AtherosclerosisVIRALNCT06217471
Influenza A VIRus and Destabilization of Atherosclerotic Carotid Plaques
An observational study of Atherosclerosis, run by IRCCS Policlinico S. Donato at 1 site in Italy.
Trial summary
Atherosclerosis is the main cause of cardiovascular diseases and is characterized by the accumulation of lipids and inflammatory cells such as macrophages and lymphocytes within the vessel wall of large and medium-sized arteries, forming so-called plaques. Read more about this study
- Who is it for?
- Any age
- Conditions the study is for
- Atherosclerosis
- What is being tested?
- Carotid Endoarterectomy
- Type of treatment
- Surgery or procedure
- How many people
- 160 participants
- Where
- 1 siteItaly
- Study dates
- 18 Feb 2020to 9 Mar 2023
- Phase
- Observational
- Are there results?
- None posted in the registry
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 Any age
- All sexes
- Child, Adult, Older adult
Study population: Patients coming to the Vascular Surgery Unit of the IRCCS Policlinico San Donato to undergo carotid endarterectomy surgery for significant carotid stenosis
Who may be able to join
- adult patients (age > 18 years) who have given their consent to participate in the study, belonging to the Vascular Surgery Unit of the IRCCS Policlinico San Donato to undergo carotid endarterectomy surgery for significant carotid stenosis (in accordance with the Guidelines International guidelines, asymptomatic patients with carotid stenosis > 80% according to ECST and symptomatic patients with stenosis > 70% according to ECST
Who cannot join
- Minor patients
- Pregnant/breastfeeding women
- Patients who have not provided their consent to participate in the study.
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Role of Influenza A VIRus in the Biomolecular Pathogenesis of the Destabilization of Atherosclerotic Carotid Plaques
Atherosclerosis is the main cause of cardiovascular diseases and is characterized by the accumulation of lipids and inflammatory cells such as macrophages and lymphocytes within the vessel wall of large and medium-sized arteries, forming so-called plaques. The underlying molecular mechanisms are not yet clearly understood. In particular, it is not yet clear what factors can cause the "destabilization" of atherosclerotic plaques, thus making them more vulnerable and prone to triggering acute cardiovascular events. Infectious agents have also been implicated in the pathogenesis of atherosclerosis. Some of them would be able to spread from the infected tissue and migrate to endothelial cells, promoting the secretion of inflammatory mediators and the oxidation of low-density lipoproteins (LDL), their accumulation in vascular cells and the formation of foam cells , fundamental mechanisms especially in the formation of vulnerable plaques.
Recently, many studies have shown that the influenza virus can also play a role in the destabilization of atherosclerotic plaques. However, the role of influenza A virus (IVA) infection and related vaccination in the destabilization of atherosclerotic plaques is still controversial. Furthermore, the underlying molecular mechanisms are still a matter of investigation.
Based on these data, we hypothesized that IV A infection may promote the destabilization of atherosclerotic plaques through a chronic postinfection immune response. This response would lead to systemic and local changes in the expression of pro-atherosclerotic cytokines and chemokines resulting in increased recruitment of monocyte macrophages and upregulation of the expression of scavenger receptors on the surface of macrophages with greater affinity for oxidized LDL (CD36 and Lectins- Like-oxLDL-receptor 1).
Read the detailed description
The following data will be collected anonymously from the medical records:
- personal details (age, sex);
- comorbidity (presence of cardiovascular risk factors: arterial hypertension, smoking, dyslipidemia, ischemic heart disease, COPD, diabetes mellitus; chronic renal failure, history of cerebrovascular ischemic events);
- history of flu vaccination;
- clinical (weight, height); As per clinical practice, patients will undergo carotid endarterectomy surgery. Upon entry into the operating room, patients will be taken 4 ml of blood in 4 tubes with a specific anticoagulant (EDTA), from a peripheral venous access already positioned for the surgical procedure regardless of the study. These blood samples will be stored and processed appropriately for individual analyses.
Samples of atherosclerotic plaque removed during surgery will also be stored appropriately for subsequent investigations.
The data collected will be entered into the dedicated e-CRF and appropriately analyzed.
Use of blood samples Peripheral blood mononuclear cells (PBMC) will be separated and isolated from the venous blood sample using a Percoll gradient. These cells will be appropriately stimulated with influenza A virus antigens using specific commercial kits. This process will allow the evaluation of immune reactivity to the virus, both in the group of patients with vulnerable carotid plaque (group A) and in those with non-vulnerable plaque (group B). On the serum of the same samples, the quantitative expression of some cytokines/chemokines involved in inflammation and the atherosclerotic process (IL-6, IL-1β, TNF-α, IFN-γ, MCP-1) will be evaluated using the ELISA method).
The appropriate antibody evaluation will also be performed to test for any acute IV A infections.
Use of vascular samples Histology investigations will be carried out on atherosclerotic plaque samples which will allow determining the vulnerability or otherwise of the plaque, in such a way as to define the two groups of patients (A, vulnerable plaque; B, non-vulnerable plaque) to be analysed. and compare.
Western-Blot assays and immunohistochemical analyzes will also be performed on the same samples to evaluate the quantitative and qualitative expression of some molecules (V-CAM, I-CAM, E-Selectins) and receptors that identify scavenger macrophage cells (CD36 and Lectins -Like Ox-LDL-Receptor 1.
Finally, the same samples will be subjected to ELISA analysis for the quantitative research of the same cytokines/chemokines evaluated on the blood sample via RT-PCR. The possible presence of viral RNA will be evaluated on the atherosclerotic plaques by one step RT-PCR, as well as the T-specific cell reactivity to the IV A virus after the preparation of appropriate cell cultures which will be stimulated with the same commercial kit used to stimulate the PMBC of peripheral blood, according to the method described by Keller et al. Collaterally, the possible presence of viral or bacterial DNA in the plaques will be checked. In particular, the presence of DNA from Human Polyomaviruses and Human Herpesviruses (herpes simplex virus 7 and 2, varicella zoster virus, Epstein-Barr virus, human cytomegalovirus, human herpesvirus 6) and Chlamydia will be analyzed through Real Time PCR.
Evaluation of specific T-cell reactivity to virus IV A Taking as reference the method described by Keller et al, the stimulation index (SI) will be evaluated, both on the blood sample and on the atherosclerotic plaque, as the average count per minute (cpm) of cultures with the virus, divided by the mean cpm of parallel cultures without viruses.
Subsequently, the reactivity will be calculated based on the ratio between the SI of the plaque T cells and the SI of the peripheral blood T cells for each patient, defining responsive patients if the ratio is > 2 (patients with SI of the T cells T of the plaque significantly higher than those of the peripheral blood), and not responsive if the ratio is < 2 (in the latter case, patients with SI of the T cells of the peripheral blood greater than those of the plaque, or with SI of the T cells Plaque T not significantly higher than those of peripheral blood).
- Conditions
- Atherosclerosis
- Being tested
- Carotid Endoarterectomy
- Medical subject headings
- Atherosclerosis
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Carotid EndoarterectomyProcedure or surgery
Surgical removal of atherosclerotic plaque from the carotid artery, collection of blood samples
What is being measured
The primary outcome is the main question the study is designed to answer.
antigenic specificity of IV T cells
To test the antigenic specificity of IV T cells in carotid plaques and blood samples (peripheral blood mononuclear immune cells - PBMCs) of patients undergoing carotid endarterectomy (CEA) using the Stimulation Index, comparing results among a group of patients with vulnerable carotid plaque (group A) and a group of patients with stable plaque (group B, controls). Collaterally, the presence of viral RNA in the carotid plaques of patients in both groups will be evaluated; Blood samples will also be evaluated with serology for the presence of antibodies against IV A.
Measured: through study completion, an average of 3 years
presence of viral RNA
The presence of viral RNA in the carotid plaques and in the blood of patients in both groups will be evaluated using real-time PCR.
Measured: through study completion, an average of 3 years
expression of inflammatory chemokines/cytokines
Evaluate and compare the expression of inflammatory chemokines/cytokines involved in the recruitment and differentiation of monocytes (especially IL-6, IL-1β, TNF-α, IFN-γ, MCP-1), in the carotid plaque and in the blood peripheral of both groups; the results will be correlated to those obtained in objective 1.
Measured: through study completion, an average of 3 years
expression of adhesion molecules and scavenger receptors
To evaluate and compare the expression of adhesion molecules and scavenger receptors with high affinity for oxLDL (CD36 and lectin-like oxLDL receptor) in carotid plaques between the two groups. The results will be correlated to those obtained in objectives 1 and 2.
Measured: through study completion, an average of 3 years
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted22 Jan 2024
- Study start18 Feb 2020
- Primary completion9 Mar 2023
- Study completion9 Mar 2023
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (6)Papers the sponsor has linked to this study.
- Other trials for AtherosclerosisStudies of the same condition, open and under way.
- More trials run by IRCCS Policlinico S. DonatoThe sponsor's other registered studies.
- 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
- Other
- Time perspective
- Cross-sectional
- Enrolment
- 160 participants (actual)
Sponsor and investigators
- Lead sponsor
- IRCCS Policlinico S. Donato
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Daniela Mazzaccaro, IRCCS Policlinico S. Donato
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06217471
- Sponsor's protocol ID
- VIRAL V1 - 131/int/2019
- Acronym
- VIRAL
- Status last verified
- Jan 2024
- First submitted
- 27 Dec 2023
- Last updated
- 22 Jan 2024
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Madjid M, Naghavi M, Litovsky S, Casscells SW. Influenza and cardiovascular disease: a new opportunity for prevention and the need for further studies. Circulation. 2003 Dec 2;108(22):2730-6. doi: 10.1161/01.CIR.0000102380.47012.92. Epub 2003 Nov 10. No abstract available.
PubMed 14610013Chistiakov DA, Melnichenko AA, Myasoedova VA, Grechko AV, Orekhov AN. Mechanisms of foam cell formation in atherosclerosis. J Mol Med (Berl). 2017 Nov;95(11):1153-1165. doi: 10.1007/s00109-017-1575-8. Epub 2017 Aug 7.
PubMed 28785870Guan X, Yang W, Sun X, Wang L, Ma B, Li H, Zhou J. Association of influenza virus infection and inflammatory cytokines with acute myocardial infarction. Inflamm Res. 2012 Jun;61(6):591-8. doi: 10.1007/s00011-012-0449-3. Epub 2012 Feb 29.
PubMed 22373653Keller TT, van der Meer JJ, Teeling P, van der Sluijs K, Idu MM, Rimmelzwaan GF, Levi M, van der Wal AC, de Boer OJ. Selective expansion of influenza A virus-specific T cells in symptomatic human carotid artery atherosclerotic plaques. Stroke. 2008 Jan;39(1):174-9. doi: 10.1161/STROKEAHA.107.491282. Epub 2007 Nov 29.
PubMed 18048854Haidari M, Wyde PR, Litovsky S, Vela D, Ali M, Casscells SW, Madjid M. Influenza virus directly infects, inflames, and resides in the arteries of atherosclerotic and normal mice. Atherosclerosis. 2010 Jan;208(1):90-6. doi: 10.1016/j.atherosclerosis.2009.07.028. Epub 2009 Jul 24.
PubMed 19665123Ricotta JJ, Aburahma A, Ascher E, Eskandari M, Faries P, Lal BK; Society for Vascular Surgery. Updated Society for Vascular Surgery guidelines for management of extracranial carotid disease. J Vasc Surg. 2011 Sep;54(3):e1-31. doi: 10.1016/j.jvs.2011.07.031.
PubMed 21889701
Study at a glance
From the registry record, last updated by the sponsor on 22 Jan 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Role of Influenza A VIRus in the Biomolecular Pathogenesis of the Destabilization of Atherosclerotic Carotid Plaques
- ClinicalTrials.gov ID
- NCT06217471
- Acronym / sponsor ID
- VIRAL / VIRAL V1 - 131/int/2019
- Conditions
- Atherosclerosis
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 160 participants (actual)
- Lead sponsor
- IRCCS Policlinico S. DonatoUniversity, hospital or other
- Study start
- 18 Feb 2020 (actual)
- Primary completion
- 9 Mar 2023 (actual)
- Study completion
- 9 Mar 2023 (actual)
- First posted
- 22 Jan 2024 (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.
Atherosclerosis is the main cause of cardiovascular diseases and is characterized by the accumulation of lipids and inflammatory cells such as macrophages and lymphocytes within the vessel wall of large and medium-sized arteries, forming so-called plaques. The underlying molecular mechanisms are not yet clearly understood. In particular, it is not yet clear what factors can cause the "destabilization" of atherosclerotic plaques, thus making them more vulnerable and prone to triggering acute cardiovascular events. Infectious agents have also been implicated in the pathogenesis of atherosclerosis. Some of them would be able to spread from the infected tissue and migrate to endothelial cells, promoting the secretion of inflammatory mediators and the oxidation of low-density lipoproteins (LDL), their accumulation in vascular cells and the formation of foam cells , fundamental mechanisms especially in the formation of vulnerable plaques.
Recently, many studies have shown that the influenza virus can also play a role in the destabilization of atherosclerotic plaques. However, the role of influenza A virus (IVA) infection and related vaccination in the destabilization of atherosclerotic plaques is still controversial. Furthermore, the underlying molecular mechanisms are still a matter of investigation.
Based on these data, we hypothesized that IV A infection may promote the destabilization of atherosclerotic plaques through a chronic postinfection immune response. This response would lead to systemic and local changes in the expression of pro-atherosclerotic cytokines and chemokines resulting in increased recruitment of monocyte macrophages and upregulation of the expression of scavenger receptors on the surface of macrophages with greater affinity for oxidized LDL (CD36 and Lectins- Like-oxLDL-receptor 1).
Detailed description
The following data will be collected anonymously from the medical records:
- personal details (age, sex);
- comorbidity (presence of cardiovascular risk factors: arterial hypertension, smoking, dyslipidemia, ischemic heart disease, COPD, diabetes mellitus; chronic renal failure, history of cerebrovascular ischemic events);
- history of flu vaccination;
- clinical (weight, height); As per clinical practice, patients will undergo carotid endarterectomy surgery. Upon entry into the operating room, patients will be taken 4 ml of blood in 4 tubes with a specific anticoagulant (EDTA), from a peripheral venous access already positioned for the surgical procedure regardless of the study. These blood samples will be stored and processed appropriately for individual analyses.
Samples of atherosclerotic plaque removed during surgery will also be stored appropriately for subsequent investigations.
The data collected will be entered into the dedicated e-CRF and appropriately analyzed.
Use of blood samples Peripheral blood mononuclear cells (PBMC) will be separated and isolated from the venous blood sample using a Percoll gradient. These cells will be appropriately stimulated with influenza A virus antigens using specific commercial kits. This process will allow the evaluation of immune reactivity to the virus, both in the group of patients with vulnerable carotid plaque (group A) and in those with non-vulnerable plaque (group B). On the serum of the same samples, the quantitative expression of some cytokines/chemokines involved in inflammation and the atherosclerotic process (IL-6, IL-1β, TNF-α, IFN-γ, MCP-1) will be evaluated using the ELISA method).
The appropriate antibody evaluation will also be performed to test for any acute IV A infections.
Use of vascular samples Histology investigations will be carried out on atherosclerotic plaque samples which will allow determining the vulnerability or otherwise of the plaque, in such a way as to define the two groups of patients (A, vulnerable plaque; B, non-vulnerable plaque) to be analysed. and compare.
Western-Blot assays and immunohistochemical analyzes will also be performed on the same samples to evaluate the quantitative and qualitative expression of some molecules (V-CAM, I-CAM, E-Selectins) and receptors that identify scavenger macrophage cells (CD36 and Lectins -Like Ox-LDL-Receptor 1.
Finally, the same samples will be subjected to ELISA analysis for the quantitative research of the same cytokines/chemokines evaluated on the blood sample via RT-PCR. The possible presence of viral RNA will be evaluated on the atherosclerotic plaques by one step RT-PCR, as well as the T-specific cell reactivity to the IV A virus after the preparation of appropriate cell cultures which will be stimulated with the same commercial kit used to stimulate the PMBC of peripheral blood, according to the method described by Keller et al. Collaterally, the possible presence of viral or bacterial DNA in the plaques will be checked. In particular, the presence of DNA from Human Polyomaviruses and Human Herpesviruses (herpes simplex virus 7 and 2, varicella zoster virus, Epstein-Barr virus, human cytomegalovirus, human herpesvirus 6) and Chlamydia will be analyzed through Real Time PCR.
Evaluation of specific T-cell reactivity to virus IV A Taking as reference the method described by Keller et al, the stimulation index (SI) will be evaluated, both on the blood sample and on the atherosclerotic plaque, as the average count per minute (cpm) of cultures with the virus, divided by the mean cpm of parallel cultures without viruses.
Subsequently, the reactivity will be calculated based on the ratio between the SI of the plaque T cells and the SI of the peripheral blood T cells for each patient, defining responsive patients if the ratio is > 2 (patients with SI of the T cells T of the plaque significantly higher than those of the peripheral blood), and not responsive if the ratio is < 2 (in the latter case, patients with SI of the T cells of the peripheral blood greater than those of the plaque, or with SI of the T cells Plaque T not significantly higher than those of peripheral blood).
Study design
- Observational model
- Other
- Time perspective
- Cross-sectional
Who may qualify
- Sex
- All
- Age groups
- Child, Adult, Older adult
- Study population
- Patients coming to the Vascular Surgery Unit of the IRCCS Policlinico San Donato to undergo carotid endarterectomy surgery for significant carotid stenosis
Key inclusion criteria (1 listed)
- adult patients (age > 18 years) who have given their consent to participate in the study, belonging to the Vascular Surgery Unit of the IRCCS Policlinico San Donato to undergo carotid endarterectomy surgery for significant carotid stenosis (in accordance with the Guidelines International guidelines, asymptomatic patients with carotid stenosis > 80% according to ECST and symptomatic patients with stenosis > 70% according to ECST
Key exclusion criteria (3 listed)
- Minor patients
- Pregnant/breastfeeding women
- Patients who have not provided their consent to participate in the study.
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 |
|---|---|---|
| Carotid EndoarterectomySurgical removal of atherosclerotic plaque from the carotid artery, collection of blood samples | Procedure or surgery | – |
Primary outcome
antigenic specificity of IV T cells
Time frame: through study completion, an average of 3 years
To test the antigenic specificity of IV T cells in carotid plaques and blood samples (peripheral blood mononuclear immune cells - PBMCs) of patients undergoing carotid endarterectomy (CEA) using the Stimulation Index, comparing results among a group of patients with vulnerable carotid plaque (group A) and a group of patients with stable plaque (group B, controls). Collaterally, the presence of viral RNA in the carotid plaques of patients in both groups will be evaluated; Blood samples will also be evaluated with serology for the presence of antibodies against IV A.
presence of viral RNA
Time frame: through study completion, an average of 3 years
The presence of viral RNA in the carotid plaques and in the blood of patients in both groups will be evaluated using real-time PCR.
expression of inflammatory chemokines/cytokines
Time frame: through study completion, an average of 3 years
Evaluate and compare the expression of inflammatory chemokines/cytokines involved in the recruitment and differentiation of monocytes (especially IL-6, IL-1β, TNF-α, IFN-γ, MCP-1), in the carotid plaque and in the blood peripheral of both groups; the results will be correlated to those obtained in objective 1.
expression of adhesion molecules and scavenger receptors
Time frame: through study completion, an average of 3 years
To evaluate and compare the expression of adhesion molecules and scavenger receptors with high affinity for oxLDL (CD36 and lectin-like oxLDL receptor) in carotid plaques between the two groups. The results will be correlated to those obtained in objectives 1 and 2.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 22 Jan 2024.
- Results publication: PubMed 14610013Madjid M, Naghavi M, Litovsky S, Casscells SW. Influenza and cardiovascular disease: a new opportunity for prevention and the need for further studies. Circulation. 2003 Dec 2;108(22):2730-6. doi: 10.1161/01.CIR.0000102380.47012.92. Epub 2003 Nov 10. No abstract available.
- Results publication: PubMed 28785870Chistiakov DA, Melnichenko AA, Myasoedova VA, Grechko AV, Orekhov AN. Mechanisms of foam cell formation in atherosclerosis. J Mol Med (Berl). 2017 Nov;95(11):1153-1165. doi: 10.1007/s00109-017-1575-8. Epub 2017 Aug 7.
- Results publication: PubMed 22373653Guan X, Yang W, Sun X, Wang L, Ma B, Li H, Zhou J. Association of influenza virus infection and inflammatory cytokines with acute myocardial infarction. Inflamm Res. 2012 Jun;61(6):591-8. doi: 10.1007/s00011-012-0449-3. Epub 2012 Feb 29.
- Results publication: PubMed 18048854Keller TT, van der Meer JJ, Teeling P, van der Sluijs K, Idu MM, Rimmelzwaan GF, Levi M, van der Wal AC, de Boer OJ. Selective expansion of influenza A virus-specific T cells in symptomatic human carotid artery atherosclerotic plaques. Stroke. 2008 Jan;39(1):174-9. doi: 10.1161/STROKEAHA.107.491282. Epub 2007 Nov 29.
- Results publication: PubMed 19665123Haidari M, Wyde PR, Litovsky S, Vela D, Ali M, Casscells SW, Madjid M. Influenza virus directly infects, inflames, and resides in the arteries of atherosclerotic and normal mice. Atherosclerosis. 2010 Jan;208(1):90-6. doi: 10.1016/j.atherosclerosis.2009.07.028. Epub 2009 Jul 24.
- Results publication: PubMed 21889701Ricotta JJ, Aburahma A, Ascher E, Eskandari M, Faries P, Lal BK; Society for Vascular Surgery. Updated Society for Vascular Surgery guidelines for management of extracranial carotid disease. J Vasc Surg. 2011 Sep;54(3):e1-31. doi: 10.1016/j.jvs.2011.07.031.
- Individual participant dataSharing planned: Undecided
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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. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
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 Atherosclerosis, run by IRCCS Policlinico S. Donato at 1 site in Italy.
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 1 inclusion and 3 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: finished, as of the sponsor's last update on 22 Jan 2024. 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 Italy. 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?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
antigenic specificity of IV T cells (time frame: through study completion, an average of 3 years). The study lists 4 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT06217471, which also lists 6 linked publications.
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 22 Jan 2024.