Jiawei Zhao; Rui Zhao; Yuzhu Chen; Lina Cui; Xianqin Ma; Jiawen Chen; Fuhong Dong; Tong Lin; Jinfeng Tan; Tianyu Wu; Chengmei Jin; Lili Xiu; Wei Wang; Lulu Li; Yini Wang; Senqing Jiang; Huai Yu; Jingbo Hou; Chao Fang; Jiannan Dai; Bo Yu

doi:10.4244/EIJ-D-25-00648

Long-term clinical outcomes of non-culprit plaque rupture in STEMI

Jiawei Zhao¹^,², MD; Rui Zhao¹^,², MD; Yuzhu Chen¹^,², MD; Lina Cui¹^,², MD; Xianqin Ma¹^,², MD; Jiawen Chen¹^,², MD; Fuhong Dong¹^,², MD; Tong Lin¹^,², MD; Jinfeng Tan¹^,², MD; Tianyu Wu¹^,², MD; Chengmei Jin¹^,², MD; Lili Xiu¹^,², MD; Wei Wang¹^,², MD; Lulu Li¹, MS; Yini Wang¹^,²^,³, MD, PhD; Senqing Jiang¹^,², MD, PhD; Huai Yu¹^,², MD, PhD; Jingbo Hou¹^,²^,⁴, MD, PhD; Chao Fang¹^,²^,⁴, MD, PhD; Jiannan Dai¹^,²^,³^,⁴, MD, PhD; Bo Yu¹^,²^,⁴, MD, PhD

Abstract

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.

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