammation and its potential to induce graft failure.",
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T1 - High-pressure distention of the saphenous vein during preparation results in increased markers of inflammation

T2 - A potential mechanism for graft failure

AU - Khaleel, Maseeha S.

AU - Dorheim, Tracy A.

AU - Duryee, Michael J.

AU - Durbin, Harold E.

AU - Bussey, Walter D.

AU - Garvin, Robert P.

AU - Klassen, Lynell Warren

AU - Thiele, Geoffrey Milton

AU - Anderson, Daniel R

PY - 2012/2/1

Y1 - 2012/2/1

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AB - Background: Coronary artery disease is the single leading cause of death in the United States. Commonly it is treated with coronary bypass grafting using the saphenous vein (SV) or internal mammary artery (IMA) as a conduit. Unfortunately, the SV has much lower patency rates compared with the IMA. Several hypotheses exist as to why occlusion occurs more commonly in SV grafts than in IMA grafts. However detailed studies in this area have been limited. This study investigates the effects of pressure distention on inflammation in SV conduit used in coronary artery bypass grafting (CABG). Methods: Saphenous vein distention pressure was measured intraoperatively during 48 CABG procedures. A segment of SV was excised from the conduit before distention. Because the vein was used for coronary artery grafting, sequential pieces were archived for evaluation. Real-time polymerase chain reaction (RT-PCR) and immunohistochemical analyses were performed to investigate a change in the expression of biomarkers. Results: Upregulation of various biomarkers occurred. These biomarkers included scavenger receptors A and B (SR-A, SR-B), toll-like receptors 2 and 4 (TLR2, TLR4), platelet endothelial cell adhesion molecule (PECAM), vascular cell adhesion molecule (VCAM), and intercellular cell adhesion molecule (ICAM) in segments of SV that were subjected to distention. Immunohistochemical results mirrored RT-PCR findings. A significant correlation was observed between biomarkers and pressure values. Conclusions: These studies demonstrate that markers of inflammation are upregulated in response to SV distention. The data suggest that the pressure used in graft preparation procedures should be regulated to avoid inflammation and its potential to induce graft failure.

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KW - cluster of differentiation

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KW - internal mammary artery

KW - intracellular adhesion molecule

KW - lipopolysaccharide

KW - platelet endothelial cell adhesion molecule

KW - platelet-derived growth factor

KW - saphenous vein

KW - scavenger receptor

KW - toll-like receptor

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