Cardiovascular DiseasePhase 4NCT06263452
Beta-Blocker Influences on Inflammatory and Neural Responses to Stress
A Phase 4 study testing Propranolol in people with Cardiovascular Disease, run by University of North Carolina, Chapel Hill at 1 site in United States.
Trial summary
The purpose of this study is to map the neural and molecular mechanisms underlying psychological stress-induced changes in inflammation which could reveal new targets for intervention to reduce the risk of cardiovascular disease. Read more about this study
- Who is it for?
- Ages 18 to 30 yearsHealthy volunteers can take part
- Conditions the study is for
- Cardiovascular Disease
- What is being tested?
- Propranolol
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 120 participants
- Where
- 1 siteUnited States
- Study dates
- 1 May 2024to Feb 2027
- Phase
- Phase 4
- 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 30 years
- All sexes
- Healthy volunteers accepted
- Adult
Who may be able to join
- Ages 18-30 years
- Right-handed
- Fluent in English reading, writing, and speaking at least at a 10th grade level
- Body mass index (BMI) less than or equal to 35 kg/m^2
Who cannot join
- Assessed as screening, reassessed at Session I:
- Non-removeable metal devices/implants/objects in the body
- Severe claustrophobia (assessed by self-report)
- Currently pregnant
- Left-handed
- Body mass index (BMI) greater than 35 kg/m^2
Show all 21Show fewer
- History of fainting spells or any heart condition
- History of or present low resting heart rate (< 60 BPM) and/or low blood pressure (systolic blood pressure < 80mmHg)
- Self-reported physical illnesses: diabetes, cardiovascular diseases, high blood pressure, inflammatory bowel diseases, rheumatoid arthritis, asthma, autoimmune disease, Crohn's disease, ulcerative colitis, lupus
- Any self-reported diagnosed mental illness
- Current use of prescription medications (except hormonal contraceptives)
- Current or recent regular nicotine/tobacco use (cigarettes, e-cigarettes, vape, chewing tobacco, nicotine gum)
- Current regular (daily or almost daily) recreational drug use = 4 or more times per week
- Instructed against during Session I, reassessed at Session II:
- Received any vaccine within the past two weeks
- Severe sleep disturbance (3-4 hours of sleep loss) the night before Session II
- Vigorous physical activity on the day of Session II
- Acute illness or allergy symptoms on the day of Session II
- Usage of over-the-counter medications on the day of Session II
- Usage of recreational drugs within 48 hours of Session II
- Usage of alcohol on the day of Session II
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
Social Neuroscience and Health Laboratory
Chapel Hill, North Carolina, 27514
Keely A Muscatell, PhD, 916-495-7661, kmuscatell@unc.edu
Jessica R Cohen, PhD
About this study
The purpose of this study is to map the neural and molecular mechanisms underlying psychological stress-induced changes in inflammation which could reveal new targets for intervention to reduce the risk of cardiovascular disease.
Read the detailed description
The proposed work will conduct a mechanistic clinical trial utilizing the non-selective beta-adrenergic receptor blocker propranolol to examine the role of beta-adrenergic signaling in shaping neural and inflammatory responses to stress. The investigators will focus on beta-adrenergic signaling given seminal pre-clinical work showing that this molecular pathway is an important driver of stress-related increases in inflammation, and initial human neuroimaging work showing that beta-blockade leads to changes in neural responses to negative stimuli. Here, the investigators will bring these two previously disparate lines of work together to determine how experimentally blocking one critical stress-signaling pathway shapes neural activity and inflammatory responses to stress. In doing so, the investigators will be advancing knowledge by mapping mechanisms (i.e., beta-adrenergic signaling), offering methodological improvements (i.e., moving beyond correlation to using pharmacological manipulations to provide causal evidence), and identifying intervention targets (i.e., the neurocognitive systems that shift activity/connectivity in response to beta-blockade). In sum, the work proposed herein is significant because it will address the mechanisms by which one critical risk factor, psychological stress, may ultimately lead to cardiovascular disease via inflammation. The proposed study also offers significant methodological improvements over past work by using neuroimaging to identify neurocognitive pathways, and pharmacology to provide causal experimental evidence to move us beyond correlation. Finally, this project is significant because it could provide insight into novel targets for future interventions.
- Conditions
- Cardiovascular Disease
- Being tested
- Propranolol, Placebo
- Keywords
- Beta-Blockade, Inflammation, Neuroimaging
- Medical subject headings
- Cardiovascular Diseases, Inflammation
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
PropranololDrug
Also called Inderal, Propranolol hydrochloride
Tablet encapsulated to visually look identical to the placebo.
PlaceboDrug
Also called Sugar pill
Encapsulated sugar pill to visually look identical to the experimental condition.
| Study group | Role | What they receive |
|---|---|---|
| Propranolol | Experimental | Propranolol tablet, 40mg, one-time, orally Receives: Drug: Propranolol |
| Placebo | Placebo comparator | Encapsulated placebo tablet Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change in levels of pro-inflammatory cytokine interleukin-6 in response to social stress
Blood plasma will be analyzed for levels of pro-inflammatory cytokine interleukin-6 (IL-6), from baseline, a baseline after drug administration, a sample 90-minutes after the stress task (T-90) measured in pg/mL. The timeline was determined on meta-analytic work showing changes in the inflammatory cytokine IL-6 are largest at 90 minutes post-stress.
Measured: Post-drug baseline to 90-minutes post-stress task (T-90)
Change in levels of inflammatory gene expression in response to social stress
Whole blood samples will be collected in PaxGene tubes and analyzed for changes in inflammatory gene expression from baseline, a baseline after drug administration, and 30-minutes after the stress task (T-30), measured in gene transcript counts per million. The timeline is based on the Principal Investigator's work showing that changes in pro-inflammatory gene expression are observed 30-minutes post-stress.
Measured: Post-drug baseline to 30-minutes post-stress task (T-30)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted16 Feb 2024
- Study start1 May 2024
- Primary completionFeb 2027 (estimated)
- Study completionFeb 2027 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (58)Papers the sponsor has linked to this study.
- Other trials for Cardiovascular DiseaseStudies of the same condition, open and under way.
- More trials run by University of North Carolina, Chapel HillThe 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
- Interventional
- Phase
- Phase 4
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Model description
- Subjects (n = 60 per condition, N = 120) will either take a one-time, 40mg dose of propranolol or an encapsulated placebo.
- Masking
- Triple blind
- Who is masked
- Participant, Care provider, Investigator
- Enrolment
- 120 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of North Carolina, Chapel Hill
- Sponsor type
- University, hospital or other
- Collaborators
- National Heart, Lung, and Blood Institute (NHLBI), University of California, Los Angeles, Dartmouth College
- Responsible party
- Sponsor
- Investigators
- Keely Muscatell, PhD, Principal investigator, University of North Carolina, Chapel Hill
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06263452
- Sponsor's protocol ID
- 23-2768
- Other IDs
- 1R01HL157422-01
- Status last verified
- Nov 2026
- First submitted
- 31 Jan 2024
- Last updated
- 5 Nov 2026
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- Yes
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Mehta NK, Abrams LR, Myrskyla M. US life expectancy stalls due to cardiovascular disease, not drug deaths. Proc Natl Acad Sci U S A. 2020 Mar 31;117(13):6998-7000. doi: 10.1073/pnas.1920391117. Epub 2020 Mar 16.
PubMed 32179670Virani SS, Alonso A, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, Chamberlain AM, Chang AR, Cheng S, Delling FN, Djousse L, Elkind MSV, Ferguson JF, Fornage M, Khan SS, Kissela BM, Knutson KL, Kwan TW, Lackland DT, Lewis TT, Lichtman JH, Longenecker CT, Loop MS, Lutsey PL, Martin SS, Matsushita K, Moran AE, Mussolino ME, Perak AM, Rosamond WD, Roth GA, Sampson UKA, Satou GM, Schroeder EB, Shah SH, Shay CM, Spartano NL, Stokes A, Tirschwell DL, VanWagner LB, Tsao CW; American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart Disease and Stroke Statistics-2020 Update: A Report From the American Heart Association. Circulation. 2020 Mar 3;141(9):e139-e596. doi: 10.1161/CIR.0000000000000757. Epub 2020 Jan 29.
PubMed 31992061Lagraauw HM, Kuiper J, Bot I. Acute and chronic psychological stress as risk factors for cardiovascular disease: Insights gained from epidemiological, clinical and experimental studies. Brain Behav Immun. 2015 Nov;50:18-30. doi: 10.1016/j.bbi.2015.08.007. Epub 2015 Aug 6.
PubMed 26256574Gianaros PJ, Jennings JR. Host in the machine: A neurobiological perspective on psychological stress and cardiovascular disease. Am Psychol. 2018 Nov;73(8):1031-1044. doi: 10.1037/amp0000232.
PubMed 30394781Chida Y, Steptoe A. Greater cardiovascular responses to laboratory mental stress are associated with poor subsequent cardiovascular risk status: a meta-analysis of prospective evidence. Hypertension. 2010 Apr;55(4):1026-32. doi: 10.1161/HYPERTENSIONAHA.109.146621. Epub 2010 Mar 1.
PubMed 20194301Ginty AT, Kraynak TE, Fisher JP, Gianaros PJ. Cardiovascular and autonomic reactivity to psychological stress: Neurophysiological substrates and links to cardiovascular disease. Auton Neurosci. 2017 Nov;207:2-9. doi: 10.1016/j.autneu.2017.03.003. Epub 2017 Mar 16.
PubMed 28391987Hong S, Dimitrov S, Cheng T, Redwine L, Pruitt C, Mills PJ, Ziegler MG, Green JM, Shaikh F, Wilson K. Beta-adrenergic receptor mediated inflammation control by monocytes is associated with blood pressure and risk factors for cardiovascular disease. Brain Behav Immun. 2015 Nov;50:31-38. doi: 10.1016/j.bbi.2015.08.012. Epub 2015 Aug 20.
PubMed 26300225Devereux RB, Alderman MH. Role of preclinical cardiovascular disease in the evolution from risk factor exposure to development of morbid events. Circulation. 1993 Oct;88(4 Pt 1):1444-55. doi: 10.1161/01.cir.88.4.1444.
PubMed 8403291Black PH, Garbutt LD. Stress, inflammation and cardiovascular disease. J Psychosom Res. 2002 Jan;52(1):1-23. doi: 10.1016/s0022-3999(01)00302-6.
PubMed 11801260Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000 Mar 23;342(12):836-43. doi: 10.1056/NEJM200003233421202.
PubMed 10733371Pepys MB, Hirschfield GM, Tennent GA, Gallimore JR, Kahan MC, Bellotti V, Hawkins PN, Myers RM, Smith MD, Polara A, Cobb AJ, Ley SV, Aquilina JA, Robinson CV, Sharif I, Gray GA, Sabin CA, Jenvey MC, Kolstoe SE, Thompson D, Wood SP. Targeting C-reactive protein for the treatment of cardiovascular disease. Nature. 2006 Apr 27;440(7088):1217-21. doi: 10.1038/nature04672.
PubMed 16642000Irwin MR, Cole SW. Reciprocal regulation of the neural and innate immune systems. Nat Rev Immunol. 2011 Aug 5;11(9):625-32. doi: 10.1038/nri3042.
PubMed 21818124Flaa A, Eide IK, Kjeldsen SE, Rostrup M. Sympathoadrenal stress reactivity is a predictor of future blood pressure: an 18-year follow-up study. Hypertension. 2008 Aug;52(2):336-41. doi: 10.1161/HYPERTENSIONAHA.108.111625. Epub 2008 Jun 23.
PubMed 18574074Bosch JA, Berntson GG, Cacioppo JT, Dhabhar FS, Marucha PT. Acute stress evokes selective mobilization of T cells that differ in chemokine receptor expression: a potential pathway linking immunologic reactivity to cardiovascular disease. Brain Behav Immun. 2003 Aug;17(4):251-9. doi: 10.1016/s0889-1591(03)00054-0.
PubMed 12831827McEwen BS, Gianaros PJ. Central role of the brain in stress and adaptation: links to socioeconomic status, health, and disease. Ann N Y Acad Sci. 2010 Feb;1186:190-222. doi: 10.1111/j.1749-6632.2009.05331.x.
PubMed 20201874
Study at a glance
From the registry record, last updated by the sponsor on 5 Nov 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Beta-Blocker Influences on Inflammatory and Neural Responses to Stress
- ClinicalTrials.gov ID
- NCT06263452
- Acronym / sponsor ID
- 23-2768
- Conditions
- Cardiovascular Disease
- Keywords
- Beta-Blockade, Inflammation, Neuroimaging
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- Recruiting
- Enrolment
- 120 participants (estimated)
- Lead sponsor
- University of North Carolina, Chapel HillUniversity, hospital or other
- Collaborators
- National Heart, Lung, and Blood Institute (NHLBI), University of California, Los Angeles, Dartmouth College
- Study start
- 1 May 2024 (actual)
- Primary completion
- Feb 2027 (estimated)
- Study completion
- Feb 2027 (estimated)
- First posted
- 16 Feb 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.
The purpose of this study is to map the neural and molecular mechanisms underlying psychological stress-induced changes in inflammation which could reveal new targets for intervention to reduce the risk of cardiovascular disease.
Detailed description
The proposed work will conduct a mechanistic clinical trial utilizing the non-selective beta-adrenergic receptor blocker propranolol to examine the role of beta-adrenergic signaling in shaping neural and inflammatory responses to stress. The investigators will focus on beta-adrenergic signaling given seminal pre-clinical work showing that this molecular pathway is an important driver of stress-related increases in inflammation, and initial human neuroimaging work showing that beta-blockade leads to changes in neural responses to negative stimuli. Here, the investigators will bring these two previously disparate lines of work together to determine how experimentally blocking one critical stress-signaling pathway shapes neural activity and inflammatory responses to stress. In doing so, the investigators will be advancing knowledge by mapping mechanisms (i.e., beta-adrenergic signaling), offering methodological improvements (i.e., moving beyond correlation to using pharmacological manipulations to provide causal evidence), and identifying intervention targets (i.e., the neurocognitive systems that shift activity/connectivity in response to beta-blockade). In sum, the work proposed herein is significant because it will address the mechanisms by which one critical risk factor, psychological stress, may ultimately lead to cardiovascular disease via inflammation. The proposed study also offers significant methodological improvements over past work by using neuroimaging to identify neurocognitive pathways, and pharmacology to provide causal experimental evidence to move us beyond correlation. Finally, this project is significant because it could provide insight into novel targets for future interventions.
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind (participant, care provider, investigator)
- Number of arms
- 2
- Model description
- Subjects (n = 60 per condition, N = 120) will either take a one-time, 40mg dose of propranolol or an encapsulated placebo.
| Arm | Type | Receives |
|---|---|---|
| Propranolol | Experimental | Drug: PropranololPropranolol tablet, 40mg, one-time, orally |
| Placebo | Placebo comparator | Drug: PlaceboEncapsulated placebo tablet |
Who may qualify
- Ages
- 18 to 30 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (4 listed)
- Ages 18-30 years
- Right-handed
- Fluent in English reading, writing, and speaking at least at a 10th grade level
- Body mass index (BMI) less than or equal to 35 kg/m^2
Key exclusion criteria (21 listed)
- Non-removeable metal devices/implants/objects in the body
- Severe claustrophobia (assessed by self-report)
- Currently pregnant
- Left-handed
- Body mass index (BMI) greater than 35 kg/m^2
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 |
|---|---|---|
| PropranololAlso: Inderal, Propranolol hydrochlorideTablet encapsulated to visually look identical to the placebo. | Drug | Propranolol |
| PlaceboAlso: Sugar pillEncapsulated sugar pill to visually look identical to the experimental condition. | Drug | Placebo |
Primary outcome
Change in levels of pro-inflammatory cytokine interleukin-6 in response to social stress
Time frame: Post-drug baseline to 90-minutes post-stress task (T-90)
Blood plasma will be analyzed for levels of pro-inflammatory cytokine interleukin-6 (IL-6), from baseline, a baseline after drug administration, a sample 90-minutes after the stress task (T-90) measured in pg/mL. The timeline was determined on meta-analytic work showing changes in the inflammatory cytokine IL-6 are largest at 90 minutes post-stress.
Change in levels of inflammatory gene expression in response to social stress
Time frame: Post-drug baseline to 30-minutes post-stress task (T-30)
Whole blood samples will be collected in PaxGene tubes and analyzed for changes in inflammatory gene expression from baseline, a baseline after drug administration, and 30-minutes after the stress task (T-30), measured in gene transcript counts per million. The timeline is based on the Principal Investigator's work showing that changes in pro-inflammatory gene expression are observed 30-minutes post-stress.
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 5 Nov 2026.
- Background: PubMed 32179670Mehta NK, Abrams LR, Myrskyla M. US life expectancy stalls due to cardiovascular disease, not drug deaths. Proc Natl Acad Sci U S A. 2020 Mar 31;117(13):6998-7000. doi: 10.1073/pnas.1920391117. Epub 2020 Mar 16.
- Background: PubMed 31992061Virani SS, Alonso A, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, Chamberlain AM, Chang AR, Cheng S, Delling FN, Djousse L, Elkind MSV, Ferguson JF, Fornage M, Khan SS, Kissela BM, Knutson KL, Kwan TW, Lackland DT, Lewis TT, Lichtman JH, Longenecker CT, Loop MS, Lutsey PL, Martin SS, Matsushita K, Moran AE, Mussolino ME, Perak AM, Rosamond WD, Roth GA, Sampson UKA, Satou GM, Schroeder EB, Shah SH, Shay CM, Spartano NL, Stokes A, Tirschwell DL, VanWagner LB, Tsao CW; American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart Disease and Stroke Statistics-2020 Update: A Report From the American Heart Association. Circulation. 2020 Mar 3;141(9):e139-e596. doi: 10.1161/CIR.0000000000000757. Epub 2020 Jan 29.
- Background: PubMed 26256574Lagraauw HM, Kuiper J, Bot I. Acute and chronic psychological stress as risk factors for cardiovascular disease: Insights gained from epidemiological, clinical and experimental studies. Brain Behav Immun. 2015 Nov;50:18-30. doi: 10.1016/j.bbi.2015.08.007. Epub 2015 Aug 6.
- Background: PubMed 30394781Gianaros PJ, Jennings JR. Host in the machine: A neurobiological perspective on psychological stress and cardiovascular disease. Am Psychol. 2018 Nov;73(8):1031-1044. doi: 10.1037/amp0000232.
- Background: PubMed 20194301Chida Y, Steptoe A. Greater cardiovascular responses to laboratory mental stress are associated with poor subsequent cardiovascular risk status: a meta-analysis of prospective evidence. Hypertension. 2010 Apr;55(4):1026-32. doi: 10.1161/HYPERTENSIONAHA.109.146621. Epub 2010 Mar 1.
- Background: PubMed 28391987Ginty AT, Kraynak TE, Fisher JP, Gianaros PJ. Cardiovascular and autonomic reactivity to psychological stress: Neurophysiological substrates and links to cardiovascular disease. Auton Neurosci. 2017 Nov;207:2-9. doi: 10.1016/j.autneu.2017.03.003. Epub 2017 Mar 16.
- Background: PubMed 26300225Hong S, Dimitrov S, Cheng T, Redwine L, Pruitt C, Mills PJ, Ziegler MG, Green JM, Shaikh F, Wilson K. Beta-adrenergic receptor mediated inflammation control by monocytes is associated with blood pressure and risk factors for cardiovascular disease. Brain Behav Immun. 2015 Nov;50:31-38. doi: 10.1016/j.bbi.2015.08.012. Epub 2015 Aug 20.
- Background: PubMed 8403291Devereux RB, Alderman MH. Role of preclinical cardiovascular disease in the evolution from risk factor exposure to development of morbid events. Circulation. 1993 Oct;88(4 Pt 1):1444-55. doi: 10.1161/01.cir.88.4.1444.
- Background: PubMed 11801260Black PH, Garbutt LD. Stress, inflammation and cardiovascular disease. J Psychosom Res. 2002 Jan;52(1):1-23. doi: 10.1016/s0022-3999(01)00302-6.
- Background: PubMed 10733371Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000 Mar 23;342(12):836-43. doi: 10.1056/NEJM200003233421202.
- Background: PubMed 16642000Pepys MB, Hirschfield GM, Tennent GA, Gallimore JR, Kahan MC, Bellotti V, Hawkins PN, Myers RM, Smith MD, Polara A, Cobb AJ, Ley SV, Aquilina JA, Robinson CV, Sharif I, Gray GA, Sabin CA, Jenvey MC, Kolstoe SE, Thompson D, Wood SP. Targeting C-reactive protein for the treatment of cardiovascular disease. Nature. 2006 Apr 27;440(7088):1217-21. doi: 10.1038/nature04672.
- Background: PubMed 21818124Irwin MR, Cole SW. Reciprocal regulation of the neural and innate immune systems. Nat Rev Immunol. 2011 Aug 5;11(9):625-32. doi: 10.1038/nri3042.
- Individual participant dataSharing planned: No
Related trials for Cardiovascular Disease
Active, not recruitingPhase 3
ENDOTHELION Study Group: Effect of Bosentan in NAION Patients
Ischemic Optic Neuropathy
Active, not recruiting
Digital Reinforcement of Motivational Interviewing Micro-Skills Among Primary Care Healthcare Professionals
Hypertension (Without Type 2 Diabetes Mellitus)
Not yet recruitingPhase 2
Study of YKST02 in Adults With Relapsed or Refractory Multiple Myeloma
Relapsed or Refractory Multiple Myeloma (RRMM)
RecruitingPhase 2
Engaging T-cells to Eliminate MRD in Newly Diagnosed Myeloma Optimizing Response With Talquetmab and Teclistamab (ROTATE)
Multiple Myeloma
Recruiting
PAW-Hydrogel for Chronic Wound Healing
Diabetic Foot Ulcer (DFU), Pressure Ulcer (PU)
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.
Keely Muscatell, PhD principal investigator
University of North Carolina, Chapel Hill
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 4 study testing Propranolol in people with Cardiovascular Disease, run by University of North Carolina, Chapel Hill 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 4 inclusion and 21 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 5 Nov 2026. 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. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 4 studies take place after a treatment is approved, to learn more about its long-term benefits and risks in everyday use.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
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 Jonathan Bunting, BS (9164957661, jonb@unc.edu), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Change in levels of pro-inflammatory cytokine interleukin-6 in response to social stress (time frame: Post-drug baseline to 90-minutes post-stress task (T-90)). The study lists 2 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 NCT06263452, which also lists 58 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 5 Nov 2026.