JACC. Cardiovascular imaging
July 6, 2026 · via Europe PMC
Association of Hemodynamic Disease Severity and Distribution With Risk of Future Acute Coronary Syndrome.
Yang S, Chung JW, Park SH, +59 more, Koo BK.
AI summary — for doctors, generated from the abstract only
Both how severe and how focal or diffuse coronary disease is on CT-derived hemodynamics helped identify vessels that later caused acute coronary syndrome.
What was studied
EMERALD-II, an international case-control study of 351 ACS patients (873 vessels) who had coronary CTA 1 month to 3 years before the event, analysing FFRCT and pullback pressure gradient PPGCT.
Key findings
- Lower FFRCT and higher PPGCT were each independently associated with ACS (OR per 0.1 FFRCT increase 0.71, 95% CI 0.65-0.77)
- Mean FFRCT was 0.74 and mean PPGCT 0.54
- Hemodynamic disease pattern added prognostic value beyond lumen and plaque features
- Higher PPGCT added risk particularly when maximal FFRCT drop was 0.10 or more
Clinical relevance
Cardiologists using coronary CT may find that the distribution of disease, not only severity, informs risk of future events.
Who should care
Limitations
It is a case-control design with CTA at varying intervals before the event, so prediction in routine care is not directly demonstrated.
CT-based hemodynamic patterns may complement plaque assessment for identifying high-risk vessels.
This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.
Abstract
Background
Although physiological assessment has been used in decision-making for revascularization, its role in predicting the future risk of acute coronary syndrome (ACS) remains underexplored.
Objectives
This study aims to investigate the independent and combined prognostic significance of hemodynamic disease severity and distribution in identifying ACS culprit vessels, in conjunction with lumen and plaque characteristics.
Methods
The EMERALD-II study is an international, multicenter, internal case-control study enrolling 351 patients with ACS who underwent coronary computed tomography angiography (CTA) 1 month to 3 years before the event. Culprit and nonculprit vessels were identified by matching invasive coronary angiography with coronary CTA findings. High-risk plaque (HRP) characteristics, including minimum lumen area 2, plaque burden ≥70%, low-attenuation plaque, positive remodeling, spotty calcification, and napkin-ring sign, were assessed by a core laboratory, with HRP defined as ≥3 HRP characteristics. From coronary CTA, the authors derived both the hemodynamic severity of the disease (fractional flow reserve derived from computed tomography [FFRCT]) and its spatial distribution (diffuse vs focal), as assessed by the pullback pressure gradient derived from coronary CTA (PPGCT). Vessels were categorized into 4 hemodynamic disease patterns: nonischemic (FFRCT >0.80), hemodynamic diffuse (FFRCT ≤0.80 and PPGCT ≤0.50), mixed (FFRCT ≤0.80 and 0.50 CT ≤0.60), and focal disease (FFRCT ≤0.80 and PPGCT >0.60).
Results
Among 873 vessels, the mean FFRCT was 0.74 ± 0.17 and the mean PPGCT was 0.54 ± 0.14. Both lower FFRCT and higher PPGCT were independently associated with higher ACS risk (OR per 0.1 increase in FFRCT: 0.71 [95% CI: 0.65-0.77]; P CT (differences in FFRCT across the lesion) demonstrated superior model performance compared with models incorporating FFRCT and PPGCT, higher PPGCT was additionally associated with increased ACS risk, particularly among vessels with maximal ΔFFRCT ≥0.10.
Conclusions
Hemodynamic disease distribution, as measured by PPGCT, complements FFRCT in predicting ACS risk. The integration of hemodynamic disease patterns provides additional prognostic value beyond lumen and plaque characteristics, with hemodynamic focal disease emerging as an independent predictor and a potential therapeutic target for ACS prevention. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary CT Angiography and Computational Fluid Dynamics II [EMERALD II]; NCT03591328).
DOI
10.1016/j.jcmg.2026.05.012
PMID
42412030
Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.
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