Muhua Cao1, Linlin Zhao1, Xuefeng Ren1, Tianyu Wu1, Guang Yang1, Zhuo Du1, Huai Yu1, Jiannan Dai1, Lulu Li1, Yini Wang1, Guo Wei1, Lijia Ma1, Lei Xing1, Yingfeng Tu1, Shaohong Fang1, Jinwei Tian1, Haibo Jia1, Gary S Mintz2, Bo Yu3. 1. Department of Cardiology, Second Affiliated Hospital of Harbin Medical University, Harbin, China; Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China. 2. Cardiovascular Research Foundation, New York, New York, USA. 3. Department of Cardiology, Second Affiliated Hospital of Harbin Medical University, Harbin, China; Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China. Electronic address: yubodr@163.com.
Abstract
OBJECTIVES: This study sought to investigate nonculprit plaque characteristics in patients with ST-segment elevation myocardial infarction (STEMI) presenting with plaque erosion (PE) and plaque rupture (PR). Pancoronary vulnerability was considered at nonculprit sites: 1) the CLIMA (Relationship Between OCT Coronary Plaque Morphology and Clinical Outcome) study (NCT02883088) defined high-risk plaques with simultaneous presence of 4 optical coherence tomography (OCT) features (minimum lumen area <3.5 mm2; fibrous cap thickness [FCT] <75 μm; maximum lipid arc >180º; and macrophage accumulation); and 2) the presence of plaque ruptures or thin-cap fibroatheromas (TCFA). BACKGROUND: PE is a unique clinical entity associated with better outcomes than PR. There is limited evidence regarding pancoronary plaque characteristics of patients with culprit PE versus culprit PR. METHODS: Between October 2016 and September 2018, 523 patients treated by 3-vessel OCT at the time of primary percutaneous intervention were included with 152 patients excluded from final analysis. RESULTS: Overall, 458 nonculprit plaques were identified in 202 STEMI patients with culprit PE; and 1,027 nonculprit plaques were identified in 321 STEMI patients with culprit PR. At least 1 CLIMA-defined OCT nonculprit high-risk plaque was seen in 11.4% of patients with culprit PE, but twice as many patients were seen with culprit PR (25.2%; p < 0.001). This proportion was also seen when individual high-risk features were analyzed separately. When patients with PE were divided by a heterogeneous substrate (fibrous or lipid-rich plaque) underlying the culprit site, the prevalence of nonculprits with FCT <75 μm, macrophages, and TCFA showed a significant gradient from PE(Fibrous) to PElipid-rich plaque (LRP) to PR. Interestingly, nonculprit rupture was rarely found in patients with culprit PE(Fibrous) (1.9%), although it was exhibited with comparable prevalence in patients with culprit PE(LRP) (16.3%) versus PR (17.8%). Culprit PE predicted decreased pancoronary vulnerability independent of conventional risk factors. CONCLUSIONS: STEMI patients with culprit PE have a limited pancoronary vulnerability that may explain better outcomes in these patients than in STEMI patients with culprit PR.
OBJECTIVES: This study sought to investigate nonculprit plaque characteristics in patients with ST-segment elevation myocardial infarction (STEMI) presenting with plaque erosion (PE) and plaque rupture (PR). Pancoronary vulnerability was considered at nonculprit sites: 1) the CLIMA (Relationship Between OCT Coronary Plaque Morphology and Clinical Outcome) study (NCT02883088) defined high-risk plaques with simultaneous presence of 4 optical coherence tomography (OCT) features (minimum lumen area <3.5 mm2; fibrous cap thickness [FCT] <75 μm; maximum lipid arc >180º; and macrophage accumulation); and 2) the presence of plaque ruptures or thin-cap fibroatheromas (TCFA). BACKGROUND: PE is a unique clinical entity associated with better outcomes than PR. There is limited evidence regarding pancoronary plaque characteristics of patients with culprit PE versus culprit PR. METHODS: Between October 2016 and September 2018, 523 patients treated by 3-vessel OCT at the time of primary percutaneous intervention were included with 152 patients excluded from final analysis. RESULTS: Overall, 458 nonculprit plaques were identified in 202 STEMI patients with culprit PE; and 1,027 nonculprit plaques were identified in 321 STEMI patients with culprit PR. At least 1 CLIMA-defined OCT nonculprit high-risk plaque was seen in 11.4% of patients with culprit PE, but twice as many patients were seen with culprit PR (25.2%; p < 0.001). This proportion was also seen when individual high-risk features were analyzed separately. When patients with PE were divided by a heterogeneous substrate (fibrous or lipid-rich plaque) underlying the culprit site, the prevalence of nonculprits with FCT <75 μm, macrophages, and TCFA showed a significant gradient from PE(Fibrous) to PElipid-rich plaque (LRP) to PR. Interestingly, nonculprit rupture was rarely found in patients with culprit PE(Fibrous) (1.9%), although it was exhibited with comparable prevalence in patients with culprit PE(LRP) (16.3%) versus PR (17.8%). Culprit PE predicted decreased pancoronary vulnerability independent of conventional risk factors. CONCLUSIONS: STEMI patients with culprit PE have a limited pancoronary vulnerability that may explain better outcomes in these patients than in STEMI patients with culprit PR.
Authors: Elisa Ceriani; Azzurra Marceca; Antonio Lanfranchi; Stefano De Vita; Riccardo Schiavon; Francesco Casella; Daniela Torzillo; Marta Del Medico; Diego Ruggiero; Alberto Barosi; Chiara Cogliati Journal: Intern Emerg Med Date: 2021-05-21 Impact factor: 3.397