ST Elevation Myocardial InfarctionPICNICNCT06506448
Risk Characterization of Non-culprit Vessels in Patients Undergoing Primary PCI for ST-elevation MI in Multivessel Disease
An observational study of ST Elevation Myocardial Infarction, run by University Hospital Southampton NHS Foundation Trust at 3 sites in United Kingdom.
Trial summary
Most heart attacks occur because a clot forms in a coronary artery blocking blood flow. Without blood heart muscle dies. Untreated, clots can cause a specific type of heart attack -ST-elevation myocardial infarction (STEMI). Read more about this study
- Who is it for?
- Ages 18 to 85 years
- Conditions the study is for
- ST Elevation Myocardial Infarction
- What is being tested?
- CT Coronary Angiography
- How many people
- 320 participants
- Where
- 3 sitesUnited Kingdom
- Study dates
- 20 Jan 2025to Jan 2029
- 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 85 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Patients presenting with ST elevation myocardial infarction who are found to have significant stenoses in the non-infarct related artery(s) defined as coronary stenosis >50% by visual estimation
Who may be able to join
- Ability to provide written informed consent (post PPCI)
- Age 18 years to 85 years
- Presentation of acute STEMI within 12 hours of symptom on-set
- Culprit artery PPCI
- Coronary stenosis of > 50% diameter stenosis by visual estimation in NIRA with a minimum diameter of 2.5mm
Who cannot join
- Cardiogenic shock
- Decompensated heart failure requiring intubation, inotropes, or intra-aortic balloon counter pulsation
- Refractory ventricular arrhythmia
- Previous coronary artery bypass surgery (CABG)
- Stent thrombosis and in stent restenosis
- An intention before inclusion into the study to revascularize a non-culprit lesion
Show all 24Show fewer
- Active malignancy or inflammatory disorders such as rheumatoid arthritis or inflammatory bowel disease
- Severe valvular heart disease requiring surgery
- Planned surgical revascularisation
- Active participation in another study/trial
- < 12 months life expectancy
- Contraindication to CTCA
- Presence of internal defibrillator
- Known allergy to iodinated contrast
- Pregnancy
- Contraindication to intravenous beta blockade
- Contraindication to acute sublingual nitrate administration
- Mechanical prosthetic heart valve
- Advanced renal impairment (creatinine >200)
- Significant valve disease (sever aortic stenosis or regurgitation; severe mitral regurgitation)
- Angiographic exclusion criteria
- NIRA stenosis of 50% or more in the left main stem or the ostia of both the left anterior descending and circumflex arteries
- < TIMI (thrombolysis in myocardial infarction) flow grade 3 in the NIRA,
- Evidence of thrombus in the NIRA.
Trial locations and contacts
3 sites in 1 country. Contact the study team or a site near you to ask about taking part.
United Kingdom3 sites, 3 recruiting
- Recruiting
University Hospitals Dorset NHS Foundation Trust
Bournemouth, Dorset, BH15 2JB
Jonathan Hinton, MD, 01202303626, jonathan.hinton@uhd.nhs.uk
- Recruiting
University Hospital Southampton NHS Foundation Trust
Southampton, Hampshire, SO16 6YD
Nick Curzen, BM (Hons) PhD FRCP, nick.curzen@uhs.nhs.uk
Nick Curzen, BM(Hons) PhD FRCP
- Recruiting
Royal Stoke University Hospital
Stoke-on-Trent, Staffordshire, ST4 6QG
Mamas Mamas, 01782 715444, mamasmamas1@yahoo.co.uk
About this study
Official title: Anatomical, Physiological and Inflammatory Characterization of the Non-Culprit Vessels in Patients Undergoing Primary PCI for ST-Elevation Myocardial Infarction in the Presence of Multivessel Disease Toward a Personalised Approach to Complete Revascularisation After Primary PCI
Most heart attacks occur because a clot forms in a coronary artery blocking blood flow. Without blood heart muscle dies. Untreated, clots can cause a specific type of heart attack -ST-elevation myocardial infarction (STEMI). STEMI patients are treated immediately by finding the blocked artery ("culprit" lesion) using a dye injected into the coronary arteries and then by unblocking the artery using balloons and stents. This procedure - primary angioplasty - is offered 24/7 and limits the size of heart attacks and saves lives.
Cardiologists know how to treat STEMI patients but it's less clear what to do about narrowings in other coronary arteries ("bystander" disease). This is important - if they're left alone some bystander lesions can cause future events including heart attacks or angina. Recent trials compared stenting ALL the bystander narrowings after primary angioplasty, with stenting none and showed some benefit from stenting all of them ("complete revascularisation").
Read more
However, complete revascularisation carries extra risk, putting patients through more complicated procedures and using up resource. A blanket strategy of complete revascularisation of ALL bystander narrowings in ALL STEMI patients is unlikely to be the correct answer as only a small minority of these patients have further events.
In PICNIC the investigators want to identify bystander narrowings most likely to cause a future event, and those unlikely to do so. The study can then test the hypothesis that only the high-risk bystander narrowings need stenting, and the others can be treated with tablets only. Investigators will study patients using specialised imaging techniques from coronary artery CT scans and levels of inflammation to see which narrowings cause future events and which do not. If this can be done, a case can be made to test complete revascularisation only in bystander narrowings that look high risk.
Read the detailed description
Approximately 50% of patients presenting with an acute ST-segment elevation myocardial infarction (STEMI) have multivessel coronary artery disease (CAD). Five randomized studies have shown that complete revascularization, either at the time of primary percutaneous coronary intervention (PPCI) or within 45 days of the index admission, is safe and reduces the risk of repeat coronary revascularization and myocardial infarction (MI), particularly in the non-infarct related artery (NIRA). Despite these improvements in clinical outcomes, no study to date has provided a mechanistic insight as to how complete revascularization of chronic bystander disease may lead to the observed benefit. Indeed, the randomized studies, through the variable nature of their results (reduction in MI versus revascularization etc), have suggested the possibility that there are differing mechanisms for the observed benefit. The data would also be consistent with the concept that not all patients undergoing primary PCI with bystander disease require or benefit from complete revascularisation. This is an important possibility with important potential implications for resource utilisation and patient experience.
The investigators hypothesize that the susceptibility of non-culprit disease to ischaemic events after primary PCI is variable between individuals, and possibly even between their coronary vessels and lesions. Specifically, the investigators postulate that this susceptibility may be related to multiple factors including their anatomical and physiological vulnerability, and their local vascular inflammatory status. In order to test this hypothesis, the investigators will systematically examine the following parameters in each bystander coronary vessel in patients who present with STEMI and are undergoing primary PCI of the culprit vessel:
- markers of systemic inflammatory status
- plaque anatomy including lesion severity and markers of lesion vulnerability on CTCA
- assessment of individual coronary vessel inflammation using CT-derived fat attenuation index
- vessel physiology using FFRCT (fractional flow reserve from computed tomography) incorporating wall shear stress and axial plaque stress.
Aims
The aims of this study are to address the following research questions:
- What are the anatomical, physiological \& inflammatory features of lesions in the NIRA(s) of patients presenting with STEMI who are treated with a strategy of culprit-only PPCI?
- Is there an association between these anatomical, physiological \& inflammatory features and the risk of non-culprit lesions causing adverse events in STEMI patients with significant bystander disease in the NIRA(s)?
- Conditions
- ST Elevation Myocardial Infarction
- Being tested
- CT Coronary Angiography
- Keywords
- Primary percutaneous coronary intervention, Infarct related artery, Non-infarct related artery, Computerised Tomography Coronary Angiography CTCA, Fractional Flow Reserve from CT (FFRct), Fat Attenuation Index (FAI), Inflammation
- Medical subject headings
- ST Elevation Myocardial Infarction, Inflammation
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
CT Coronary AngiographyDiagnostic test
Also called FFRCT and plaque analysis (HeartFlow) and Fat Attenuation Index (Caristo)
CTCA for anatomical, physiological, plaque composition and inflammatory assessment of coronary arteries
| Study group | Role | What they receive |
|---|---|---|
| STEMI patients with multivessel disease | 320 patients undergoing primary angioplasty for ST-elevation myocardial infarction (STEMI) who have bystander disease in a main coronary artery with at least one stenosis of 50% or more Receives: Diagnostic Test: CT Coronary Angiography |
What is being measured
The primary outcome is the main question the study is designed to answer.
Correlation between major adverse cardiac & cerebrovascular events (MACCE) and CTCA-derived anatomical, physiological, plaque & inflammatory characteristics and serum inflammatory markers at 2 years
Correlation between:
- major adverse cardiac \& cerebrovascular events (MACCE) defined as the composite of all-cause mortality, cardiovascular death, cardiac arrest, acute coronary syndrome (unstable angina, NSTEMI, or STEMI), additional revascularization by CABG or PCI, rehospitalisation for angina, heart failure, stroke, ventricular or atrial fibrillation or tachyarrhythmia at 2 years \&:
- Anatomical \& physiological characteristics of coronary vessels/lesions in the NIRA(s) as assessed by CTCA parameters (FFRCT + FAI + plaque characteristics)
Measured: 2 years
Secondary outcomes (4)
Correlation between major adverse cardiac & cerebrovascular events (MACCE) and components of CTCA-derived anatomical, physiological, plaque & inflammatory characteristics and serum inflammatory markers at 1 year
Correlation between:
- major adverse cardiac \& cerebrovascular events (MACCE) defined as the composite of all-cause mortality, cardiovascular death, cardiac arrest, acute coronary syndrome (unstable angina, NSTEMI, or STEMI), additional revascularization by CABG or PCI, rehospitalisation for angina, heart failure, stroke, ventricular or atrial fibrillation or tachyarrhythmia at 1 year \&:
- Anatomical \& physiological characteristics of coronary vessels/lesions in the NIRA(s) as assessed by CTCA/FFRCT/FAI parameters between individual components of MACCE
Measured: 1 year
Correlation between anatomical, physiological & serum inflammatory markers and future adverse events at 3 years
Correlation between:
- major adverse cardiac \& cerebrovascular events (MACCE) defined as the composite of all-cause mortality, cardiovascular death, cardiac arrest, acute coronary syndrome (unstable angina, NSTEMI, or STEMI), additional revascularization by CABG or PCI, rehospitalisation for angina, heart failure, stroke, ventricular or atrial fibrillation or tachyarrhythmia at 3 years \&:
- Anatomical \& physiological characteristics of coronary vessels/lesions in the NIRA(s) as assessed by CTCA/FFRCT/FAI parameters between individual components of MACCE
Measured: 3 years
Development of a risk score to predict clinical events based upon individual-, vessel- & lesion-specific factors
To build a multidimensional AI-mediated deep learning model that uses the following data inputs (a) blood biomarkers, (b) CTCA lesion severity, (c) CTCA conventional plaque characteristics (e.g. spotty calcification etc); (d) FFRCT-derived plaque characteristic (ie adverse plaque and haemodynamic characteristics); (d) FAI-derived output; (e) clinical characteristics in order to correlate them with clinical events. The model will then be used to develop a risk score
Measured: 1 year
Development of a risk score to predict clinical events based upon individual-, vessel- & lesion-specific factors
To build a multidimensional AI-mediated deep learning model that uses the following data inputs (a) blood biomarkers, (b) CTCA lesion severity, (c) CTCA conventional plaque characteristics (e.g. spotty calcification etc); (d) FFRCT-derived plaque characteristic (ie adverse plaque and haemodynamic characteristics); (d) FAI-derived output; (e) clinical characteristics in order to correlate them with clinical events. The model will then be used to develop a risk score
Measured: 3 years
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted17 Jul 2024
- Study start20 Jan 2025
- Primary completionMar 2026 (estimated)
- Study completionJan 2029 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (1)Papers the sponsor has linked to this study.
- Other trials for ST Elevation Myocardial InfarctionStudies 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
- Cohort
- Time perspective
- Prospective
- Enrolment
- 320 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University Hospital Southampton NHS Foundation Trust
- Sponsor type
- University, hospital or other
- Collaborators
- Boston Scientific Corporation, HeartFlow, Inc., Wessex Heartbeat, Caristo
- Responsible party
- Sponsor
- Investigators
- Nick Curzen, PhD, Principal investigator, University Hospital Southampton NHS Foundation Trust
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06506448
- Sponsor's protocol ID
- RHMCAR0647
- Acronym
- PICNIC
- Status last verified
- Sep 2025
- First submitted
- 22 May 2024
- Last updated
- 23 Sep 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No: Not applicable. There will be no individual participant data available to other researchers.
Publications
Heller T, Ong P, Sechtem U, Bekeredjian R. Management of multivessel disease in patients with ST-segment elevation myocardial infarction: questioning routine immediate complete revascularization in all patients. Coron Artery Dis. 2026 Dec 1;37(8):625-633. doi: 10.1097/MCA.0000000000001661. Epub 2026 Jul 10.
PubMed 42423587
Study at a glance
From the registry record, last updated by the sponsor on 23 Sep 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Anatomical, Physiological and Inflammatory Characterization of the Non-Culprit Vessels in Patients Undergoing Primary PCI for ST-Elevation Myocardial Infarction in the Presence of Multivessel Disease Toward a Personalised Approach to Complete Revascularisation After Primary PCI
- ClinicalTrials.gov ID
- NCT06506448
- Acronym / sponsor ID
- PICNIC / RHMCAR0647
- Conditions
- ST Elevation Myocardial Infarction
- Keywords
- Primary percutaneous coronary intervention, Infarct related artery, Non-infarct related artery, Computerised Tomography Coronary Angiography CTCA, Fractional Flow Reserve from CT (FFRct), Fat Attenuation Index (FAI), Inflammation
- Study type
- Observational
- Recruitment status
- Recruiting
- Enrolment
- 320 participants (estimated)
- Lead sponsor
- University Hospital Southampton NHS Foundation TrustUniversity, hospital or other
- Collaborators
- Boston Scientific Corporation, HeartFlow, Inc., Wessex Heartbeat, Caristo
- Study start
- 20 Jan 2025 (actual)
- Primary completion
- Mar 2026 (estimated)
- Study completion
- Jan 2029 (estimated)
- First posted
- 17 Jul 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.
Most heart attacks occur because a clot forms in a coronary artery blocking blood flow. Without blood heart muscle dies. Untreated, clots can cause a specific type of heart attack -ST-elevation myocardial infarction (STEMI). STEMI patients are treated immediately by finding the blocked artery ("culprit" lesion) using a dye injected into the coronary arteries and then by unblocking the artery using balloons and stents. This procedure - primary angioplasty - is offered 24/7 and limits the size of heart attacks and saves lives.
Cardiologists know how to treat STEMI patients but it's less clear what to do about narrowings in other coronary arteries ("bystander" disease). This is important - if they're left alone some bystander lesions can cause future events including heart attacks or angina. Recent trials compared stenting ALL the bystander narrowings after primary angioplasty, with stenting none and showed some benefit from stenting all of them ("complete revascularisation").
However, complete revascularisation carries extra risk, putting patients through more complicated procedures and using up resource. A blanket strategy of complete revascularisation of ALL bystander narrowings in ALL STEMI patients is unlikely to be the correct answer as only a small minority of these patients have further events.
In PICNIC the investigators want to identify bystander narrowings most likely to cause a future event, and those unlikely to do so. The study can then test the hypothesis that only the high-risk bystander narrowings need stenting, and the others can be treated with tablets only. Investigators will study patients using specialised imaging techniques from coronary artery CT scans and levels of inflammation to see which narrowings cause future events and which do not. If this can be done, a case can be made to test complete revascularisation only in bystander narrowings that look high risk.
Detailed description
Approximately 50% of patients presenting with an acute ST-segment elevation myocardial infarction (STEMI) have multivessel coronary artery disease (CAD). Five randomized studies have shown that complete revascularization, either at the time of primary percutaneous coronary intervention (PPCI) or within 45 days of the index admission, is safe and reduces the risk of repeat coronary revascularization and myocardial infarction (MI), particularly in the non-infarct related artery (NIRA). Despite these improvements in clinical outcomes, no study to date has provided a mechanistic insight as to how complete revascularization of chronic bystander disease may lead to the observed benefit. Indeed, the randomized studies, through the variable nature of their results (reduction in MI versus revascularization etc), have suggested the possibility that there are differing mechanisms for the observed benefit. The data would also be consistent with the concept that not all patients undergoing primary PCI with bystander disease require or benefit from complete revascularisation. This is an important possibility with important potential implications for resource utilisation and patient experience.
The investigators hypothesize that the susceptibility of non-culprit disease to ischaemic events after primary PCI is variable between individuals, and possibly even between their coronary vessels and lesions. Specifically, the investigators postulate that this susceptibility may be related to multiple factors including their anatomical and physiological vulnerability, and their local vascular inflammatory status. In order to test this hypothesis, the investigators will systematically examine the following parameters in each bystander coronary vessel in patients who present with STEMI and are undergoing primary PCI of the culprit vessel:
- markers of systemic inflammatory status
- plaque anatomy including lesion severity and markers of lesion vulnerability on CTCA
- assessment of individual coronary vessel inflammation using CT-derived fat attenuation index
- vessel physiology using FFRCT (fractional flow reserve from computed tomography) incorporating wall shear stress and axial plaque stress.
Aims
The aims of this study are to address the following research questions:
- What are the anatomical, physiological \& inflammatory features of lesions in the NIRA(s) of patients presenting with STEMI who are treated with a strategy of culprit-only PPCI?
- Is there an association between these anatomical, physiological \& inflammatory features and the risk of non-culprit lesions causing adverse events in STEMI patients with significant bystander disease in the NIRA(s)?
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| STEMI patients with multivessel disease | – | Diagnostic Test: CT Coronary Angiography320 patients undergoing primary angioplasty for ST-elevation myocardial infarction (STEMI) who have bystander disease in a main coronary artery with at least one stenosis of 50% or more |
Who may qualify
- Ages
- 18 to 85 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients presenting with ST elevation myocardial infarction who are found to have significant stenoses in the non-infarct related artery(s) defined as coronary stenosis >50% by visual estimation
Key inclusion criteria (5 listed)
- Ability to provide written informed consent (post PPCI)
- Age 18 years to 85 years
- Presentation of acute STEMI within 12 hours of symptom on-set
- Culprit artery PPCI
- Coronary stenosis of > 50% diameter stenosis by visual estimation in NIRA with a minimum diameter of 2.5mm
Key exclusion criteria (24 listed)
- Cardiogenic shock
- Decompensated heart failure requiring intubation, inotropes, or intra-aortic balloon counter pulsation
- Refractory ventricular arrhythmia
- Previous coronary artery bypass surgery (CABG)
- Stent thrombosis and in stent restenosis
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 |
|---|---|---|
| CT Coronary AngiographyAlso: FFRCT and plaque analysis (HeartFlow) and Fat Attenuation Index (Caristo)CTCA for anatomical, physiological, plaque composition and inflammatory assessment of coronary arteries | Diagnostic test | STEMI patients with multivessel disease |
Primary outcome
Correlation between major adverse cardiac & cerebrovascular events (MACCE) and CTCA-derived anatomical, physiological, plaque & inflammatory characteristics and serum inflammatory markers at 2 years
Time frame: 2 years
Correlation between: 1. major adverse cardiac \& cerebrovascular events (MACCE) defined as the composite of all-cause mortality, cardiovascular death, cardiac arrest, acute coronary syndrome (unstable angina, NSTEMI, or STEMI), additional revascularization by CABG or PCI, rehospitalisation for angina, heart failure, stroke, ventricular or atrial fibrillation or tachyarrhythmia at 2 years \&: 2. Anatomical \& physiological characteristics of coronary vessels/lesions in the NIRA(s) as assessed by CTCA parameters (FFRCT + FAI + plaque characteristics)
4 secondary outcomes
Correlation between major adverse cardiac & cerebrovascular events (MACCE) and components of CTCA-derived anatomical, physiological, plaque & inflammatory characteristics and serum inflammatory markers at 1 year
Time frame: 1 year
Correlation between anatomical, physiological & serum inflammatory markers and future adverse events at 3 years
Time frame: 3 years
Development of a risk score to predict clinical events based upon individual-, vessel- & lesion-specific factors
Time frame: 1 year
Development of a risk score to predict clinical events based upon individual-, vessel- & lesion-specific factors
Time frame: 3 years
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 23 Sep 2025.
- Derived from this study: PubMed 42423587Heller T, Ong P, Sechtem U, Bekeredjian R. Management of multivessel disease in patients with ST-segment elevation myocardial infarction: questioning routine immediate complete revascularization in all patients. Coron Artery Dis. 2026 Dec 1;37(8):625-633. doi: 10.1097/MCA.0000000000001661. Epub 2026 Jul 10.
- Individual participant dataSharing planned: No. Not applicable. There will be no individual participant data available to other researchers.
Related trials for ST Elevation Myocardial Infarction
RecruitingPhase 4
Early Single Antiplatelet Therapy After IVUS-Guided PCI in Acute Coronary Syndrome
Acute Coronary Syndromes, STEMI
RecruitingPhase 2
Prevention of Reperfusion Injury Outcomes Through Effective Cardioprotection Targeting Myocardial Infarction
Myocardial Infarction, Reperfusion Injury
Not yet recruitingObservational study
Incremental Prognostic Utility of CBC-derived Inflammatory Indices After Incomplete Coronary Revascularization: Association With 12-months Cardiovascular Outcomes
STEMI, High Risk NSTEMI
RecruitingObservational study
SuperSaturated Oxygen Comprehensive Observational Registry
STEMI - ST Elevation Myocardial Infarction, AMI
RecruitingPhase 4
Efficacy and Safety of a Half-dose Bolus of r-SAK Prior to Primary PCI in ST-elevation Myocardial Infarction
ST Elevation Myocardial Infarction
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.
Nick Curzen, PhD principal investigator
University Hospital Southampton NHS Foundation Trust
3 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of ST Elevation Myocardial Infarction, run by University Hospital Southampton NHS Foundation Trust at 3 sites in United Kingdom.
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 24 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 23 Sep 2025. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 3 sites in United Kingdom. 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 Zoe Nicholas (02381208538, zoe.nicholas@uhs.nhs.uk), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Correlation between major adverse cardiac & cerebrovascular events (MACCE) and CTCA-derived anatomical, physiological, plaque & inflammatory characteristics and serum inflammatory markers at 2 years (time frame: 2 years). 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 NCT06506448, which also lists 1 linked publication.
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 23 Sep 2025.