Key result
Non-culprit plaque rupture in STEMI is linked to poor long-term outcomes driven by non-ruptured TCFA.
Why the study?
Does the presence of non-culprit plaque rupture predict long-term MACE in STEMI patients?
Cohort (n=930)
Does the presence of non-culprit plaque rupture predict long-term MACE in STEMI patients?
Hazard Ratio: 2.25 (95% CI 1.13–4.49)
p-value: p=0.021
In STEMI patients, the poor long-term prognosis associated with non-culprit plaque rupture is predominantly driven by the presence of non-ruptured thin-cap fibroatheroma (TCFA), which better identifies lesions at increased risk of subsequent events.
Non-ruptured TCFA may identify high-risk lesions in STEMI; challenges consensus on plaque rupture and leaves open prospective validation.
BACKGROUND: The role of non-culprit plaque rupture (a sign of pancoronary vulnerability) on long-term clinical outcomes remains unclear. AIMS: We aimed to investigate the association between non-culprit plaque rupture and long-term clinical outcomes. METHODS: ST-segment elevation myocardial infarction (STEMI) patients who had undergone 3-vessel optical coherence tomography before interventional therapy were studied. Patients and lesions were categorised into groups with and without non-culprit plaque rupture. Furthermore, non-ruptured thin-cap fibroatheroma (TCFA) was defined as a lesion with TCFA but not plaque rupture. All enrolled patients were followed for up to 5 years. The study endpoint was major adverse cardiac events (MACE), including cardiac death, non-fatal myocardial infarction, and unplanned ischaemia-driven revascularisation. RESULTS: A total of 930 STEMI patients with 3,660 non-culprit lesions were included. Non-culprit plaque rupture was detected in 165 patients and 209 lesions. During a median 4.1-year follow-up, non-culprit lesion-related MACE occurred more frequently in patients with versus without plaque rupture (hazard ratio [HR] 2.25, 95% confidence interval [CI]: 1.13-4.49; p=0.021). However, non-culprit lesion-related MACE were similar for lesions with versus without plaque rupture (HR 0.05, 95% CI: 0.00-24.68; p=0.336). Furthermore, non-ruptured TCFA was identified in 214 patients and 281 lesions. Multivariable analysis demonstrated that non-ruptured TCFA was significantly associated with non-culprit lesion-related MACE, whereas plaque rupture was not, at both the patient and lesion levels. CONCLUSIONS: Patients with non-culprit plaque rupture had a poor long-term prognosis, which is predominantly due to the effect of non-ruptured TCFA. Non-ruptured TCFA, not plaque rupture, can identify lesions at increased risk of subsequent events.
No takes yet. Share an insight, caveat, or question.
Zhao et al. (2025) conducted a cohort in ST-segment elevation myocardial infarction (STEMI) (n=930). Non-culprit plaque rupture vs. Without non-culprit plaque rupture was evaluated on Major adverse cardiac events (MACE), including cardiac death, non-fatal myocardial infarction, and unplanned ischaemia-driven revascularisation (HR 2.25, 95% CI 1.13-4.49, p=0.021). Non-culprit plaque rupture was associated with increased MACE (HR 2.25; 95% CI 1.13-4.49; p=0.021), but multivariable analysis showed this risk was driven by non-ruptured TCFA, not plaque rupture.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: