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Photochemical Tissue Passivation Reduces Vein Graft Intimal Hyperplasia in a Swine Model of Arteriovenous Bypass Grafting

View Article: PubMed Central - PubMed

ABSTRACT

Background: Bypass grafting remains the standard of care for coronary artery disease and severe lower extremity ischemia. Efficacy is limited by poor long‐term venous graft patency secondary to intimal hyperplasia (IH) caused by venous injury upon exposure to arterial pressure. We investigate whether photochemical tissue passivation (PTP) treatment of vein grafts modulates smooth muscle cell (SMC) proliferation and migration, and inhibits development of IH.

Methods and results: PTP was performed at increasing fluences up to 120 J/cm2 on porcine veins. Tensiometry performed to assess vessel elasticity/stiffness showed increased stiffness with increasing fluence until plateauing at 90 J/cm2 (median, interquartile range [IQR]). At 90 J/cm2, PTP‐treated vessels had a 10‐fold greater Young's modulus than untreated controls (954 [IQR, 2217] vs 99 kPa [IQR, 63]; P=0.03). Each pig received a PTP‐treated and untreated carotid artery venous interposition graft. At 4‐weeks, intimal/medial areas were assessed. PTP reduced the degree of IH by 66% and medial hypertrophy by 49%. Intimal area was 3.91 (IQR, 1.2) and 1.3 mm2 (IQR, 0.97; P≤0.001) in untreated and PTP‐treated grafts, respectively. Medial area was 9.2 (IQR, 3.2) and 4.7 mm2 (IQR, 2.0; P≤0.001) in untreated and PTP‐treated grafts, respectively. Immunohistochemistry was performed to assess alpha‐smooth muscle actin (SMA) and proliferating cell nuclear antigen (PCNA). Objectively, there were less SMA‐positive cells within the intima/media of PTP‐treated vessels than controls. There was an increase in PCNA‐positive cells within control vein grafts (18% [IQR, 5.3]) versus PTP‐treated vein grafts (5% [IQR, 0.9]; P=0.02).

Conclusions: By strengthening vein grafts, PTP decreases SMC proliferation and migration, thereby reducing IH.

No MeSH data available.


A, Average peak load at 0.5‐mm extension for venous samples with increasing fluence. Fluence zero represents the vein before photochemical tissue passivation treatment. B, Average Young's modulus of elasticity for venous samples with increasing fluence. Fluence zero represents the vein before PTP treatment.
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jah31663-fig-0002: A, Average peak load at 0.5‐mm extension for venous samples with increasing fluence. Fluence zero represents the vein before photochemical tissue passivation treatment. B, Average Young's modulus of elasticity for venous samples with increasing fluence. Fluence zero represents the vein before PTP treatment.

Mentions: The average peak load at 0.5‐mm extension and the average Young's modulus of elasticity for venous samples increased with increasing fluence, until plateauing by a fluence of 90 J/cm2 (Figure 2A and 2B). The peak load at 0.5‐mm extension for PTP‐treated vessels with a fluence of 90 J/cm2 was significantly greater than untreated controls (0.0469 [IQR, 0.0766] vs 0.0075 N [IQR, 0.0011]; P=0.028). Additionally, the Young's modulus was 10‐fold greater for PTP‐treated vessels with a fluence of 90 J/cm2 than for untreated controls (954 [IQR, 2217] vs 99 kPa [IQR, 63]; P=0.028). Because there was no statistically significant difference between treatment fluences of 90 and 120 J/cm2, we chose to utilize a fluence of 90 J/cm2 for vessel compliance testing.


Photochemical Tissue Passivation Reduces Vein Graft Intimal Hyperplasia in a Swine Model of Arteriovenous Bypass Grafting
A, Average peak load at 0.5‐mm extension for venous samples with increasing fluence. Fluence zero represents the vein before photochemical tissue passivation treatment. B, Average Young's modulus of elasticity for venous samples with increasing fluence. Fluence zero represents the vein before PTP treatment.
© Copyright Policy - creativeCommonsBy-nc-nd
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5015302&req=5

jah31663-fig-0002: A, Average peak load at 0.5‐mm extension for venous samples with increasing fluence. Fluence zero represents the vein before photochemical tissue passivation treatment. B, Average Young's modulus of elasticity for venous samples with increasing fluence. Fluence zero represents the vein before PTP treatment.
Mentions: The average peak load at 0.5‐mm extension and the average Young's modulus of elasticity for venous samples increased with increasing fluence, until plateauing by a fluence of 90 J/cm2 (Figure 2A and 2B). The peak load at 0.5‐mm extension for PTP‐treated vessels with a fluence of 90 J/cm2 was significantly greater than untreated controls (0.0469 [IQR, 0.0766] vs 0.0075 N [IQR, 0.0011]; P=0.028). Additionally, the Young's modulus was 10‐fold greater for PTP‐treated vessels with a fluence of 90 J/cm2 than for untreated controls (954 [IQR, 2217] vs 99 kPa [IQR, 63]; P=0.028). Because there was no statistically significant difference between treatment fluences of 90 and 120 J/cm2, we chose to utilize a fluence of 90 J/cm2 for vessel compliance testing.

View Article: PubMed Central - PubMed

ABSTRACT

Background: Bypass grafting remains the standard of care for coronary artery disease and severe lower extremity ischemia. Efficacy is limited by poor long‐term venous graft patency secondary to intimal hyperplasia (IH) caused by venous injury upon exposure to arterial pressure. We investigate whether photochemical tissue passivation (PTP) treatment of vein grafts modulates smooth muscle cell (SMC) proliferation and migration, and inhibits development of IH.

Methods and results: PTP was performed at increasing fluences up to 120 J/cm2 on porcine veins. Tensiometry performed to assess vessel elasticity/stiffness showed increased stiffness with increasing fluence until plateauing at 90 J/cm2 (median, interquartile range [IQR]). At 90 J/cm2, PTP‐treated vessels had a 10‐fold greater Young's modulus than untreated controls (954 [IQR, 2217] vs 99 kPa [IQR, 63]; P=0.03). Each pig received a PTP‐treated and untreated carotid artery venous interposition graft. At 4‐weeks, intimal/medial areas were assessed. PTP reduced the degree of IH by 66% and medial hypertrophy by 49%. Intimal area was 3.91 (IQR, 1.2) and 1.3 mm2 (IQR, 0.97; P≤0.001) in untreated and PTP‐treated grafts, respectively. Medial area was 9.2 (IQR, 3.2) and 4.7 mm2 (IQR, 2.0; P≤0.001) in untreated and PTP‐treated grafts, respectively. Immunohistochemistry was performed to assess alpha‐smooth muscle actin (SMA) and proliferating cell nuclear antigen (PCNA). Objectively, there were less SMA‐positive cells within the intima/media of PTP‐treated vessels than controls. There was an increase in PCNA‐positive cells within control vein grafts (18% [IQR, 5.3]) versus PTP‐treated vein grafts (5% [IQR, 0.9]; P=0.02).

Conclusions: By strengthening vein grafts, PTP decreases SMC proliferation and migration, thereby reducing IH.

No MeSH data available.