Coronary Artery Disease (CAD)NCT06956924
Abdominal Aortic Calcium and CAD-RADS 2.0
A study testing CCTA in people with Coronary Artery Disease (CAD), run by Chang Gung Memorial Hospital at 1 site in Taiwan.
Trial summary
Background: Abdominal aortic calcium (AAC) is a marker of systemic atherosclerosis and may predict cardiovascular outcomes similarly to coronary artery calcium (CAC). This study evaluates the predictive efficacy of CT-based AAC scores for coronary plaque burden and stenosis using the CAD-RADS 2.0 classification… Read more about this study
- Who is it for?
- Ages 60 years and older
- Conditions the study is for
- Coronary Artery Disease (CAD)
- What is being tested?
- CCTA
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 68 participants
- Where
- 1 siteTaiwan
- Study dates
- 1 Jun 2021to 31 May 2023
- Phase
- Interventional
- 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 60 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- patients with chest pain or discomfort who were scheduled to undergo cardiac CT for CAC and CCTA
- determined by the treating physician for the evaluation of CAD
Who cannot join
- severe allergies to contrast agents
- metallic implants in the lumbar spine
- renal function abnormalities (estimated glomerular filtration rate [eGFR] < 60)
- abdominal aortic aneurysms
- prior coronary artery stent placements or bypass surgery
Trial locations and contacts
1 site in 1 country.
Taiwan1 site
Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
Kaohsiung City, Niao Sung, 833
About this study
Official title: CT-Based Abdominal Aortic Calcium Score and CAD-RADS 2.0 in Elderly Chest Pain: A Cohort Study
Background: Abdominal aortic calcium (AAC) is a marker of systemic atherosclerosis and may predict cardiovascular outcomes similarly to coronary artery calcium (CAC). This study evaluates the predictive efficacy of CT-based AAC scores for coronary plaque burden and stenosis using the CAD-RADS 2.0 classification system.
Methods: A prospective cohort of 68 patients (mean age 67.5 years) with chest pain underwent cardiac CT for CAC, AAC scoring, and coronary computed tomography angiography (CCTA) at Kaohsiung Chang Gung Memorial Hospital (June 2021-May 2023). AAC scores were quantified using the Agatston method across 8 cm and 5 cm aortic segments, and outcomes were analyzed based on CAD-RADS 2.0 and plaque burden classifications.
Read the detailed description
Introduction Coronary artery calcium (CAC) scoring, developed and validated using computed tomography (CT), is a well-established technique for quantifying coronary atherosclerosis and assessing cardiovascular risk, thereby guiding preventive therapeutic strategies. Similarly, abdominal aortic calcium (AAC) is a biomarker indicating the degree of calcification within the abdominal aorta, reflecting systemic atherosclerosis. AAC has been shown to predict cardiovascular morbidity and mortality.
AAC can be assessed using two common methods: Kidney, Ureter, and Bladder (KUB) plain film radiography and CT. Studies have demonstrated a correlation between AAC and CAC scores, with AAC suggesting the presence of asymptomatic coronary artery disease (CAD). This highlights the potential importance of quantifying AAC in predicting CAD.
Coronary Computed Tomography Angiography (CCTA) enables direct visualization of coronary artery lumen stenosis, atherosclerotic plaque composition, and high-risk plaque features, such as low attenuation, spot calcification, positive remodeling, and the napkin ring sign. CCTA is particularly valuable in patients with stable chest pain, given its high sensitivity and specificity in detecting CAD. Furthermore, it plays a critical role in guiding decisions regarding coronary revascularization procedures. Beyond assessing coronary artery stenosis and atherosclerotic plaque characteristics, analyzing plaque volume and burden provides prognostic value in stratifying the risk of acute coronary syndrome (ACS) in patients with stable chest pain undergoing CCTA.
The Coronary Artery Disease Reporting and Data System (CAD-RADS) is a comprehensive framework designed to standardize the assessment of disease severity and guide treatment decisions in patients with CAD. Initially published in 2016, CAD-RADS employs a categorical system based on coronary artery stenosis and high-risk plaque characteristics as modifiers. The 2022 update, CAD-RADS 2.0, incorporates plaque burden as a new subclassification and assesses lesion-specific ischemia using CT fractional flow reserve (CT-FFR) or myocardial CT perfusion (CTP). CAD-RADS aims to standardize CCTA reporting and improve communication with referring physicians, including recommendations.
Previous studies have indicated a correlation between AAC and CAC, with AAC quantification linked to traditional cardiovascular risk factors and cardiovascular events. Additionally, CT-based AAC quantification can predict future cardiovascular events in asymptomatic adults. However, few studies have explored whether AAC correlates with non-calcified coronary artery plaques or the degree of coronary artery stenosis. This study aims to investigate the correlation between CT-based AAC scores and coronary plaque burden and stenosis, using the CAD-RADS 2.0 classification system.
Materials and Methods Study Population This prospective cohort study enrolled patients aged 60 years and older who presented to the cardiovascular department at Kaohsiung Chang Gung Memorial Hospital between June 2021 and May 2023. Inclusion criteria were patients with chest pain or discomfort who were scheduled to undergo cardiac CT for CAC and CCTA, as determined by the treating physician for the evaluation of CAD. Exclusion criteria included: (1) severe allergies to contrast agents, (2) metallic implants in the lumbar spine, (3) renal function abnormalities (estimated glomerular filtration rate [eGFR] < 60), (4) abdominal aortic aneurysms, and (5) prior coronary artery stent placements or bypass surgery. The study received approval from the Research Ethics Committee of Kaohsiung Chang Gung Memorial Hospital, Taiwan. Written informed consent was obtained from all participants. Initially, 80 patients were enrolled; however, two withdrew for personal reasons, one was excluded due to the discovery of an incidental abdominal aortic aneurysm, and nine were excluded due to prior coronary artery stent placement. Consequently, 68 patients were included in the final analysis.
Patient demographics were reviewed, including age, gender, and the presence of hypertension, diabetes mellitus, lipid profiles (total cholesterol, HDL, and LDL levels from the closest pre-CCTA tests), smoking status, and body mass index (BMI). Hypertension was defined as a history of antihypertensive medication use or resting blood pressure readings of ≥ 140 mmHg systolic or ≥ 90 mmHg diastolic. Diabetes mellitus was defined as a fasting plasma glucose level ≥ 126 mg/dL or prior use of oral hypoglycemic agents or insulin. Smoking status was based on any history of smoking at least one cigarette daily before CCTA.
The data collected were used to assess 10-year atherosclerotic cardiovascular disease (ASCVD) risk, categorized into three groups: low to borderline risk (< 7.4%), intermediate risk (7.5% to 19.9%), and high risk (≥ 20%) according to the guidelines of the American College of Cardiology.
Image Acquisition CCTA and Non-Enhanced Abdominal CT Scan Protocol CCTA was performed using a 640-slice multislice CT scanner (Canon Aquilion One Genesis, Canon Medical Systems, Japan). All participants received sublingual nitroglycerin (0.3 mg) to promote coronary vasodilation prior to imaging. The first phase involved an unenhanced, prospective electrocardiogram (ECG)-gated volume scan for CAC assessment, configured to 120 kVp and 50 mAs with a field of view (FOV) of 16 cm to ensure comprehensive cardiac coverage. Imaging was performed with a rotation time of 0.275 seconds and a slice thickness of 2 mm. Following this, an abdominal aorta scan was performed using a non-ECG-gated sequential scan mode, maintaining identical settings of 120 kVp and 2 mm slice thickness. The inferior aspect of the L5 vertebral body endplate was used as the caudal extent of the abdominal volume to be imaged, covering the iliac bifurcation of the infrarenal abdominal aorta while minimizing radiation exposure to the pelvic genital organs.
For the enhanced CCTA scans, intravenous contrast medium was delivered using a tailored volume of Omnipaque 350 (Iohexol, GE Healthcare, Chicago, IL, USA), calculated at a 1:1 ratio relative to the patient's body weight, capped at a maximum dose of 65 milliliters (mL). Contrast infusion was performed at a rate of 4-5 mL/s, followed by a saline flush of 50 mL at the same rate. Image acquisition was synchronized with the cardiac cycle using automated peak enhancement detection in the ascending aorta, triggering the scan upon reaching a threshold of 100 Hounsfield units (HU), with imaging beginning after a 5-second delay.
The data acquisition protocol was tailored to each patient's heart rate and rhythm. Specifically, a prospectively ECG-triggered volume scan was used to account for heart rates and rhythms, capturing predefined scanning areas during R-R intervals, especially in instances of frequent ectopic beats or irregular heart rates noted during pre-scan ECG monitoring. Imaging system parameters included a gantry rotation time of 0.275 seconds, collimation of 0.5 mm, tube voltage settings ranging from 100 kV to 120 kV, and a tube current-time product between 200 mAs and 450 mAs, with adjustments based on the patient's BMI.
Image Analysis CAC and AAC were quantitatively assessed using the Vitrea workstation (version 7.4.0.462, Vital Images, Plymouth, MN) following the Agatston method. Calcification was identified as a plaque ≥ 1 mm² with a density exceeding a threshold of 130 HU, which was automatically quantified for both AAC and CAC areas. The AAC and CAC scores were calculated by multiplying the area of each region by a weighted score corresponding to the highest density of calcification: 1 for 130-199 HU, 2 for 200-299 HU, 3 for 300-399 HU, and 4 for densities ≥ 400 HU. Three abdominal aortic coverage areas were analyzed, with the aortoiliac bifurcation serving as the caudal boundary (Figure 1). The first coverage (AAC-all) included the entire abdominal aorta from the superior rim of the celiac trunk origin to the aortoiliac bifurcation. The second coverage (AAC-8cm) extended 8 cm cranially from the aortoiliac bifurcation, comprising 40 slices of 2 mm each, while the third coverage (AAC-5cm) extended 5 cm cranially from the aortoiliac bifurcation, comprising 25 slices of 2 mm each.
The CAD-RADS 2.0 classification system was used to assess the severity of coronary stenosis across five distinct categories: CAD-RADS 0 (no visible stenosis, 0% maximal coronary stenosis), CAD-RADS 1 (minimal stenosis, 1-24%), CAD-RADS 2 (mild stenosis, 25-49%), CAD-RADS 3 (moderate stenosis, 50-69%), CAD-RADS 4 (severe stenosis, subdivided into 4A [70-99%] and 4B [left main >50% or three-vessel obstructive disease]), and CAD-RADS 5 (100% occlusion). The plaque burden classification within CAD-RADS 2.0 includes a "P" designation, ranging from P1 to P4, to quantify overall plaque volume. Two assessment methodologies, CAC scoring and the segment involvement score (SIS), were employed: P1 indicated mild plaque burden (CAC of 1-100 or SIS ≤ 2), P2 indicated moderate plaque burden (CAC of 101-300 or SIS 3-4), P3 indicated severe plaque burden (CAC of 301-999 or SIS 5-7), and P4 indicated extensive plaque burden (CAC ≥1000 or SIS ≥8). The most severe classification from these two assessments determined the P subclassification. The study cohort was categorized into two distinct groups based on AAC-all scores of 300, adapted from the CAC score of 300 to differentiate plaque burden into mild to moderate and severe to extensive categories.
The outcome measures in this study were categorized based on the 2022 Coronary Artery Disease-Reporting and Data System (CAD-RADS), which classifies coronary artery stenosis and plaque burden into distinct categories without the use of specific measurement units. Coronary artery stenosis was graded using a numeric scale from 0 to 5, with higher numbers indicating greater severity of stenosis. Plaque volume was categorized using a classification system ranging from P1 to P4, with P4 representing the highest plaque burden.
Statistical Analysis Statistical analysis was performed using SPSS version 22.0 (IBM SPSS, Chicago, IL, USA). Interobserver agreement for CAD-RADS 2.0 was evaluated using Cohen's kappa coefficient, categorized as poor (< 0.20), fair (0.20-0.39), moderate (0.40-0.59), substantial (0.60-0.79), and excellent (≥ 0.80). Prior to analysis, data distribution normality was assessed using the Kolmogorov-Smirnov test. Quantitative data were summarized as mean ± standard deviation or median (interquartile range, IQR) if not normally distributed. A significance level of p < 0.05 was set. Continuous variables were compared using independent t-tests or Mann-Whitney U tests, while chi-square or Fisher's exact tests were applied to categorical variables as appropriate. One-way ANOVA or Kruskal-Wallis one-way ANOVA was used to assess differences in AAC across CAD-RADS categories and plaque burden subclassifications. Spearman correlation analysis was used to examine the relationship between CAC scores and various AAC score coverage areas, with coefficients ranging from very weak to very strong. The effectiveness of different AAC scores was assessed using receiver operating characteristic (ROC) curves to identify optimal cut-offs for predicting CAD-RADS categories and coronary plaque burden, with CAD-RADS categories stratified into groups 0-2 and 3-5, and coronary plaque burden divided into groups P1-P2 (mild to moderate) and P3-P4 (severe to extensive).
- Conditions
- Coronary Artery Disease (CAD)
- Being tested
- CCTA
- Keywords
- Coronary Artery Disease (CAD), Abdominal Aortic Calcium (AAC), Coronary Artery Calcium (CAC), CAD-RADS 2.0 Classification, Coronary Plaque Burden
- Medical subject headings
- Coronary Artery Disease
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
CCTADiagnostic test
The data acquisition protocol was tailored to each patient's heart rate and rhythm. Specifically, a prospectively ECG-triggered volume scan was used to account for heart rates and rhythms, capturing predefined scanning areas during R-R intervals, especially in instances of frequent ectopic beats or irregular heart rates noted during pre-scan ECG monitoring. Imaging system parameters included a gantry rotation time of 0.275 seconds, collimation of 0.5 mm, tube voltage settings ranging from 100 kV to 120 kV, and a tube current-time product between 200 mAs and 450 mAs, with adjustments based on the patient's BMI.
| Study group | Role | What they receive |
|---|---|---|
| CCTA and Non-Enhanced Abdominal CT Scan Protocol | Experimental | CCTA was performed using a 640-slice multislice CT scanner (Canon Aquilion One Genesis, Canon Medical Systems, Japan). All participants received sublingual nitroglycerin (0.3 mg) to promote coronary vasodilation prior to imaging. The first phase involved an unenhanced, prospective electrocardiogram (ECG)-gated volume scan for CAC assessment, configured to 120 kVp and 50 mAs with a field of view (FOV) of 16 cm to ensure comprehensive cardiac coverage. Imaging was performed with a rotation time of 0.275 seconds and a slice thickness of 2 mm. Following this, an abdominal aorta scan was performed using a non-ECG-gated sequential scan mode, maintaining identical settings of 120 kVp and 2 mm slice thickness. The inferior aspect of the L5 vertebral body endplate was used as the caudal extent of the abdominal volume to be imaged, covering the iliac bifurcation of the infrarenal abdominal aorta while minimizing radiation exposure to the pelvic genital organs. Receives: Diagnostic Test: CCTA |
What is being measured
The primary outcome is the main question the study is designed to answer.
Image Analysis
The CAD-RADS 2.0 classification system was used to assess the severity of coronary stenosis across five distinct categories: CAD-RADS 0 (no visible stenosis, 0% maximal coronary stenosis), CAD-RADS 1 (minimal stenosis, 1-24%), CAD-RADS 2 (mild stenosis, 25-49%), CAD-RADS 3 (moderate stenosis, 50-69%), CAD-RADS 4 (severe stenosis, subdivided into 4A [70-99%] and 4B [left main >50% or three-vessel obstructive disease]), and CAD-RADS 5 (100% occlusion).
The outcome measures in this study were categorized based on the 2022 Coronary Artery Disease-Reporting and Data System (CAD-RADS), which classifies coronary artery stenosis and plaque burden into distinct categories without the use of specific measurement units. Coronary artery stenosis was graded using a numeric scale from 0 to 5, with higher numbers indicating greater severity of stenosis. Plaque volume was categorized using a classification system ranging from P1 to P4, with P4 representing the highest plaque burden.
Measured: From enrollment to the end of treatment at 1 week
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted4 May 2025
- Study start1 Jun 2021
- Primary completion31 May 2023
- Study completion31 May 2023
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (31)Papers the sponsor has linked to this study.
- Other trials for Coronary Artery Disease (CAD)Studies of the same condition, open and under way.
- More trials run by Chang Gung Memorial HospitalThe 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 N/A
- Primary purpose
- Diagnosis
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 68 participants (actual)
Sponsor and investigators
- Lead sponsor
- Chang Gung Memorial Hospital
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Chien-Chang Liao, M.D., Study director, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06956924
- Sponsor's protocol ID
- liao1009_01
- Other IDs
- CMRPG8L0731
- Status last verified
- Apr 2025
- First submitted
- 16 Apr 2025
- Last updated
- 4 May 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided: If I want to share, I must get the Kaohsiung Chang Gung Memorial Hospital's consent
Publications
Takayama Y, Yasuda Y, Suzuki S, Shibata Y, Tatami Y, Shibata K, Niwa M, Sawai A, Morimoto R, Kato S, Ishii H, Maruyama S, Murohara T. Relationship between abdominal aortic and coronary artery calcification as detected by computed tomography in chronic kidney disease patients. Heart Vessels. 2016 Jul;31(7):1030-7. doi: 10.1007/s00380-015-0712-y. Epub 2015 Jul 12.
PubMed 26164596Briet M, Burns KD. Chronic kidney disease and vascular remodelling: molecular mechanisms and clinical implications. Clin Sci (Lond). 2012 Oct;123(7):399-416. doi: 10.1042/CS20120074.
PubMed 22671427van Rosendael AR, van den Hoogen IJ, Gianni U, Ma X, Tantawy SW, Bax AM, Lu Y, Andreini D, Al-Mallah MH, Budoff MJ, Cademartiri F, Chinnaiyan K, Choi JH, Conte E, Marques H, de Araujo Goncalves P, Gottlieb I, Hadamitzky M, Leipsic JA, Maffei E, Pontone G, Shin S, Kim YJ, Lee BK, Chun EJ, Sung JM, Lee SE, Virmani R, Samady H, Sato Y, Stone PH, Berman DS, Narula J, Blankstein R, Min JK, Lin FY, Shaw LJ, Bax JJ, Chang HJ. Association of Statin Treatment With Progression of Coronary Atherosclerotic Plaque Composition. JAMA Cardiol. 2021 Nov 1;6(11):1257-1266. doi: 10.1001/jamacardio.2021.3055.
PubMed 34406326Schousboe JT, Claflin D, Barrett-Connor E. Association of coronary aortic calcium with abdominal aortic calcium detected on lateral dual energy x-ray absorptiometry spine images. Am J Cardiol. 2009 Aug 1;104(3):299-304. doi: 10.1016/j.amjcard.2009.03.041. Epub 2009 Jun 6.
PubMed 19616658Williams MC, Earls JP, Hecht H. Quantitative assessment of atherosclerotic plaque, recent progress and current limitations. J Cardiovasc Comput Tomogr. 2022 Mar-Apr;16(2):124-137. doi: 10.1016/j.jcct.2021.07.001. Epub 2021 Jul 16.
PubMed 34326003Min JK, Shaw LJ, Devereux RB, Okin PM, Weinsaft JW, Russo DJ, Lippolis NJ, Berman DS, Callister TQ. Prognostic value of multidetector coronary computed tomographic angiography for prediction of all-cause mortality. J Am Coll Cardiol. 2007 Sep 18;50(12):1161-70. doi: 10.1016/j.jacc.2007.03.067. Epub 2007 Sep 4.
PubMed 17868808Williams MC, Newby DE, Dey D, Dweck MR. Response by Williams et al to Letter Regarding Article, "Low-Attenuation Noncalcified Plaque on Coronary Computed Tomography Angiography Predicts Myocardial Infarction: Results From the Multicenter SCOT-HEART Trial (Scottish Computed Tomography of the HEART)". Circulation. 2020 Oct 20;142(16):e244-e245. doi: 10.1161/CIRCULATIONAHA.120.049840. Epub 2020 Oct 19. No abstract available.
PubMed 33074760Sama C, Abdelhaleem A, Velu D, Ditah Chobufo M, Fongwen NT, Budoff MJ, Roberts M, Balla S, Mills JD, Njim TN, Greathouse M, Zeb I, Hamirani YS. Non-calcified plaque in asymptomatic patients with zero coronary artery calcium score: A systematic review and meta-analysis. J Cardiovasc Comput Tomogr. 2024 Jan-Feb;18(1):43-49. doi: 10.1016/j.jcct.2023.10.002. Epub 2023 Oct 9.
PubMed 37821352Devia-Rodriguez R, Derksen M, de Groot K, Vedder IR, Zeebregts CJ, Bokkers RPH, Pol RA, de Vries JPM, Schuurmann RCL. Validation of a Length-Adjusted Abdominal Arterial Calcium Score Method for Contrast-Enhanced CT Scans. Diagnostics (Basel). 2023 Jun 1;13(11):1934. doi: 10.3390/diagnostics13111934.
PubMed 37296786Mori S, Takaya T, Kinugasa M, Ito T, Takamine S, Fujiwara S, Nishii T, Kono AK, Inoue T, Satomi-Kobayashi S, Rikitake Y, Okita Y, Hirata K. Three-dimensional quantification and visualization of aortic calcification by multidetector-row computed tomography: a simple approach using a volume-rendering method. Atherosclerosis. 2015 Apr;239(2):622-8. doi: 10.1016/j.atherosclerosis.2014.12.041. Epub 2014 Dec 24.
PubMed 25554696Oishi H, Horibe H, Yamase Y, Ueyama C, Takemoto Y, Shigeta T, Hibino T, Kondo T, Suzuki S, Ishii H, Murohara T. Predictive value of abdominal aortic calcification index for mid-term cardiovascular events in patients with acute coronary syndrome. Heart Vessels. 2020 May;35(5):620-629. doi: 10.1007/s00380-019-01527-6. Epub 2019 Nov 9.
PubMed 31707516Chuang ML, Leslie RW, Massaro JM, Manders ES, Fox CS, Hoffmann U, O'Donnell CJ. Distribution of abdominal aortic calcium by computed tomography: impact of analysis method on quantitative calcium score. Acad Radiol. 2013 Nov;20(11):1422-8. doi: 10.1016/j.acra.2013.08.008.
PubMed 24119355Agatston AS, Janowitz WR, Hildner FJ, Zusmer NR, Viamonte M Jr, Detrano R. Quantification of coronary artery calcium using ultrafast computed tomography. J Am Coll Cardiol. 1990 Mar 15;15(4):827-32. doi: 10.1016/0735-1097(90)90282-t.
PubMed 2407762Grundy SM, Stone NJ, Bailey AL, Beam C, Birtcher KK, Blumenthal RS, Braun LT, de Ferranti S, Faiella-Tommasino J, Forman DE, Goldberg R, Heidenreich PA, Hlatky MA, Jones DW, Lloyd-Jones D, Lopez-Pajares N, Ndumele CE, Orringer CE, Peralta CA, Saseen JJ, Smith SC Jr, Sperling L, Virani SS, Yeboah J. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Jun 18;139(25):e1082-e1143. doi: 10.1161/CIR.0000000000000625. Epub 2018 Nov 10.
PubMed 30586774Goff DC Jr, Lloyd-Jones DM, Bennett G, Coady S, D'Agostino RB, Gibbons R, Greenland P, Lackland DT, Levy D, O'Donnell CJ, Robinson JG, Schwartz JS, Shero ST, Smith SC Jr, Sorlie P, Stone NJ, Wilson PW, Jordan HS, Nevo L, Wnek J, Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Hochman JS, Kovacs RJ, Ohman EM, Pressler SJ, Sellke FW, Shen WK, Smith SC Jr, Tomaselli GF; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014 Jun 24;129(25 Suppl 2):S49-73. doi: 10.1161/01.cir.0000437741.48606.98. Epub 2013 Nov 12. No abstract available.
PubMed 24222018
Study at a glance
From the registry record, last updated by the sponsor on 4 May 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- CT-Based Abdominal Aortic Calcium Score and CAD-RADS 2.0 in Elderly Chest Pain: A Cohort Study
- ClinicalTrials.gov ID
- NCT06956924
- Acronym / sponsor ID
- liao1009_01
- Conditions
- Coronary Artery Disease (CAD)
- Keywords
- Coronary Artery Disease (CAD), Abdominal Aortic Calcium (AAC), Coronary Artery Calcium (CAC), CAD-RADS 2.0 Classification, Coronary Plaque Burden
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 68 participants (actual)
- Lead sponsor
- Chang Gung Memorial HospitalUniversity, hospital or other
- Study start
- 1 Jun 2021 (actual)
- Primary completion
- 31 May 2023 (actual)
- Study completion
- 31 May 2023 (actual)
- First posted
- 4 May 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.
Background: Abdominal aortic calcium (AAC) is a marker of systemic atherosclerosis and may predict cardiovascular outcomes similarly to coronary artery calcium (CAC). This study evaluates the predictive efficacy of CT-based AAC scores for coronary plaque burden and stenosis using the CAD-RADS 2.0 classification system.
Methods: A prospective cohort of 68 patients (mean age 67.5 years) with chest pain underwent cardiac CT for CAC, AAC scoring, and coronary computed tomography angiography (CCTA) at Kaohsiung Chang Gung Memorial Hospital (June 2021-May 2023). AAC scores were quantified using the Agatston method across 8 cm and 5 cm aortic segments, and outcomes were analyzed based on CAD-RADS 2.0 and plaque burden classifications.
Detailed description
Introduction Coronary artery calcium (CAC) scoring, developed and validated using computed tomography (CT), is a well-established technique for quantifying coronary atherosclerosis and assessing cardiovascular risk, thereby guiding preventive therapeutic strategies. Similarly, abdominal aortic calcium (AAC) is a biomarker indicating the degree of calcification within the abdominal aorta, reflecting systemic atherosclerosis. AAC has been shown to predict cardiovascular morbidity and mortality.
AAC can be assessed using two common methods: Kidney, Ureter, and Bladder (KUB) plain film radiography and CT. Studies have demonstrated a correlation between AAC and CAC scores, with AAC suggesting the presence of asymptomatic coronary artery disease (CAD). This highlights the potential importance of quantifying AAC in predicting CAD.
Coronary Computed Tomography Angiography (CCTA) enables direct visualization of coronary artery lumen stenosis, atherosclerotic plaque composition, and high-risk plaque features, such as low attenuation, spot calcification, positive remodeling, and the napkin ring sign. CCTA is particularly valuable in patients with stable chest pain, given its high sensitivity and specificity in detecting CAD. Furthermore, it plays a critical role in guiding decisions regarding coronary revascularization procedures. Beyond assessing coronary artery stenosis and atherosclerotic plaque characteristics, analyzing plaque volume and burden provides prognostic value in stratifying the risk of acute coronary syndrome (ACS) in patients with stable chest pain undergoing CCTA.
The Coronary Artery Disease Reporting and Data System (CAD-RADS) is a comprehensive framework designed to standardize the assessment of disease severity and guide treatment decisions in patients with CAD. Initially published in 2016, CAD-RADS employs a categorical system based on coronary artery stenosis and high-risk plaque characteristics as modifiers. The 2022 update, CAD-RADS 2.0, incorporates plaque burden as a new subclassification and assesses lesion-specific ischemia using CT fractional flow reserve (CT-FFR) or myocardial CT perfusion (CTP). CAD-RADS aims to standardize CCTA reporting and improve communication with referring physicians, including recommendations.
Previous studies have indicated a correlation between AAC and CAC, with AAC quantification linked to traditional cardiovascular risk factors and cardiovascular events. Additionally, CT-based AAC quantification can predict future cardiovascular events in asymptomatic adults. However, few studies have explored whether AAC correlates with non-calcified coronary artery plaques or the degree of coronary artery stenosis. This study aims to investigate the correlation between CT-based AAC scores and coronary plaque burden and stenosis, using the CAD-RADS 2.0 classification system.
Materials and Methods Study Population This prospective cohort study enrolled patients aged 60 years and older who presented to the cardiovascular department at Kaohsiung Chang Gung Memorial Hospital between June 2021 and May 2023. Inclusion criteria were patients with chest pain or discomfort who were scheduled to undergo cardiac CT for CAC and CCTA, as determined by the treating physician for the evaluation of CAD. Exclusion criteria included: (1) severe allergies to contrast agents, (2) metallic implants in the lumbar spine, (3) renal function abnormalities (estimated glomerular filtration rate [eGFR] < 60), (4) abdominal aortic aneurysms, and (5) prior coronary artery stent placements or bypass surgery. The study received approval from the Research Ethics Committee of Kaohsiung Chang Gung Memorial Hospital, Taiwan. Written informed consent was obtained from all participants. Initially, 80 patients were enrolled; however, two withdrew for personal reasons, one was excluded due to the discovery of an incidental abdominal aortic aneurysm, and nine were excluded due to prior coronary artery stent placement. Consequently, 68 patients were included in the final analysis.
Patient demographics were reviewed, including age, gender, and the presence of hypertension, diabetes mellitus, lipid profiles (total cholesterol, HDL, and LDL levels from the closest pre-CCTA tests), smoking status, and body mass index (BMI). Hypertension was defined as a history of antihypertensive medication use or resting blood pressure readings of ≥ 140 mmHg systolic or ≥ 90 mmHg diastolic. Diabetes mellitus was defined as a fasting plasma glucose level ≥ 126 mg/dL or prior use of oral hypoglycemic agents or insulin. Smoking status was based on any history of smoking at least one cigarette daily before CCTA.
The data collected were used to assess 10-year atherosclerotic cardiovascular disease (ASCVD) risk, categorized into three groups: low to borderline risk (< 7.4%), intermediate risk (7.5% to 19.9%), and high risk (≥ 20%) according to the guidelines of the American College of Cardiology.
Image Acquisition CCTA and Non-Enhanced Abdominal CT Scan Protocol CCTA was performed using a 640-slice multislice CT scanner (Canon Aquilion One Genesis, Canon Medical Systems, Japan). All participants received sublingual nitroglycerin (0.3 mg) to promote coronary vasodilation prior to imaging. The first phase involved an unenhanced, prospective electrocardiogram (ECG)-gated volume scan for CAC assessment, configured to 120 kVp and 50 mAs with a field of view (FOV) of 16 cm to ensure comprehensive cardiac coverage. Imaging was performed with a rotation time of 0.275 seconds and a slice thickness of 2 mm. Following this, an abdominal aorta scan was performed using a non-ECG-gated sequential scan mode, maintaining identical settings of 120 kVp and 2 mm slice thickness. The inferior aspect of the L5 vertebral body endplate was used as the caudal extent of the abdominal volume to be imaged, covering the iliac bifurcation of the infrarenal abdominal aorta while minimizing radiation exposure to the pelvic genital organs.
For the enhanced CCTA scans, intravenous contrast medium was delivered using a tailored volume of Omnipaque 350 (Iohexol, GE Healthcare, Chicago, IL, USA), calculated at a 1:1 ratio relative to the patient's body weight, capped at a maximum dose of 65 milliliters (mL). Contrast infusion was performed at a rate of 4-5 mL/s, followed by a saline flush of 50 mL at the same rate. Image acquisition was synchronized with the cardiac cycle using automated peak enhancement detection in the ascending aorta, triggering the scan upon reaching a threshold of 100 Hounsfield units (HU), with imaging beginning after a 5-second delay.
The data acquisition protocol was tailored to each patient's heart rate and rhythm. Specifically, a prospectively ECG-triggered volume scan was used to account for heart rates and rhythms, capturing predefined scanning areas during R-R intervals, especially in instances of frequent ectopic beats or irregular heart rates noted during pre-scan ECG monitoring. Imaging system parameters included a gantry rotation time of 0.275 seconds, collimation of 0.5 mm, tube voltage settings ranging from 100 kV to 120 kV, and a tube current-time product between 200 mAs and 450 mAs, with adjustments based on the patient's BMI.
Image Analysis CAC and AAC were quantitatively assessed using the Vitrea workstation (version 7.4.0.462, Vital Images, Plymouth, MN) following the Agatston method. Calcification was identified as a plaque ≥ 1 mm² with a density exceeding a threshold of 130 HU, which was automatically quantified for both AAC and CAC areas. The AAC and CAC scores were calculated by multiplying the area of each region by a weighted score corresponding to the highest density of calcification: 1 for 130-199 HU, 2 for 200-299 HU, 3 for 300-399 HU, and 4 for densities ≥ 400 HU. Three abdominal aortic coverage areas were analyzed, with the aortoiliac bifurcation serving as the caudal boundary (Figure 1). The first coverage (AAC-all) included the entire abdominal aorta from the superior rim of the celiac trunk origin to the aortoiliac bifurcation. The second coverage (AAC-8cm) extended 8 cm cranially from the aortoiliac bifurcation, comprising 40 slices of 2 mm each, while the third coverage (AAC-5cm) extended 5 cm cranially from the aortoiliac bifurcation, comprising 25 slices of 2 mm each.
The CAD-RADS 2.0 classification system was used to assess the severity of coronary stenosis across five distinct categories: CAD-RADS 0 (no visible stenosis, 0% maximal coronary stenosis), CAD-RADS 1 (minimal stenosis, 1-24%), CAD-RADS 2 (mild stenosis, 25-49%), CAD-RADS 3 (moderate stenosis, 50-69%), CAD-RADS 4 (severe stenosis, subdivided into 4A [70-99%] and 4B [left main >50% or three-vessel obstructive disease]), and CAD-RADS 5 (100% occlusion). The plaque burden classification within CAD-RADS 2.0 includes a "P" designation, ranging from P1 to P4, to quantify overall plaque volume. Two assessment methodologies, CAC scoring and the segment involvement score (SIS), were employed: P1 indicated mild plaque burden (CAC of 1-100 or SIS ≤ 2), P2 indicated moderate plaque burden (CAC of 101-300 or SIS 3-4), P3 indicated severe plaque burden (CAC of 301-999 or SIS 5-7), and P4 indicated extensive plaque burden (CAC ≥1000 or SIS ≥8). The most severe classification from these two assessments determined the P subclassification. The study cohort was categorized into two distinct groups based on AAC-all scores of 300, adapted from the CAC score of 300 to differentiate plaque burden into mild to moderate and severe to extensive categories.
The outcome measures in this study were categorized based on the 2022 Coronary Artery Disease-Reporting and Data System (CAD-RADS), which classifies coronary artery stenosis and plaque burden into distinct categories without the use of specific measurement units. Coronary artery stenosis was graded using a numeric scale from 0 to 5, with higher numbers indicating greater severity of stenosis. Plaque volume was categorized using a classification system ranging from P1 to P4, with P4 representing the highest plaque burden.
Statistical Analysis Statistical analysis was performed using SPSS version 22.0 (IBM SPSS, Chicago, IL, USA). Interobserver agreement for CAD-RADS 2.0 was evaluated using Cohen's kappa coefficient, categorized as poor (< 0.20), fair (0.20-0.39), moderate (0.40-0.59), substantial (0.60-0.79), and excellent (≥ 0.80). Prior to analysis, data distribution normality was assessed using the Kolmogorov-Smirnov test. Quantitative data were summarized as mean ± standard deviation or median (interquartile range, IQR) if not normally distributed. A significance level of p < 0.05 was set. Continuous variables were compared using independent t-tests or Mann-Whitney U tests, while chi-square or Fisher's exact tests were applied to categorical variables as appropriate. One-way ANOVA or Kruskal-Wallis one-way ANOVA was used to assess differences in AAC across CAD-RADS categories and plaque burden subclassifications. Spearman correlation analysis was used to examine the relationship between CAC scores and various AAC score coverage areas, with coefficients ranging from very weak to very strong. The effectiveness of different AAC scores was assessed using receiver operating characteristic (ROC) curves to identify optimal cut-offs for predicting CAD-RADS categories and coronary plaque burden, with CAD-RADS categories stratified into groups 0-2 and 3-5, and coronary plaque burden divided into groups P1-P2 (mild to moderate) and P3-P4 (severe to extensive).
Study design
- Primary purpose
- Diagnosis
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| CCTA and Non-Enhanced Abdominal CT Scan Protocol | Experimental | Diagnostic Test: CCTACCTA was performed using a 640-slice multislice CT scanner (Canon Aquilion One Genesis, Canon Medical Systems, Japan). All participants received sublingual nitroglycerin (0.3 mg) to promote coronary vasodilation prior to imaging. The first phase involved an unenhanced, prospective electrocardiogram (ECG)-gated volume scan for CAC assessment, configured to 120 kVp and 50 mAs with a field of view (FOV) of 16 cm to ensure comprehensive cardiac coverage. Imaging was performed with a rotation time of 0.275 seconds and a slice thickness of 2 mm. Following this, an abdominal aorta scan was performed using a non-ECG-gated sequential scan mode, maintaining identical settings of 120 kVp and 2 mm slice thickness. The inferior aspect of the L5 vertebral body endplate was used as the caudal extent of the abdominal volume to be imaged, covering the iliac bifurcation of the infrarenal abdominal aorta while minimizing radiation exposure to the pelvic genital organs. |
Who may qualify
- Ages
- 60 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (2 listed)
- patients with chest pain or discomfort who were scheduled to undergo cardiac CT for CAC and CCTA
- determined by the treating physician for the evaluation of CAD
Key exclusion criteria (5 listed)
- severe allergies to contrast agents
- metallic implants in the lumbar spine
- renal function abnormalities (estimated glomerular filtration rate [eGFR] < 60)
- abdominal aortic aneurysms
- prior coronary artery stent placements or bypass surgery
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 |
|---|---|---|
| CCTAThe data acquisition protocol was tailored to each patient's heart rate and rhythm. Specifically, a prospectively ECG-triggered volume scan was used to account for heart rates and rhythms, capturing predefined scanning areas during R-R intervals, especially in instances of frequent ectopic beats or irregular heart rates noted during pre-scan ECG monitoring. Imaging system parameters included a gantry rotation time of 0.275 seconds, collimation of 0.5 mm, tube voltage settings ranging from 100 kV to 120 kV, and a tube current-time product between 200 mAs and 450 mAs, with adjustments based on the patient's BMI. | Diagnostic test | CCTA and Non-Enhanced Abdominal CT Scan Protocol |
Primary outcome
Image Analysis
Time frame: From enrollment to the end of treatment at 1 week
The CAD-RADS 2.0 classification system was used to assess the severity of coronary stenosis across five distinct categories: CAD-RADS 0 (no visible stenosis, 0% maximal coronary stenosis), CAD-RADS 1 (minimal stenosis, 1-24%), CAD-RADS 2 (mild stenosis, 25-49%), CAD-RADS 3 (moderate stenosis, 50-69%), CAD-RADS 4 (severe stenosis, subdivided into 4A [70-99%] and 4B [left main >50% or three-vessel obstructive disease]), and CAD-RADS 5 (100% occlusion). The outcome measures in this study were categorized based on the 2022 Coronary Artery Disease-Reporting and Data System (CAD-RADS), which classifies coronary artery stenosis and plaque burden into distinct categories without the use of specific measurement units. Coronary artery stenosis was graded using a numeric scale from 0 to 5, with higher numbers indicating greater severity of stenosis. Plaque volume was categorized using a classification system ranging from P1 to P4, with P4 representing the highest plaque burden.
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 4 May 2025.
- Results publication: PubMed 26164596Takayama Y, Yasuda Y, Suzuki S, Shibata Y, Tatami Y, Shibata K, Niwa M, Sawai A, Morimoto R, Kato S, Ishii H, Maruyama S, Murohara T. Relationship between abdominal aortic and coronary artery calcification as detected by computed tomography in chronic kidney disease patients. Heart Vessels. 2016 Jul;31(7):1030-7. doi: 10.1007/s00380-015-0712-y. Epub 2015 Jul 12.
- Results publication: PubMed 22671427Briet M, Burns KD. Chronic kidney disease and vascular remodelling: molecular mechanisms and clinical implications. Clin Sci (Lond). 2012 Oct;123(7):399-416. doi: 10.1042/CS20120074.
- Results publication: PubMed 34406326van Rosendael AR, van den Hoogen IJ, Gianni U, Ma X, Tantawy SW, Bax AM, Lu Y, Andreini D, Al-Mallah MH, Budoff MJ, Cademartiri F, Chinnaiyan K, Choi JH, Conte E, Marques H, de Araujo Goncalves P, Gottlieb I, Hadamitzky M, Leipsic JA, Maffei E, Pontone G, Shin S, Kim YJ, Lee BK, Chun EJ, Sung JM, Lee SE, Virmani R, Samady H, Sato Y, Stone PH, Berman DS, Narula J, Blankstein R, Min JK, Lin FY, Shaw LJ, Bax JJ, Chang HJ. Association of Statin Treatment With Progression of Coronary Atherosclerotic Plaque Composition. JAMA Cardiol. 2021 Nov 1;6(11):1257-1266. doi: 10.1001/jamacardio.2021.3055.
- Results publication: PubMed 19616658Schousboe JT, Claflin D, Barrett-Connor E. Association of coronary aortic calcium with abdominal aortic calcium detected on lateral dual energy x-ray absorptiometry spine images. Am J Cardiol. 2009 Aug 1;104(3):299-304. doi: 10.1016/j.amjcard.2009.03.041. Epub 2009 Jun 6.
- Results publication: PubMed 34326003Williams MC, Earls JP, Hecht H. Quantitative assessment of atherosclerotic plaque, recent progress and current limitations. J Cardiovasc Comput Tomogr. 2022 Mar-Apr;16(2):124-137. doi: 10.1016/j.jcct.2021.07.001. Epub 2021 Jul 16.
- Results publication: PubMed 17868808Min JK, Shaw LJ, Devereux RB, Okin PM, Weinsaft JW, Russo DJ, Lippolis NJ, Berman DS, Callister TQ. Prognostic value of multidetector coronary computed tomographic angiography for prediction of all-cause mortality. J Am Coll Cardiol. 2007 Sep 18;50(12):1161-70. doi: 10.1016/j.jacc.2007.03.067. Epub 2007 Sep 4.
- Results publication: PubMed 33074760Williams MC, Newby DE, Dey D, Dweck MR. Response by Williams et al to Letter Regarding Article, "Low-Attenuation Noncalcified Plaque on Coronary Computed Tomography Angiography Predicts Myocardial Infarction: Results From the Multicenter SCOT-HEART Trial (Scottish Computed Tomography of the HEART)". Circulation. 2020 Oct 20;142(16):e244-e245. doi: 10.1161/CIRCULATIONAHA.120.049840. Epub 2020 Oct 19. No abstract available.
- Results publication: PubMed 37821352Sama C, Abdelhaleem A, Velu D, Ditah Chobufo M, Fongwen NT, Budoff MJ, Roberts M, Balla S, Mills JD, Njim TN, Greathouse M, Zeb I, Hamirani YS. Non-calcified plaque in asymptomatic patients with zero coronary artery calcium score: A systematic review and meta-analysis. J Cardiovasc Comput Tomogr. 2024 Jan-Feb;18(1):43-49. doi: 10.1016/j.jcct.2023.10.002. Epub 2023 Oct 9.
- Results publication: PubMed 37296786Devia-Rodriguez R, Derksen M, de Groot K, Vedder IR, Zeebregts CJ, Bokkers RPH, Pol RA, de Vries JPM, Schuurmann RCL. Validation of a Length-Adjusted Abdominal Arterial Calcium Score Method for Contrast-Enhanced CT Scans. Diagnostics (Basel). 2023 Jun 1;13(11):1934. doi: 10.3390/diagnostics13111934.
- Results publication: PubMed 25554696Mori S, Takaya T, Kinugasa M, Ito T, Takamine S, Fujiwara S, Nishii T, Kono AK, Inoue T, Satomi-Kobayashi S, Rikitake Y, Okita Y, Hirata K. Three-dimensional quantification and visualization of aortic calcification by multidetector-row computed tomography: a simple approach using a volume-rendering method. Atherosclerosis. 2015 Apr;239(2):622-8. doi: 10.1016/j.atherosclerosis.2014.12.041. Epub 2014 Dec 24.
- Results publication: PubMed 31707516Oishi H, Horibe H, Yamase Y, Ueyama C, Takemoto Y, Shigeta T, Hibino T, Kondo T, Suzuki S, Ishii H, Murohara T. Predictive value of abdominal aortic calcification index for mid-term cardiovascular events in patients with acute coronary syndrome. Heart Vessels. 2020 May;35(5):620-629. doi: 10.1007/s00380-019-01527-6. Epub 2019 Nov 9.
- Results publication: PubMed 24119355Chuang ML, Leslie RW, Massaro JM, Manders ES, Fox CS, Hoffmann U, O'Donnell CJ. Distribution of abdominal aortic calcium by computed tomography: impact of analysis method on quantitative calcium score. Acad Radiol. 2013 Nov;20(11):1422-8. doi: 10.1016/j.acra.2013.08.008.
- Individual participant dataSharing planned: Undecided. If I want to share, I must get the Kaohsiung Chang Gung Memorial Hospital's consent
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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.
Chien-Chang Liao, M.D. study director
Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing CCTA in people with Coronary Artery Disease (CAD), run by Chang Gung Memorial Hospital at 1 site in Taiwan.
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 2 inclusion and 5 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 4 May 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 Taiwan. 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?
Image Analysis (time frame: From enrollment to the end of treatment at 1 week). 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 NCT06956924, which also lists 31 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 4 May 2025.