Endothelial Function and Vein Graft Remodeling

NCT ID: NCT00831090

Last Updated: 2022-09-23

Basic Information

• Recruitment Status: COMPLETED
• Total Enrollment: 55 participants
• Study Classification: OBSERVATIONAL
• Study Start Date: 2009-01-31
• Study Completion Date: 2015-01-16

Brief Summary

The purpose of this study is to better understand why some vein bypass grafts develop narrowing. Evidence suggests that there is a relationship between inflammatory markers in the blood and the narrowing that occurs in blood vessels. In this study, we will look at inflammatory markers in the blood and how well the vein graft functions.

Detailed Description

Despite the acceptance of catheter-based approaches to lower extremity reconstruction, bypass with autogenous vein remains the most durable option. In the United States alone there are approximately 100,000 lower extremity bypass procedures performed yearly. However, 30-50% of these grafts either occlude or require revision in the first 5 years.

Traditional Framingham cardiovascular risk factors such as dyslipidemia and diabetes do not predict which grafts are at risk for failure. Therefore other variables such as hemodynamic factors or endothelial function may be important in identifying vulnerable vein grafts. The applicant has previously noted that vein grafts undergo dramatic geometric remodeling within the first month after implantation into the arterial circulation. This is partly driven by hemodynamic forces such as shear stress and is thought to be related to endothelial function. Shear stress is positively correlated with early (0-1 month) luminal enlargement. This adaptive response is important to maintain bypass graft patency. However, there is considerable amount of variability in this response unaccounted for by shear stress alone. The applicant has further shown that baseline systemic inflammation dampens the ability for adequate vein graft luminal expansion and therefore may uncouple the mechano-chemical signal transduction at the endothelial level. Therefore, this study will examine the relationship between circulating levels of inflammatory mediators and endothelial function in a cohort of patients undergoing lower extremity arterial reconstruction with autogenous vein.

Conditions

Peripheral Arterial Disease; Cardiovascular Disease

Study Design

• Observational Model Type: COHORT
• Study Time Perspective: PROSPECTIVE

Eligibility Criteria

Inclusion Criteria

• Age > 22 or < 90 years
• Undergoing lower extremity (infrainguinal) bypass using autologous vein for the treatment of disabling claudication or critical limb ischemia secondary to chronic atherosclerotic occlusive disease
• Able to understand, give, and take part in the consent process

Exclusion Criteria

• Age < 22 or > 90 years
• Grafts employing prosthetic or other non-autologous vein material in any part (e.g. composite grafts). [Patch angioplasty of inflow and outflow vessel permissible with any material]
• Vasculitis, trauma, acute embolic disease as etiology of limb ischemia
• History of diagnosed hypercoagulable state
• Evidence of active infection - pneumonia, urinary tract, etc., requiring medical therapy
• Evidence of significant local sepsis in foot or limb prior to bypass
• Patients taking immunosuppressant medications (steroids, chemotherapeutic agents)
• Other concurrent significant illness within 30 days
• Non-English speakers

• Minimum Eligible Age: 22 Years
• Maximum Eligible Age: 89 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: No

Sponsors

National Heart, Lung, and Blood Institute (NHLBI)

NIH

Sponsor Role: collaborator

University of California, San Francisco

OTHER

Sponsor Role: lead

Responsible Party

Responsibility Role: SPONSOR

Principal Investigators

Warren J. Gasper, M.D.

Role: PRINCIPAL_INVESTIGATOR

University of California, San Francisco

Locations

San Francisco Veterans Affairs Medical Center

San Francisco, California, United States

University of California, San Francisco

San Francisco, California, United States

Countries

United States

Other Identifiers

HL92163-01

Identifier Type: -

Identifier Source: secondary_id

10-02338

Identifier Type: -

Identifier Source: org_study_id