Non-invasive bed-side measurement of systemic endothelial function in patients undergoing abdominal aortic aneurysm repair; modulation by ascorbic acid - AAAAA

Status

Active, not recruiting

Phases

Phase 2

Study type

Interventional

Source

EU CTR

Registry ID

EUCTR2006-006887-44-GB

Enrollment

Registered

2007-05-15

Start date

2007-06-19

Completion date

Unknown

Last updated

2020-10-13

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Abdominal Aortic Aneurysm MedDRA version: 9.1 Level: LLT Classification code 10049871 Term: Abdominal aortic aneurysm haemorrhage

Interventions

Trade Name: Ascorbic Acid Injection BPC 500mg/5ml or Pascorbin Product Name: Ascorbic Acid Injection Pharmaceutical Form: Solution for injection Pharmaceutical form of the placebo: Intravenous infusi

Eligibility

Sex/Gender

All

Inclusion criteria

Inclusion criteria: Adult patients admitted for elective open repair of AAA in the Royal Victoria Hospital, Belfast will be eligible for inclusion in the study. Are the trial subjects under 18? no Number of subjects for this age range: F.1.2 Adults (18-64 years) yes F.1.2.1 Number of subjects for this age range F.1.3 Elderly (>=65 years) yes F.1.3.1 Number of subjects for this age range

Exclusion criteria

Exclusion criteria: Exclusion criteria will be prior antioxidant therapy, known allergy to ascorbic acid or agents specified in the standardised anaesthetic protocol and lack of consent.

Design outcomes

Primary

Measure	Time frame
Main Objective: The aim of this pilot study is to investigate the acute effects of ascorbic acid supplementation on systemic and pulmonary endothelial function in the immediate post-operative period following AAA repair. ;Secondary Objective: ;Primary end point(s): As this is a phase II clinical study, several outcomes will be evaluated to determine whether treatment with ascorbic acid attenuates important surrogate physiological outcomes. The primary endpoint of this clinical study is to evaluate the efficacy of ascorbic acid to reduce endothelial dysfunction as measured by the change in plasma vWF at 4 hours following removal of the aortic cross-clamp. The following surrogate markers will also be assessed: 1) Systemic endothelial function as assessed by a) plasma adhesion molecules, ICAM, VCAM and E-selectin b) albumin creatinine ratio (ACR) c) Non-invasive assessment of the change in AIx in response to an endothelial dependent and endothelial independent vasodilator as described below. 2) Pulmonary endothelial function as assessed by the pulmonary dead space fraction. Exhaled breath condensate will be collected and its pH recorded, also the concentration of LTB4; a marker of pulmonary inflammation. In addition the PO2:FiO2 ratio will be recorded as a clinical indicator of pulmonary function when the dead space fraction is measured. 3) Oxidative stress as measured by a) serum lipid peroxides b) urinary F2 isoprostanes c) exhaled breath condensate concentration of hydrogen peroxide and myeloperoxidase. Although the incidence of intensive care admission, cardiac complications, length of hospital stay and survival will be recorded, these important clinical outcomes are not included as major outcome measures as the study is not adequately powered to assess these outcomes.	—

Measure

Time frame

Main Objective: The aim of this pilot study is to investigate the acute effects of ascorbic acid supplementation on systemic and pulmonary endothelial function in the immediate post-operative period following AAA repair. ;Secondary Objective: ;Primary end point(s): As this is a phase II clinical study, several outcomes will be evaluated to determine whether treatment with ascorbic acid attenuates important surrogate physiological outcomes. The primary endpoint of this clinical study is to evaluate the efficacy of ascorbic acid to reduce endothelial dysfunction as measured by the change in plasma vWF at 4 hours following removal of the aortic cross-clamp. The following surrogate markers will also be assessed: 1) Systemic endothelial function as assessed by a) plasma adhesion molecules, ICAM, VCAM and E-selectin b) albumin creatinine ratio (ACR) c) Non-invasive assessment of the change in AIx in response to an endothelial dependent and endothelial independent vasodilator as described below. 2) Pulmonary endothelial function as assessed by the pulmonary dead space fraction. Exhaled breath condensate will be collected and its pH recorded, also the concentration of LTB4; a marker of pulmonary inflammation. In addition the PO2:FiO2 ratio will be recorded as a clinical indicator of pulmonary function when the dead space fraction is measured. 3) Oxidative stress as measured by a) serum lipid peroxides b) urinary F2 isoprostanes c) exhaled breath condensate concentration of hydrogen peroxide and myeloperoxidase. Although the incidence of intensive care admission, cardiac complications, length of hospital stay and survival will be recorded, these important clinical outcomes are not included as major outcome measures as the study is not adequately powered to assess these outcomes.

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Countries

United Kingdom

Outcome results

None listed

Source: EU CTR (via WHO ICTRP) · Data processed: Feb 4, 2026