Key result
Future culprit vessels show ~8-point higher maximal radial wall strain than nonculprit vessels before ACS.
Why the study?
Angiography-derived radial wall strain (RWS) is associated with plaque vulnerability, but whether elevated RWS demonstrates culprit-vessel predominance or a broader multivessel distribution within the same patient before ACS was unknown.
Does angiography-derived maximal radial wall strain (RWSmax) demonstrate culprit-vessel predominance compared to nonculprit vessels within the same patient prior to acute coronary syndrome?
Observational (n=101)
Yes
Does angiography-derived maximal radial wall strain (RWSmax) demonstrate culprit-vessel predominance compared to nonculprit vessels within the same patient prior to acute coronary syndrome?
Prior to acute coronary syndrome, angiography-derived radial wall strain is significantly higher in the future culprit vessel compared to nonculprit vessels within the same patient, despite frequent multivessel elevation.
May aid culprit vessel identification in ACS; leaves open prospective validation before clinical adoption.
Background Angiography-derived radial wall strain (RWS) is a biomechanical index associated with plaque vulnerability. Whether elevated RWS demonstrates culprit-vessel predominance or broader multivessel distribution within the same patient is unknown. Objectives The objective of the study was to compare maximal RWS (RWSmax) in the future culprit vessel with nonculprit vessels within the same patient and assess its association with time to acute coronary syndrome (ACS). Methods In the multicenter CULPRIT-STRAIN study, consecutive ACS patients with a prior coronary angiogram (≥3 months before event) were identified from a prospectively maintained registry ( NCT04185285 ). RWSmax was measured in all 3 epicardial coronary arteries at the index angiogram. The primary endpoint was within-patient comparison of culprit vs nonculprit RWSmax; secondary endpoints included its association with index-to-ACS interval and the prevalence of multivessel biomechanical elevation. Results Among 101 patients (303 vessels; median index-to-ACS interval, 35 months), culprit-vessel RWSmax was higher than nonculprit-vessel RWSmax (19.7% vs 11.3%; P < 0.001). The culprit vessel had the highest RWSmax in 96 patients (95.0%; P < 0.001), with a median within-patient ΔRWS of 7.0% (IQR: 3.6%-13.2%). In exploratory analysis, higher culprit-vessel RWSmax was associated with a shorter index-to-ACS interval (ρ = −0.34; P < 0.001). Overall, 60.4% of patients had ≥2 vessels with RWSmax >12%. Conclusions Among patients who developed ACS, RWSmax demonstrated marked culprit-vessel predominance despite frequent multivessel elevation, indicating a graded distribution across vessels. These retrospective findings do not establish prospective risk prediction and require validation in unselected populations with event-free controls.
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Skalidis et al. (2026) conducted an observational in Acute coronary syndrome (ACS) (n=101). Future culprit vessel (measured by angiography-derived maximal radial wall strain [RWSmax]) vs. Nonculprit epicardial coronary vessels within the same patient was evaluated on Within-patient comparison of culprit vs nonculprit maximal radial wall strain (RWSmax) (p=< 0.001). Future culprit vessels had significantly higher angiography-derived maximal radial wall strain than nonculprit vessels within the same patient prior to ACS (19.7% vs 11.3%; P < 0.001).
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