A New Way of Looking Inside Your Heart Without Surgery — Can Advanced CCTA Improve Heart-Attack Risk Prediction?

Traditional Risk Models, Coronary CT AngiographyCoronary CT angiography, or CCTA, is a CT scan done with dye in your veins that produces detailed pictures of your heart's arteries., and AI-Driven Quantitative PlaquePlaque is the buildup of cholesterol, immune cells, scar tissue, and calcium inside an artery wall. Analysis: What the Evidence Does and Does Not Show

The SCAPIS Analysis and the Shift Toward Disease-Based Risk Assessment

The Bergström et al. analysis of the Swedish CArdioPulmonary bioImage Study (SCAPISSCAPIS (Swedish CArdioPulmonary bioImage Study) is a large population imaging study of more than 25,000 Swedish adults aged 50 to 64 with no known coronary artery disease, which used coronary CT angiography to detect atherosclerosis in 42 percent of participants and significant stenosis in about 5 percent.), published online in the Journal of the American Medical Association on November 9, 2025 and in print as JAMA. 2026;335(3):245–254, is the largest population-based test to date of a simple question: does looking directly at the coronary arteriesThe coronary arteries are the small vessels that wrap around the outside of your heart and feed the heart muscle itself. tell you something that risk factorsA risk factor is something that raises your chance of developing a disease — high cholesterol particles, high blood pressure, smoking, diabetes, family history. and a calcium scoreA calcium score (coronary artery calcium score) is a number derived from a CT scan that quantifies the total amount of calcified plaque in the coronary arteries; a score of zero indicates no detectable calcified plaque, while higher scores reflect greater plaque burden and elevated cardiovascular risk. do not?¹

The study followed 24,791 individuals aged 50 to 64 years, randomly recruited from the general population at six Swedish university hospitals and free of established cardiovascular diseaseCardiovascular disease is the umbrella term for problems with the heart and blood vessels, including heart attacks, strokes, and blocked leg arteries. at baseline, for a median of 7.8 years.¹ The outcome was a first nonfatal myocardial infarctionSee Heart Attack for the full entry. or death from coronary heart diseaseCoronary heart disease is the narrowing or blockage of the arteries that supply blood to the heart muscle, caused by the buildup of atherosclerotic plaque; it is the leading cause of heart attack and cardiac death worldwide.; 304 such events occurred. The question was whether adding coronary computed tomographyComputed tomography, or CT, takes X-ray images from many angles and reconstructs them into cross-sections of the body. angiography (CCTA) findings to a model containing the Pooled Cohort Equation (PCE) and the coronary artery calcium scoreA coronary artery calcium score, or CAC score, comes from a quick CT scan that measures how much hardened plaque is in your heart's arteries. No dye, no needles, about ten minutes. (CACS) improved prediction.¹

The extent of atherosclerosisAtherosclerosis is the disease behind most heart attacks and many strokes. Cholesterol particles get stuck in the wall of an artery, the body sends immune cells to clean up, and over years that mess hardens into plaque. mattered more than any single stenosisStenosis is narrowing — usually described as a percentage, like a 70 percent blockage.. The Segment Involvement Score (SIS)A coronary CT angiography measure that counts the number of coronary artery segments (out of 18 standardized segments) containing any plaque, regardless of whether the plaque is calcified or not; in the SCAPIS study, an SIS greater than 4 was associated with a hazard ratio of 5.27 for first coronary events., which counts how many of the 18 coronary segments contain any plaque, tracked strongly with events: an SIS of 3 to 4 carried a hazard ratioA hazard ratio compares how quickly events happen in two groups. A ratio of 0.75 means events occurred at three-quarters the rate in the treated group. (HR) of 2.71 (95% CI, 1.34–5.44) and an SIS greater than 4 an HR of 5.27 (95% CI, 2.50–11.07), relative to lower scores. The presence of noncalcified atherosclerosis carried an HR of 1.66 (95% CI, 1.23–2.22).¹

Predictive variable	Hazard ratio	95% CI	Model
SIS 1–2	1.00	Reference	Fully adjusted
SIS 3–4	2.71	1.34–5.44	Fully adjusted
SIS >4	5.27	2.50–11.07	Fully adjusted
Noncalcified atherosclerosis	1.66	1.23–2.22	Fully adjusted
Stenosis ≥50%	1.22	0.89–1.69	Fully adjusted

Table 1. Association of CCTA findings with first coronary events in SCAPIS.¹ All values are from the fully adjusted model. Note that once plaque extent is accounted for, obstructive stenosis (≥50%) is not independently associated with first events in this primary-prevention cohort — the confidence intervalA confidence interval is the range of values that are statistically compatible with what a study found. crosses 1.0. Unadjusted and partially adjusted models give larger stenosis estimates and should not be quoted as if they were adjusted results.

Adding the CCTA variables to a model containing PCE and CACS improved discrimination modestly: the C-statistic rose from 0.764 to 0.779 (P = .004).¹ ReclassificationIn cardiovascular risk assessment, reclassification refers to the process by which an additional test — such as a CAC scan or ApoB measurement — moves a patient from one risk category to another, prompting a change in treatment decisions that a standard risk calculator alone would not have triggered. improved as well, with a net reclassification improvement of 0.133 (95% CI, 0.031–0.165). Among participants who went on to have an event, 14.2% were correctly moved into a higher risk category; among those who did not have an event, 1.6% were incorrectly moved upward.¹ Because the overall event rate was low, most of this reclassification occurred among people the PCE had labeled low risk (<5%) — which is precisely the group in which a missed diagnosis is most consequential, and also the group in which unnecessary treatment is hardest to justify.

The investigators themselves characterize the gain as modest.¹ That word is worth keeping. SCAPIS shows that direct imaging of plaque adds real, statistically robust information beyond risk factors and calcium scoring in a middle-aged primary-prevention population. It does not show that imaging transforms individual risk predictionRisk prediction in cardiovascular medicine refers to the use of clinical variables — such as age, blood pressure, cholesterol, and smoking status — or direct measurements such as imaging to estimate an individual's probability of suffering a heart attack or stroke within a defined time horizon., and it was not designed to show that acting on the imaging improves outcomes.

Two Different Questions: Detecting Stenosis vs Predicting Events

Much of the confusion in the popular coverage of AI-assisted CCTA comes from treating two very different performance metrics as interchangeable. They are not, and conflating them inflates the apparent capability of the technology.

• Diagnostic accuracy asks: how well does the test agree with a reference standard — typically invasive quantitative coronary angiographyQuantitative coronary angiography is a way of measuring artery narrowing precisely from angiogram images, rather than eyeballing it. (QCA) — about whether a stenosis is present right now?
• Prognostic discrimination asks: how well does the test rank people by their likelihood of having a cardiovascular event in the future?

An area under the curve (AUC) of 0.91 for the first question is not evidence of an AUC of 0.91 for the second. Diagnostic AUCs against an anatomic reference standard are systematically higher than event-prediction AUCs, because future events depend on plaque biology, hemodynamics, thrombotic propensity, treatment, and chance — not only on anatomy. The two tables below are therefore presented separately and should not be merged into a single ranking.

Diagnostic accuracy: agreement with invasive angiography

In a post hoc analysis of the PACIFIC-1A clinical study in which AI-assisted quantitative CT coronary angiography (AI-QCT) was compared head-to-head with human expert readers; AI-QCT achieved an AUC of 0.91 for detecting obstructive stenosis, outperforming level-3 expert cardiologists who scored 0.77. cohort (208 patients with new-onset stable chest pain, all of whom underwent both CCTA and invasive QCA), AI-guided quantitative CT (AI-QCT) was compared directly with human readers of differing experience for the detection of ≥50% stenosis on a per-patient basis.³

Reader	AUC (95% CI)	Task
AI-QCT	0.91 (0.87–0.95)	≥50% stenosis vs QCA
Level-3 expert reader	0.77 (0.70–0.83)	≥50% stenosis vs QCA
Level-2 reader A	0.79	≥50% stenosis vs QCA
Level-2 reader B	0.76	≥50% stenosis vs QCA

Table 2. Per-patient diagnostic accuracy for obstructive stenosis, PACIFIC-1 post hoc analysis, invasive QCA as reference standard.³ These are diagnostic AUCs. They describe agreement with invasive angiography about present anatomy. They do not describe prediction of myocardial infarction.

The correct reading of this result is that automated quantitative analysis agreed with the invasive reference standard more closely than expert visual assessment did, and did so reproducibly. That is a meaningful finding about interpretive consistency — visual CCTA reading is known to be experience-dependent and to overestimate stenosis — but it is a statement about diagnosis, not about prognosis.

Prognostic discrimination: predicting future events

In the CONFIRM2 registryA large, multinational registry of over 6,000 patients in which AI-quantified coronary plaque features were evaluated for their ability to predict major adverse cardiovascular events; the registry showed that AI-derived plaque analysis improved the area under the ROC curve for event prediction from 0.62 to 0.75 compared with standard methods., AI-QCT was tested for incremental prognostic value over the qualitative and semiquantitative measures currently recommended in practice. Adding AI-QCT improved discrimination for major adverse cardiovascular eventsA major adverse cardiovascular event, or MACE, is a bundle of bad outcomes counted together in a study — typically cardiovascular death, heart attack, and stroke. over CAD-RADSCAD-RADS (Coronary Artery Disease Reporting and Data System) is a standardized grading scale used to report findings from coronary CT angiography, ranging from 0 (no plaque or stenosis) to 5 (at least one totally occluded artery); the index patient scored CAD-RADS 0, reflecting no detectable plaque above the imaging threshold. 2.0, CACS, and the modified Duke Index.⁴

Comparator (alone)	AUC alone	AUC + AI-QCT
CAD-RADS 2.0	0.79	0.81
Coronary arteryAn artery is a blood vessel that carries blood away from the heart to the rest of the body. calcium score	0.70	0.79
Modified Duke Index	0.76	0.81
PCE + CACS (SCAPIS, + CCTA)¹	0.764	0.779

Table 3. Prognostic discrimination for future events.¹˒⁴ The CONFIRM2 rows describe specific models within one registry of symptomatic patients referred for CCTA; the SCAPIS row describes an asymptomatic general-population cohort and non-AI CCTA variables. These are not interchangeable, and none of them is a universal performance characteristic of AI-QCT.

Taken together, the honest summary is this: quantitative, AI-assisted CCTA measurements can provide incremental prognostic information beyond conventional clinical risk assessment, calcium scoring, and qualitative CCTA reads — but the magnitude of that improvement varies substantially with the population studied, the endpoint chosen, and the model specification. In the contemporary prognostic studies discussed here, reported event-prediction AUCs for AI-QCT are approximately 0.75 to 0.81 rather than 0.90.¹˒⁴

What Quantitative Plaque Analysis Measures, and Why It Matters

Traditional risk equations such as the Framingham Risk ScoreThe Framingham Risk Score is a specific ten-year heart-attack-risk calculator built from the Framingham Heart Study's decades of data — the original tool that turned "risk factors" into a number. and the Pooled Cohort EquationsThe Pooled Cohort Equations are the risk calculator the American College of Cardiology and American Heart Association currently recommend, estimating your ten-year odds of a heart attack or stroke from age, cholesterol, blood pressure, diabetes, and smoking status. infer vascular risk from surrogate variables — age, sex, blood pressureBlood pressure is the force of blood pushing against your artery walls. It is written as two numbers, like 120/80. The top number is the pressure when your heart squeezes, the bottom is when it relaxes., lipids, smokingSmoking damages the lining of your blood vessels, raises blood pressure, makes blood clot more easily, and speeds up plaque growth., diabetesDiabetes is a condition where blood sugar stays too high, either because the body makes too little insulin or because it stops responding to the insulin it makes. — rather than from the artery itself.⁹˒¹⁰ They perform reasonably at the population level and imperfectly at the individual level, because the relationship between risk factors and plaque development is heterogeneous. Two people with identical risk-factor profiles can have very different coronary arteries.

Quantitative CCTA measures the disease directly. Rather than reporting only the tightest narrowing, it characterizes plaque throughout the coronary tree by volume, composition, and vessel remodeling. Several of these features carry prognostic information:

• Total plaque volume (TPV)A quantitative measure, obtained by AI-assisted CT angiography, of the combined three-dimensional volume of all atherosclerotic deposits across the coronary arteries; high TPV is the strongest independent imaging predictor of future myocardial infarction, conferring approximately a sevenfold increase in risk in SCOT-HEART.. Higher total atherosclerotic burden is independently associated with future events across multiple cohorts. Effect sizes are study-specific and depend on the population, the units in which volume is expressed, and the covariates adjusted for; a risk estimate from one cohort should not be quoted as a general property of plaque volumePlaque volume is the total physical amount of plaque in a stretch of artery, measured in cubic millimeters..⁴˒⁵
• Noncalcified plaqueAtherosclerotic deposits within artery walls that have not yet undergone calcification; sometimes called 'soft' plaque, these lesions are lipid-rich and structurally unstable, making them more prone to rupture and acute thrombosis than calcified plaque. (NCP) volume. In CONFIRM2, each 50-mm³ increase in noncalcified plaque was associated with a 1% relative increase in MACE risk in women and 11.6% in men.⁵
• Low-attenuation plaqueLow-attenuation plaque is the very darkest, fattiest plaque on a CT scan — soft enough that X-rays pass through it easily. (≤30 HU). A CT marker associated with lipid-rich, necrotic-core plaque characteristics — an imaging correlate rather than a direct measurement of necrotic coreThe necrotic core is the dead, mushy center of an advanced plaque, built from immune cells that ate trapped cholesterol and then died in place.. In SCOT-HEART, low-attenuation plaque burdenPlaque burden is the total amount of plaque in your arteries, everywhere — not just at the single worst spot. was the strongest predictor of fatal or nonfatal myocardial infarction (adjusted HR 60 per doubling; 95% CI, 1.10–2.34), and a burden above 4% was associated with an HR of 4.65 (95% CI, 2.06–10.5).²
• Positive (outward) remodeling. Outward expansion of the vessel wall may allow substantial plaque to accumulate before marked luminal narrowing becomes apparent, which is one reason lumen-focused assessment can underestimate disease burden.

The biology underlying these measurements is more nuanced than a simple “calcium is safe, soft plaqueNon-calcified, lipid-rich atherosclerotic plaque that does not appear bright on a standard calcium score scan but is detectable by CT angiography; it is considered higher risk for rupture than fully calcified plaque. is dangerous” dichotomy. Dense calcificationCalcification is when calcium gets deposited into a plaque, turning part of it hard and bony. is generally associated with more stable lesionIn cardiology, a lesion refers to a discrete area of atherosclerotic plaque narrowing a coronary artery, typically described by the percentage of luminal obstruction it causes. The article describes four residual lesions too small in vessel diameter to accept a stent after the most critical one was treated. behavior, and calcification does often follow inflammatory injury as part of a healing response — but calcified plaqueCalcified plaque is the hardened, calcium-filled part of a plaque. It shows up brightly on a CT scan, which is what a calcium scan measures. is not inert, and calcium burden remains a strong marker of overall atherosclerotic disease. Conversely, noncalcified plaque is not synonymous with vulnerable plaqueA vulnerable plaque is one at high risk of cracking open: a thin cap, a large greasy core, active inflammation, and often outward bulging of the artery.; it is a heterogeneous category, only part of which has the lipid-rich, thin-capped phenotype associated with rupture. The useful statement is narrower and better supported: plaque composition adds prognostic information that calcium score alone does not capture.

A related point is frequently overstated in consumer coverage. It is well documented that many acute coronary events arise from lesions that were not severely obstructive on prior imaging, which is a central reason plaque burden and composition can carry information beyond stenosis severity. It does not follow that “most heart attacksA heart attack happens when blood flow to part of the heart muscle is cut off and that muscle starts to die. are caused by non-obstructive soft plaque” — that phrasing compresses several distinct issues (pre-event stenosis severity, plaque phenotypePlaque phenotype refers to the biological and structural characteristics of an atherosclerotic lesion — including the size of its lipid-rich necrotic core, fibrous cap thickness, degree of calcification, and inflammatory cell content — which together determine whether a plaque is stable or at high risk of rupturing., rupture versus erosion, and the limitations of retrospective angiographic comparison) into a single claim that the evidence does not cleanly support.

Scanner Technology: What Wide-Detector CT Actually Delivers

Contemporary wide-detector CT systems can acquire the entire heart within a single cardiac cycle in appropriately selected patients. This reduces misregistration (“stitching”) artifacts that arise when a volume is assembled from multiple heartbeats, and it permits high-quality coronary imagingNon-invasive or invasive techniques—such as quantitative coronary angiography or intravascular ultrasound—used to visualise the size and character of plaques inside the coronary arteries; the Ornish and Esselstyn work is notable for using objective coronary imaging rather than relying solely on symptom or event data. at relatively low radiation doses when protocols are optimized.

Several caveats belong alongside that statement, because they are routinely omitted:

• Marketing terms such as “640-slice” describe a reconstruction characteristic of a wide-area detector system rather than an independent measure of image quality, and they do not by themselves establish superior outcome prediction. Detector coverage (for example, 16 cm) and acquisition architecture are the more meaningful descriptors.
• Radiation dose cannot be stated as a single number. It varies with scanner generation, prospective versus retrospective gating, tube voltage and current, heart rateHeart rate is how many times your heart beats per minute. and rhythm, body habitus, scan length, and reconstruction algorithm.¹¹ Sub-millisievert coronary CTA is achievable in favorable patients with optimized protocols; it is not a general expectation.
• Spatial resolutionSpatial resolution in medical imaging refers to the smallest structure a scanner can distinguish as a separate object; coronary CT angiography has a practical resolution limit of about 0.4–0.5 mm, meaning early atherosclerotic lesions thinner than a human hair—typically 100–300 micrometers—are invisible to the scan even when biologically present. figures are scanner- and protocol-specific and should be verified against the manufacturer’s technical specification for the exact system and acquisition mode in question before being cited.
• Single-beat acquisition reduces — but does not eliminate — the need for heart-rate control, and does not eliminate motion artifact.

The practical significance of wide-detector systems for this discussion is that reproducible, lower-dose acquisition makes serial imaging more feasible, which in turn makes longitudinal plaque tracking a technically feasible clinical and research proposition. Routine serial CCTA performed specifically to monitor plaque remains an evolving strategy rather than established standard care for most patients.

Is Plaque Modifiable? EVAPORATE and the Limits of What It Shows

EVAPORATE, a randomized, double-blind, placebo-controlled trial of 80 patients with elevated triglyceridesTriglycerides are the main form of fat in your blood and in your body's storage. on statinA statin slows the enzyme your liver uses to make cholesterol. Your liver responds by pulling more cholesterol out of your blood, which is where the real benefit comes from. therapy, used serial CCTA to assess the effect of icosapent ethylIcosapent ethyl is a purified, high-dose form of the omega-3 fat EPA, sold as Vascepa. on plaque progression over 18 months. It found reduction in low-attenuation plaque volume in the treatment arm alongside progression in the placeboA placebo is a dummy treatment — a sugar pill or a saline injection — given so researchers can tell what a real drug actually does. arm.⁷

EVAPORATE is a mechanistic imaging trial. It was not an AI-QCT study and it was not powered for clinical events. It supports the proposition that plaque composition is modifiable and measurable over time; it does not validate the prognostic performance of any particular AI analysis platform, and it should not be cited as though it did.

TRANSFORM: A Trial Designed to Test the Outcome Question

TRANSFORM (NCT06112418) is a prospective, randomized, open-label, blinded-endpoint trial enrolling patients at elevated cardiovascular risk without known symptomatic disease. Participants are randomized to guideline-directed risk-factor-based care or to a care strategy driven by an AI-based coronary plaque staging system, with repeat imaging at 24 months in the imaging arm.⁸

TRANSFORM is ongoing. Its results are not yet available, and it therefore cannot be cited as evidence supporting any conclusion about the effectiveness of an imaging-guided prevention strategy. Its importance lies in what it is designed to establish: whether identifying and staging plaque earlier, and treating accordingly, actually reduces cardiovascular events compared with current practice. That is the question the existing observational and diagnostic literature cannot answer.

Impact on Clinical Decision-Making

There is reasonable evidence that quantitative plaque analysis changes what clinicians do. In the CERTAIN studyA clinical study evaluating the impact of AI-QCT coronary plaque analysis on physician treatment decisions; it found that AI-derived results changed management in 57.1% of patients, increasing statin use by 28.1%, aspirin prescribing by 23%, and reducing unnecessary downstream testing by 37%., a multicenter crossover study of 750 consecutive patients referred for CCTA at five expert sites, physicians recorded their diagnosis and management plan based on conventional site interpretation and then repeated the assessment after AI-QCT analysis.⁶

• Diagnosis or management changed in 1% of patients (P < .001).⁶
• Statin initiation or intensification increased in an additional 1% of patients, and aspirinAspirin makes blood platelets less sticky, so clots are less likely to form. initiation in an additional 23.0% (P < .001 for both).⁶
• The anticipated need for downstream noninvasive and invasive testing fell by 1% (P < .001).⁶

These are changes in physician intent measured within a study design in which the same physicians assessed the same patients twice, in a fixed order, at high-volume expert centers. That design cannot exclude ordering effects, and intent to prescribe is not the same as improved outcomes. The finding is genuinely encouraging about clinical utility and genuinely insufficient as evidence of clinical benefit.

Coverage for AI-based coronary plaque analysis has expanded among United States payers since 2024, but policies remain plan-, indication-, and region-specific. Patients and clinicians should verify coverage directly with the payer rather than relying on general statements of availability.

Sex-Specific Implications

One of the most clinically relevant findings in this literature concerns sex differences in how plaque burden translates into risk. In the CONFIRM2 registry (3,551 symptomatic patients, 49.5% women, mean follow-up 4.8 ± 2.2 years), women had roughly half the plaque burden of men and about half the MACE rate (3.2% vs 6.1%). But the relative riskRelative risk compares two groups: this group had 30 percent fewer heart attacks than that group. conferred by each increment of plaque was consistently higher in women.⁵

Plaque measure (per 50 mm³ increase)	Increase in MACE risk, women	Increase in MACE risk, men
Total plaque volume	+17.7%	+5.3%
Noncalcified plaque	+27.1%	+11.6%
Calcified plaque	+22.9%	+5.4%

Table 4. Sex-specific relative risk per 50-mm³ increment, CONFIRM2 registry (P for interaction < .001).⁵ Note that total plaque volume, noncalcified plaque, and calcified plaque have distinct values and must not be quoted interchangeably.

The clinical implication is that a plaque volume that looks reassuringly “low” by absolute standards derived largely from men may carry meaningful prognostic weight in a woman. Quantitative measurement, which reports actual volumes rather than a qualitative impression, is well suited to detecting exactly this pattern — provided the interpretation is sex-aware.

Synthesis and Conclusion

The central argument holds. Coronary CT angiography identifies atherosclerotic disease that risk-factor equations and calcium scoring do not fully characterize, and quantitative, AI-assisted analysis of those images adds diagnostic reproducibility and incremental prognostic information. SCAPIS provides strong contemporary evidence that CCTA improves prediction of first coronary events beyond the PCE and CACS in a middle-aged general population, particularly among people those tools classify as low risk.¹ CONFIRM2 shows that quantitative plaque measurement improves discrimination over the qualitative and semiquantitative measures used in practice today, and that plaque burden carries greater relative risk in women.⁴˒⁵ CERTAIN shows that clinicians change their management when given this information.⁶

What the evidence does not yet establish is equally important:

• It does not establish that AI-assisted CCTA predicts cardiovascular events with an AUC near 0.90. That figure comes from diagnostic accuracy against invasive angiography, not from event prediction.³˒⁴
• It does not establish that imaging-guided prevention improves clinical outcomes. No completed randomized trial has demonstrated this. TRANSFORM is designed to test it and has not reported.⁸
• It does not establish that any single scanner configuration or analysis platform is superior in outcome terms.

The reasonable conclusion is a strong one without being an overclaim: direct visualization and quantification of coronary plaque represents a substantive advance over inference from risk factors alone, and it identifies disease in people whom conventional tools reassure. Whether acting on that information reduces heart attacks is a question currently under randomized investigation, and the answer will come from TRANSFORM and trials like it rather than from registries, diagnostic accuracy studies, or extrapolation.

For an individual patient, the practical takeaway is unchanged by any of these caveats: finding plaque may identify an opportunity to intensify evidence-based preventive treatment, and serial CCTA studies demonstrate that plaque characteristics are measurably modifiable.⁷ The appropriate posture toward the technology is confident engagement paired with accurate expectations about what the evidence currently supports.

References

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2. Williams MC, Kwiecinski J, Doris M, et al. 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;141(18):1452-1462. doi:10.1161/CIRCULATIONAHA.119.044720
3. Bernardo R, Nurmohamed NS, Bom MJ, et al. Diagnostic accuracy in coronary CT angiography analysis: artificial intelligence versus human assessment. Open Heart. 2025;12(1):e003115. doi:10.1136/openhrt-2024-003115
4. van Rosendael A, Nakanishi R, Bax JJ, et al. Prognostic value of AI-based quantitative coronary CTA vs human reader-based visual assessment: results from the CONFIRM2 registry. JACC Cardiovasc Imaging. 2026;19(3):345-359. doi:10.1016/j.jcmg.2025.09.021
5. Feuchtner GM, Lacaita PG, Bax JJ, et al. AI-quantitative CT coronary plaque features associate with a higher relative risk in women: CONFIRM2 registry. Circ Cardiovasc Imaging. 2025;18(6):e018235. doi:10.1161/CIRCIMAGING.125.018235
6. Nurmohamed NS, Cole JH, Budoff MJ, et al. Impact of atherosclerosis imaging-quantitative computed tomography on diagnostic certainty, downstream testing, coronary revascularization, and medical therapy: the CERTAIN study. Eur Heart J Cardiovasc Imaging. 2024;25(6):857-866. doi:10.1093/ehjci/jeae029
7. Budoff MJ, Bhatt DL, Kinninger A, et al. Effect of icosapent ethyl on progression of coronary atherosclerosis in patients with elevated triglycerides on statin therapy: final results of the EVAPORATE trial. Eur Heart J. 2020;41(40):3925-3932. doi:10.1093/eurheartj/ehaa652
8. [Trial registry record] TRANSFORM — A randomized comparison of Cleerly coronary artery disease stage-based care versus risk factor-based care for primary prevention of cardiovascular events. ClinicalTrials.gov identifier NCT06112418. US National Library of Medicine. Accessed August 2026. Cited for trial design and status only; no results have been reported.
9. Goff DC Jr, Lloyd-Jones DM, Bennett G, et al. 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;129(25 suppl 2):S49-S73. doi:10.1161/01.cir.0000437741.48606.98
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11. Hausleiter J, Meyer T, Hermann F, et al. Estimated radiation dose associated with cardiac CT angiography. JAMA. 2009;301(5):500-507. doi:10.1001/jama.2009.54