Key result
ACS linked to ~6.1-fold higher odds of focal soft plaque thickening in non-culprit lesions.
Why the study?
Major adverse cardiovascular events from non-culprit lesions remain a concern in ACS, and while several CCTA high-risk features identify plaque vulnerability, the significance of soft plaque morphology in non-culprit lesions was unclear.
Is acute coronary syndrome associated with distinct soft plaque morphology (focal soft plaque thickening) in non-culprit lesions on coronary computed tomography angiography compared to chronic coronary syndrome?
Cross-Sectional (n=69)
Is acute coronary syndrome associated with distinct soft plaque morphology (focal soft plaque thickening) in non-culprit lesions on coronary computed tomography angiography compared to chronic coronary syndrome?
Answers are grounded in this paper and cite their sources.
Morphological assessment of focal soft plaque thickening on CCTA is strongly associated with ACS and may provide complementary information for characterizing vulnerable non-culprit lesions.
BACKGROUND: Major adverse cardiovascular events arising from non-culprit lesions (NCLs) remain relevant in patients with acute coronary syndrome (ACS), highlighting the need for more effective identification of vulnerable plaques. Although several coronary computed tomography angiography (CCTA)-derived high-risk features are recognized as markers of plaque vulnerability, the significance of soft plaque morphology remains unclear. This study investigated whether ACS is associated with soft plaque morphology in NCLs on CCTA. METHODS AND RESULTS: Overall, 174 NCLs from 69 patients with ACS or chronic coronary syndrome (CCS) who underwent CCTA within 1 month of percutaneous coronary intervention were analyzed. Soft plaques were classified according to the presence or absence of focal soft plaque thickening (FSPT), defined as localized thickening of the soft plaque component measuring ≥500 μm in at least one cross-sectional slice. Intravascular ultrasound (IVUS) was co-registered with CCTA in 49 lesions. The soft plaque burden did not differ significantly between NCLs in patients with ACS and CCS, whereas FSPT was more frequently observed in NCLs in patients with ACS (56.4% vs. 18.8%; p < 0.001). In multivariable analysis accounting for within-patient clustering, ACS was independently associated with FSPT (odds ratio, 6.09; 95% confidence interval, 2.72-13.60; p < 0.001). On co-registered IVUS, lesions with FSPT showed larger attenuation arcs and more frequent superficial attenuation. CONCLUSIONS: ACS was independently associated with CCTA-derived FSPT in NCLs. These exploratory findings suggest that morphological assessment of soft plaques on CCTA may provide complementary information for the characterization of NCLs. Further validation in independent cohorts is warranted.
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Hatakeyama et al. (2026) conducted a cross-sectional in Acute coronary syndrome or chronic coronary syndrome (n=69). Acute coronary syndrome (ACS) vs. Chronic coronary syndrome (CCS) was evaluated on Focal soft plaque thickening (FSPT, localized thickening of soft plaque ≥500 μm in at least one cross-sectional slice) in non-culprit lesions on CCTA (OR 6.09, 95% CI 2.72-13.60, p=< 0.001). Acute coronary syndrome was independently associated with focal soft plaque thickening in non-culprit lesions on CCTA compared with chronic coronary syndrome (OR 6.09; 95% CI 2.72-13.60; p<0.001).
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