Angiographic prevalence of occlusion myocardial infarction and the limited value of serial troponin in patients with non-ST-segment elevation acute coronary syndrome.

IF 3 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Frontiers in Cardiovascular Medicine Pub Date : 2026-10-05 eCollection Date: 2026-01-01 DOI:10.3389/fcvm.2026.1903711
Sajid Kadir, Sandeep Sasidharan, Sandipan Shringi, Mahati Dasari, Pramukh Arun Kumar
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引用次数: 0

Abstract

Background: An estimated 25%-34% of patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) are diagnosed with an occluded culprit artery during catheterization. Whether early serial troponin kinetics discriminate angiographically defined occlusion myocardial infarction (OMI) in catheterized patients with NSTE-ACS remains uncertain.

Methods: We conducted a single-center retrospective cohort study of 481 patients with NSTE-ACS who underwent coronary catheterization between 2017 and 2023. OMI was defined by a purely angiographic criterion: >90% culprit-vessel stenosis with Thrombolysis in Myocardial Infarction flow grade 0, 1, or 2. Seven contemporary sensitivity troponin I metrics (absolute values at 0, 3, and 6 h; deltas; and ratios) were evaluated by receiver operating characteristic analysis. Operating characteristics are reported with 95% confidence intervals (CIs) and likelihood ratios.

Results: Ninety-eight patients (20.4%) met the angiographic definition of OMI. These patients were younger (median, 65.5 vs. 70.0 years; p = 0.025), had fewer comorbidities, and more often presented with chest pain (92.9% vs. 82.8%; p = 0.013). The left circumflex artery was the most common culprit in OMI (36.7%). Twenty-nine patients with OMI (29.6%) had a presentation ECG classified as normal (no ST-T change or bundle branch block. No troponin metric reliably discriminated OMI from non-occlusion MI. The prespecified primary predictor, the 0-6-h change in troponin concentration, had an area under the curve (AUC) of 0.623 (95% CI, 0.544-0.703) and the best single metric, the 6-h value, of 0.654 (0.580-0.727); all seven unadjusted troponin-metric AUCs were under 0.66. At its Youden cutoff (≥0.379 ng/mL), the 6-h troponin had a sensitivity of 69.4%, a specificity of 57.7%, a positive predictive value of 27.2%, and a negative predictive value of 89.3%. The highest positive predictive value of any metric was 41.3%, the first troponin (at 0 h) identified fewer than 40% of patients with OMI at its optimal threshold, and likelihood ratios produced only limited shifts in post-test probability.

Conclusion: Among analyzable patients with NSTE-ACS undergoing catheterization, approximately one in five met the study-defined angiographic criteria for OMI. Early serial troponin kinetics showed only modest discrimination, and upper confidence bounds fell below levels expected of a standalone triage biomarker. Complementary strategies for identifying these patients, including expert ECG interpretation, warrant further study.

非st段抬高急性冠状动脉综合征患者闭塞性心肌梗死的血管造影患病率及系列肌钙蛋白的有限价值
背景:估计25%-34%的非st段抬高急性冠状动脉综合征(NSTE-ACS)患者在导管置入期间被诊断为罪魁动脉闭塞。是否早期系列肌钙蛋白动力学区分血管造影定义的闭塞性心肌梗死(OMI)导管患者NSTE-ACS仍不确定。方法:我们对2017年至2023年间接受冠状动脉导管置入的481例NSTE-ACS患者进行了单中心回顾性队列研究。OMI是由一个纯粹的血管造影标准定义的:罪魁祸首血管狭窄,心肌梗死血流等级为0、1或2。通过受试者工作特征分析评估7项当代肌钙蛋白I敏感性指标(0,3和6h时的绝对值、δ和比率)。以95%置信区间(ci)和似然比报告操作特征。结果:98例(20.4%)符合OMI的血管造影定义。这些患者较年轻(中位年龄为65.5岁对70.0岁,p = 0.025),合并症较少,更常出现胸痛(92.9%对82.8%,p = 0.013)。左旋动脉是OMI最常见的罪魁祸首(36.7%)。29例OMI患者(29.6%)的心电图表现为正常(无ST-T改变或束支传导阻滞)。没有肌钙蛋白指标能够可靠地区分OMI和非闭塞性MI。预先指定的主要预测指标,0-6小时肌钙蛋白浓度变化,曲线下面积(AUC)为0.623 (95% CI, 0.544-0.703),最佳单一指标,6小时值为0.654 (0.580-0.727);所有7个未经调整的肌钙蛋白auc均低于0.66。在约登截止值(≥0.379 ng/mL)下,6 h肌钙蛋白的敏感性为69.4%,特异性为57.7%,阳性预测值为27.2%,阴性预测值为89.3%。任何指标的最高阳性预测值为41.3%,第一个肌钙蛋白(在0小时)在其最佳阈值处识别不到40%的OMI患者,似然比仅产生有限的检测后概率变化。结论:在可分析的接受导管置入的NSTE-ACS患者中,大约五分之一的患者符合研究定义的OMI血管造影标准。早期系列肌钙蛋白动力学仅显示出适度的区分,并且上限置信度低于独立分诊生物标志物的预期水平。识别这些患者的补充策略,包括专家心电图解读,值得进一步研究。
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来源期刊
Frontiers in Cardiovascular Medicine
Frontiers in Cardiovascular Medicine Medicine-Cardiology and Cardiovascular Medicine
CiteScore
3.80
自引率
11.10%
发文量
3529
审稿时长
14 weeks
期刊介绍: Frontiers? Which frontiers? Where exactly are the frontiers of cardiovascular medicine? And who should be defining these frontiers? At Frontiers in Cardiovascular Medicine we believe it is worth being curious to foresee and explore beyond the current frontiers. In other words, we would like, through the articles published by our community journal Frontiers in Cardiovascular Medicine, to anticipate the future of cardiovascular medicine, and thus better prevent cardiovascular disorders and improve therapeutic options and outcomes of our patients.
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