Spinal Cord InjuriesNCT07227740
Testosterone Deficiency and Endothelial Dysfunction After Spinal Cord Injury
An observational study of Spinal Cord Injuries and Endothelial Dysfunction, run by Craig Hospital at 1 site in United States.
Trial summary
Heart attacks and strokes are among the most common causes of premature death in individuals living with spinal cord injury (SCI) and appear to occur earlier in life. The factors that lead to the heighten and accelerated risk of heart attacks and strokes in adults living with SCI remain poorly understood. Read more about this study
- Who is it for?
- Ages 18 to 89 years, men only
- Conditions the study is for
- Spinal Cord Injuries, Endothelial Dysfunction, Testosterone Deficiency
- What is being tested?
- Intra-arterial Infusion of Vasoactive Agents, Intra-arterial Vitamin C Infusion and Blood Sampling
- Type of treatment
- Injection or infusion
- How many people
- 48 participants
- Where
- 1 siteUnited States
- Study dates
- 15 Jul 2025to 14 Jul 2028
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 89 years
- Men only
- No healthy volunteers
- Adult, Older adult
Study population: Only male participants of all races and ethnic backgrounds aged 18-89 with a history of motor complete (AIS A/B) paraplegia (NLI T3 or Below). Time since injury <6 months at time of enrollment and diagnosed with normal and low T (Testosterone Deficiency defined as < 300ng/dL)
Who may be able to join
- Between ages 18-89 years of age
- Male Sex
- History of motor complete (AIS A/B) paraplegia (NLI T3 or Below)
- Time since injury <6 months at time of enrollment (Subacute injury)
- Testosterone Deficiency defined as < 300ng/dL
Who cannot join
- Overt cardiovascular disease assessed by a) medical history, b) physical examination c) electrocardiogram
- Anaphylaxis to betadine, lidocaine, iodine
- Active infection at time of enrollment.
- Recent surgery (<1 month) at time of enrollment.
- History smoking tobacco (currently or in the past 12 months)
- History of more than low-risk history of alcohol consumption
Show all 9Show fewer
- History of drug abuse
- History of use of cardiovascular-acting (i.e. statins, beta-blockers) therapeutics
- History of other health habits, medications, and supplements that could influence the outcome measures deemed by principal investigators and investigative team.
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
United States1 site, 1 recruiting
- Recruiting
Craig Hospital
Englewood, Colorado, 80113
Genevieve Madera, BS, 7203454640, Gmadera@craighospital.org
Andrew Park, MD, 303-789-8101, apark@craighospital.org
About this study
Official title: Testosterone Deficiency and Endothelial Dysfunction in Spinal Cord Injury Related Cardiovascular Disease Mechanistic Insights and Therapeutic Prospects
Heart attacks and strokes are among the most common causes of premature death in individuals living with spinal cord injury (SCI) and appear to occur earlier in life. The factors that lead to the heighten and accelerated risk of heart attacks and strokes in adults living with SCI remain poorly understood. The investigators aim to uncover why this happens and find ways to prevent it. Our research focuses on how important cells which line blood vessels, called endothelial cells, function after SCI. The investigators test endothelial function in live conscious people with SCI. The investigators also study signaling molecules endothelial cells release called endothelial cell derived microvesicles (EMVs), which the investigators can measure in blood to tell us the health of endothelial cells. By using these rigorous tests of vascular function, the investigators have determined that endothelial cells appear dysfunctional after SCI. The investigators also know that many men with SCI have low testosterone levels. Our team has studied testosterone's effects on endothelial dysfunction and believe low testosterone may be contributing to endothelial dysfunction after SCI. By understanding these mechanisms, the investigators hope to improve the lives of those living with SCI and reduce their risk for heart attacks and strokes. The investigators propose to study the influence of testosterone on endothelial function by using state-of-the-art clinical and laboratory experiments to assess endothelial function in men with SCI with low and normal testosterone levels.
Read the detailed description
The vascular endothelium plays a central role in atherosclerotic cardiovascular disease and may contribute to the increased risk of myocardial infarction and stroke following spinal cord injury (SCI). Endothelial dysfunction is characterized by impaired vasodilator function and reduced fibrinolytic capacity.
Endothelium-dependent vasodilation is primarily mediated by nitric oxide (NO), which induces rapid relaxation of vascular smooth muscle. Fibrinolysis is the breakdown of thrombi within blood vessels, and is facilitated by endothelial cells through the synthesis and release of tissue-type plasminogen activator (t-PA). Importantly, endothelial dysfunction often precedes detectable atherosclerosis and predicts future major vascular events.
Low testosterone (T) is a common secondary complication that occurs early after SCI, with hypogonadism being four times more prevalent in men with SCI. Testosterone has known antioxidant properties and its deficiency may contribute to endothelial dysfunction. Testosterone deficiency may represent a modifiable risk factor for vascular impairment after SCI.
This cross-sectional study will include 48 adults with subacute (<6 months), motor-complete (AIS A/B) paraplegia (neurological level T3 or below). 24 with testosterone deficiency and 24 with normal T levels. Endothelium-dependent vasodilation and t-PA capacity will be assessed via intra-arterial infusion of vasoactive drugs, with total forearm blood flow measured using venous occlusion plethysmography.
- Being tested
- Intra-arterial Infusion of Vasoactive Agents, Intra-arterial Vitamin C Infusion, Blood Sampling
- Keywords
- spinal cord injury, endothelial dysfunction, testosterone deficiency, extracellular vesicles, microvesicles, vasodilation, fibrinolysis
- Medical subject headings
- Spinal Cord Injuries, Aneurysm
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Intra-arterial Infusion of Vasoactive AgentsDiagnostic test
A catheter is placed in the brachial artery of the non-dominant arm, and small doses of vasoactive drugs acetylcholine, isoproterenol, sodium nitroprusside are infused. Forearm blood flow will be measured using venous occlusion plethysmography. The purpose of this procedure is to assess endothelium-dependent and independent vasodilation by stimulating different vascular pathways. The acetylcholine infusion is to test muscarinic receptor, nitro oxide dependent, endothelium-dependent vasodilation. Isoproterenol was selected to stimulate tissue plasminogen activator based on its specificity and effectiveness at eliciting local and rapid tissue plasminogen activator release in adult humans. Sodium nitroprusside infusion is to assess endothelium-independent vasodilation.
Intra-arterial Vitamin C InfusionDiagnostic test
Vitamin C, a potent antioxidant, will be infused into the forearm and forearm blood flow will be re-evaluated to determine whether oxidative stress contributes to endothelial dysfunction.
Blood SamplingDiagnostic test
Blood will be sampled from the antecubital vein (~50 mL) for biomarker analysis. This is to assess circulating biochemical and molecular indicators of vascular health and inflammation including levels of endothelial cell derived microvesicles.
| Study group | Role | What they receive |
|---|---|---|
| Adult Male with Subacute Traumatic Spinal Cord Injury with Normal Testosterone | 24 male participants of all races and ethnic backgrounds aged 18-89 years with a history of spinal cord injury and diagnosed with normal testosterone Receives: Diagnostic Test: Intra-arterial Infusion of Vasoactive Agents; Diagnostic Test: Intra-arterial Vitamin C Infusion; Diagnostic Test: Blood Sampling | |
| Adult Male with Subacute Traumatic Spinal Cord Injury with Low Testosterone | 24 male participants of all races and ethnic backgrounds aged 18-89 years with a history of spinal cord injury and diagnosed with low testosterone Receives: Diagnostic Test: Intra-arterial Infusion of Vasoactive Agents; Diagnostic Test: Intra-arterial Vitamin C Infusion; Diagnostic Test: Blood Sampling |
What is being measured
The primary outcome is the main question the study is designed to answer.
Endothelium-dependent vasodilation
Total forearm blood flow with be measured by strain gauge venous plethysmography under baseline conditions and under pharmacological manipulation with acetylcholine at increasing concentrations (8, 16, 32ug/ml).
Measured: Measured at baseline (without acetylcholine) and immediately after each acetylcholine dose for 3-5 minutes.
Endothelium-independent vasodilation
Total forearm blood flow with be measured by strain gauge venous plethysmography under baseline conditions and under pharmacological manipulation with sodium nitroprusside at increasing concentrations (1, 2, 4ug/ml).
Measured: Measured at baseline (without sodium nitroprusside) and immediately after each sodium nitroprusside dose for 3-5 minutes.
Tissue plasminogen activator release
Net endothelial release or uptake of t-PA and PAI-1 (both antigen and activity levels) at each dose of isoproterenol and sodium nitroprusside will be calculated as the product of the arteriovenous concentration gradient and the infused forearm plasma flow. Arteriovenous concentration gradients for both t-PA and PAI-1 antigen and activity for each subject (at each time point) will be determined by subtraction of the values measured in simultaneously collected venous and arterial blood samples
Measured: Measured at baseline and immediately after each isoproterenol and sodium nitroprusside dose for 3-5 minutes.
Endothelial cell-derived microvesicles concentration
Endothelial cell-derived microvesicles will be collected from venous blood samples and counted used flow cytometry to determine a circulating concentration.
Measured: Baseline
Endothelial cell-derived microvesicles effects of human coronary artery endothelial cells nitric oxide bioavailability.
Endothelial cell-derived microvesicles will be sorted and collected by fluorescence-activated cell sorting (FACS) flow cytometry. The endothelial cell-derived microvesicles will be co-cultured with human coronary artery endothelial cells. Endothelial Nitric Oxide Synthase and phosphorylation sites of interest will be measured by intracellular protein expression quantification of whole cell lysates by capillary electrophoresis immunoassays. Nitric oxide production will be assessed by total nitric oxide and nitrate/nitrite parameter assays
Measured: Baseline
Endothelial cell-derived microvesicles effects of human coronary artery endothelial cells reactive oxygen species and antioxidant capacity
Endothelial cell-derived microvesicles will be sorted and collected by fluorescence-activated cell sorting (FACS) flow cytometry. The endothelial cell-derived microvesicles will be co-cultured with human coronary artery endothelial cells. Super oxide dismutase and catalase expression will be measured by intracellular protein expression quantification of whole cell lysates by capillary electrophoresis immunoassays. Intracellular oxidative stress will be assessed by ROS-Glo H2O2 assay.
Measured: Baseline
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted13 Nov 2025
- Study start15 Jul 2025
- Primary completion14 Jul 2028 (estimated)
- Study completion14 Jul 2028 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Spinal Cord InjuriesStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Cross-sectional
- Enrolment
- 48 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Craig Hospital
- Sponsor type
- University, hospital or other
- Collaborators
- University of Colorado, Boulder, Denver Health and Hospital Authority, University of Colorado, Denver
- Responsible party
- Sponsor
- Investigators
- Andrew Park, MD, Principal investigator, Craig Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07227740
- Sponsor's protocol ID
- 2301643
- Other IDs
- CDMRP-SC240119
- Status last verified
- Nov 2025
- First submitted
- 11 Nov 2025
- Last updated
- 21 Nov 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Yes: Data sharing will be facilitated through active participation in Open Data Commons for SCI (ODC-SCI). ODC-SCI is a cloud-based community-governed repository to store, share, and publish research data on Spinal Cord Injury and is compliant with requirements for FAIR and trustworthy repositories established by NIH.
Study at a glance
From the registry record, last updated by the sponsor on 21 Nov 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Testosterone Deficiency and Endothelial Dysfunction in Spinal Cord Injury Related Cardiovascular Disease Mechanistic Insights and Therapeutic Prospects
- ClinicalTrials.gov ID
- NCT07227740
- Acronym / sponsor ID
- 2301643
- Keywords
- spinal cord injury, endothelial dysfunction, testosterone deficiency, extracellular vesicles, microvesicles, vasodilation, fibrinolysis
- Study type
- Observational
- Recruitment status
- Recruiting
- Enrolment
- 48 participants (estimated)
- Lead sponsor
- Craig HospitalUniversity, hospital or other
- Collaborators
- University of Colorado, Boulder, Denver Health and Hospital Authority, University of Colorado, Denver
- Study start
- 15 Jul 2025 (actual)
- Primary completion
- 14 Jul 2028 (estimated)
- Study completion
- 14 Jul 2028 (estimated)
- First posted
- 13 Nov 2025 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Heart attacks and strokes are among the most common causes of premature death in individuals living with spinal cord injury (SCI) and appear to occur earlier in life. The factors that lead to the heighten and accelerated risk of heart attacks and strokes in adults living with SCI remain poorly understood. The investigators aim to uncover why this happens and find ways to prevent it. Our research focuses on how important cells which line blood vessels, called endothelial cells, function after SCI. The investigators test endothelial function in live conscious people with SCI. The investigators also study signaling molecules endothelial cells release called endothelial cell derived microvesicles (EMVs), which the investigators can measure in blood to tell us the health of endothelial cells. By using these rigorous tests of vascular function, the investigators have determined that endothelial cells appear dysfunctional after SCI. The investigators also know that many men with SCI have low testosterone levels. Our team has studied testosterone's effects on endothelial dysfunction and believe low testosterone may be contributing to endothelial dysfunction after SCI. By understanding these mechanisms, the investigators hope to improve the lives of those living with SCI and reduce their risk for heart attacks and strokes. The investigators propose to study the influence of testosterone on endothelial function by using state-of-the-art clinical and laboratory experiments to assess endothelial function in men with SCI with low and normal testosterone levels.
Detailed description
The vascular endothelium plays a central role in atherosclerotic cardiovascular disease and may contribute to the increased risk of myocardial infarction and stroke following spinal cord injury (SCI). Endothelial dysfunction is characterized by impaired vasodilator function and reduced fibrinolytic capacity.
Endothelium-dependent vasodilation is primarily mediated by nitric oxide (NO), which induces rapid relaxation of vascular smooth muscle. Fibrinolysis is the breakdown of thrombi within blood vessels, and is facilitated by endothelial cells through the synthesis and release of tissue-type plasminogen activator (t-PA). Importantly, endothelial dysfunction often precedes detectable atherosclerosis and predicts future major vascular events.
Low testosterone (T) is a common secondary complication that occurs early after SCI, with hypogonadism being four times more prevalent in men with SCI. Testosterone has known antioxidant properties and its deficiency may contribute to endothelial dysfunction. Testosterone deficiency may represent a modifiable risk factor for vascular impairment after SCI.
This cross-sectional study will include 48 adults with subacute (<6 months), motor-complete (AIS A/B) paraplegia (neurological level T3 or below). 24 with testosterone deficiency and 24 with normal T levels. Endothelium-dependent vasodilation and t-PA capacity will be assessed via intra-arterial infusion of vasoactive drugs, with total forearm blood flow measured using venous occlusion plethysmography.
Study design
- Observational model
- Case-control
- Time perspective
- Cross-sectional
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Adult Male with Subacute Traumatic Spinal Cord Injury with Normal Testosterone | – | Diagnostic Test: Intra-arterial Infusion of Vasoactive Agents, Diagnostic Test: Intra-arterial Vitamin C Infusion, Diagnostic Test: Blood Sampling24 male participants of all races and ethnic backgrounds aged 18-89 years with a history of spinal cord injury and diagnosed with normal testosterone |
| Adult Male with Subacute Traumatic Spinal Cord Injury with Low Testosterone | – | Diagnostic Test: Intra-arterial Infusion of Vasoactive Agents, Diagnostic Test: Intra-arterial Vitamin C Infusion, Diagnostic Test: Blood Sampling24 male participants of all races and ethnic backgrounds aged 18-89 years with a history of spinal cord injury and diagnosed with low testosterone |
Who may qualify
- Ages
- 18 to 89 years
- Sex
- Male only
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Only male participants of all races and ethnic backgrounds aged 18-89 with a history of motor complete (AIS A/B) paraplegia (NLI T3 or Below). Time since injury <6 months at time of enrollment and diagnosed with normal and low T (Testosterone Deficiency defined as < 300ng/dL)
Key inclusion criteria (5 listed)
- Between ages 18-89 years of age
- Male Sex
- History of motor complete (AIS A/B) paraplegia (NLI T3 or Below)
- Time since injury <6 months at time of enrollment (Subacute injury)
- Testosterone Deficiency defined as < 300ng/dL
Key exclusion criteria (9 listed)
- Overt cardiovascular disease assessed by a) medical history, b) physical examination c) electrocardiogram
- Anaphylaxis to betadine, lidocaine, iodine
- Active infection at time of enrollment.
- Recent surgery (<1 month) at time of enrollment.
- History smoking tobacco (currently or in the past 12 months)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Intra-arterial Infusion of Vasoactive AgentsA catheter is placed in the brachial artery of the non-dominant arm, and small doses of vasoactive drugs acetylcholine, isoproterenol, sodium nitroprusside are infused. Forearm blood flow will be measured using venous occlusion plethysmography. The purpose of this procedure is to assess endothelium-dependent and independent vasodilation by stimulating different vascular pathways. The acetylcholine infusion is to test muscarinic receptor, nitro oxide dependent, endothelium-dependent vasodilation. Isoproterenol was selected to stimulate tissue plasminogen activator based on its specificity and effectiveness at eliciting local and rapid tissue plasminogen activator release in adult humans. Sodium nitroprusside infusion is to assess endothelium-independent vasodilation. | Diagnostic test | Adult Male with Subacute Traumatic Spinal Cord Injury with Low Testosterone, Adult Male with Subacute Traumatic Spinal Cord Injury with Normal Testosterone |
| Intra-arterial Vitamin C InfusionVitamin C, a potent antioxidant, will be infused into the forearm and forearm blood flow will be re-evaluated to determine whether oxidative stress contributes to endothelial dysfunction. | Diagnostic test | Adult Male with Subacute Traumatic Spinal Cord Injury with Low Testosterone, Adult Male with Subacute Traumatic Spinal Cord Injury with Normal Testosterone |
| Blood SamplingBlood will be sampled from the antecubital vein (~50 mL) for biomarker analysis. This is to assess circulating biochemical and molecular indicators of vascular health and inflammation including levels of endothelial cell derived microvesicles. | Diagnostic test | Adult Male with Subacute Traumatic Spinal Cord Injury with Low Testosterone, Adult Male with Subacute Traumatic Spinal Cord Injury with Normal Testosterone |
Primary outcome
Endothelium-dependent vasodilation
Time frame: Measured at baseline (without acetylcholine) and immediately after each acetylcholine dose for 3-5 minutes.
Total forearm blood flow with be measured by strain gauge venous plethysmography under baseline conditions and under pharmacological manipulation with acetylcholine at increasing concentrations (8, 16, 32ug/ml).
Endothelium-independent vasodilation
Time frame: Measured at baseline (without sodium nitroprusside) and immediately after each sodium nitroprusside dose for 3-5 minutes.
Total forearm blood flow with be measured by strain gauge venous plethysmography under baseline conditions and under pharmacological manipulation with sodium nitroprusside at increasing concentrations (1, 2, 4ug/ml).
Tissue plasminogen activator release
Time frame: Measured at baseline and immediately after each isoproterenol and sodium nitroprusside dose for 3-5 minutes.
Net endothelial release or uptake of t-PA and PAI-1 (both antigen and activity levels) at each dose of isoproterenol and sodium nitroprusside will be calculated as the product of the arteriovenous concentration gradient and the infused forearm plasma flow. Arteriovenous concentration gradients for both t-PA and PAI-1 antigen and activity for each subject (at each time point) will be determined by subtraction of the values measured in simultaneously collected venous and arterial blood samples
Endothelial cell-derived microvesicles concentration
Time frame: Baseline
Endothelial cell-derived microvesicles will be collected from venous blood samples and counted used flow cytometry to determine a circulating concentration.
Endothelial cell-derived microvesicles effects of human coronary artery endothelial cells nitric oxide bioavailability.
Time frame: Baseline
Endothelial cell-derived microvesicles will be sorted and collected by fluorescence-activated cell sorting (FACS) flow cytometry. The endothelial cell-derived microvesicles will be co-cultured with human coronary artery endothelial cells. Endothelial Nitric Oxide Synthase and phosphorylation sites of interest will be measured by intracellular protein expression quantification of whole cell lysates by capillary electrophoresis immunoassays. Nitric oxide production will be assessed by total nitric oxide and nitrate/nitrite parameter assays
Endothelial cell-derived microvesicles effects of human coronary artery endothelial cells reactive oxygen species and antioxidant capacity
Time frame: Baseline
Endothelial cell-derived microvesicles will be sorted and collected by fluorescence-activated cell sorting (FACS) flow cytometry. The endothelial cell-derived microvesicles will be co-cultured with human coronary artery endothelial cells. Super oxide dismutase and catalase expression will be measured by intracellular protein expression quantification of whole cell lysates by capillary electrophoresis immunoassays. Intracellular oxidative stress will be assessed by ROS-Glo H2O2 assay.
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 21 Nov 2025.
- Individual participant dataSharing planned: Yes. Data sharing will be facilitated through active participation in Open Data Commons for SCI (ODC-SCI). ODC-SCI is a cloud-based community-governed repository to store, share, and publish research data on Spinal Cord Injury and is compliant with requirements for FAIR and trustworthy repositories established by NIH.
Related trials for Spinal Cord Injuries
Recruiting
Implant for Walking After Incomplete SCI
Spinal Cord Injury (SCI), Gait
Recruiting
MindEx: A Novel, Multifocal, Cognitive Brain-Machine Interface System
Paralysis; Quadriplegic, Quadraplegia
Recruiting
tSCS Combined With Rehabilitation Training in Treating Paraplegic Patients After SCI
Spinal Cord Injury, Paraplegia, Spinal
Active, not recruitingObservational study
Natural History of Shoulder Pathology in Manual Wheelchair Users
Paraplegia, Spinal Cord Injuries
Recruiting
Neuromodulation for Metabolic Dysfunction
Spinal Cord Injuries (SCI), Prediabetes / Type 2 Diabetes
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Andrew Park, MD principal investigator
Craig Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Spinal Cord Injuries and Endothelial Dysfunction, run by Craig Hospital at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 9 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: looking for participants now, as of the sponsor's last update on 21 Nov 2025. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Genevieve Madera, BS (17203454640, Gmadera@craighospital.org), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Endothelium-dependent vasodilation (time frame: Measured at baseline (without acetylcholine) and immediately after each acetylcholine dose for 3-5 minutes.). The study lists 6 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 21 Nov 2025.