Layered plaque in patients with chronic coronary syndrome

IF 3.4 Q3 PERIPHERAL VASCULAR DISEASE

Atherosclerosis plus Pub Date : 2025-12-01 Epub Date: 2025-11-27 DOI:10.1016/j.athplu.2025.11.002

Takafumi Mito , Daisuke Kinoshita , Yoichiro Otaki , Jun Goto , Seisei Ra , Hiroe Ono , Taku Shikama , Shingo Tachibana , Shigehiko Kato , Tetsu Watanabe , Ik-Kyung Jang , Masafumi Watanabe

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Abstract

Background

Plaque disruption exposes thrombogenic substrates and triggers local thrombosis. When a fresh thrombus forms, endogenous antithrombotic mechanisms activate. The balance between these two pro- and antithrombotic mechanisms determines the outcome of plaque disruption. When thrombogenic stimuli outweigh the antithrombotic mechanisms, an occlusive thrombus forms, leading to acute coronary syndromes. When antithrombotic mechanisms dominate, a non-occlusive thrombus forms, contributing to the rapid progression of atherosclerosis. A layered or healed plaque can be identified using optical coherence tomography (OCT).

Purpose

The study aimed to investigate the association between atherothrombotic biomarkers and layered plaque at culprit lesions.

Methods

We analyzed 119 lesions in patients with chronic coronary syndrome who underwent OCT prior to percutaneous coronary intervention. Four groups of biomarkers were studied: antithrombotic, atherogenic, prothrombotic, and inflammatory. The layer index, defined as the mean layer arc multiplied by the layer length, was assessed using OCT.

Results

Patients were divided into tertiles based on each of the four groups. Among the four groups, only the antithrombotic biomarkers were significantly associated with the layer index (low vs. moderate vs. high: 0 vs. 517 vs. 719, p for trend = 0.037). This positive correlation remained significant after adjusting for confounders. In contrast, no association was found between the layer index and atherogenic, prothrombotic, or inflammatory biomarkers.

Conclusions

The antithrombotic mechanism appears to play a key role in layered plaque formation.

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慢性冠脉综合征患者的层状斑块

斑块破坏暴露血栓形成底物并引发局部血栓形成。当新血栓形成时，内源性抗血栓机制被激活。这两种促血栓和抗血栓机制之间的平衡决定了斑块破裂的结果。当血栓形成的刺激超过抗血栓机制，闭塞血栓形成，导致急性冠状动脉综合征。当抗血栓机制占主导地位时，非闭塞性血栓形成，促进动脉粥样硬化的快速进展。层状或愈合的斑块可以使用光学相干断层扫描（OCT）识别。目的研究动脉粥样硬化血栓生物标志物与罪魁祸首病变层状斑块之间的关系。方法分析119例经皮冠状动脉介入治疗前行OCT检查的慢性冠状动脉综合征病变。研究了四组生物标志物：抗血栓、致动脉粥样硬化、促血栓和炎症。层指数定义为平均层弧乘以层长，使用oct进行评估。结果根据四组的每一组将患者分为三层。在四组中，只有抗血栓生物标志物与层指数显著相关（低、中、高：0、517、719，p为趋势= 0.037）。在调整混杂因素后，这种正相关仍然显著。相反，没有发现层指数与动脉粥样硬化、血栓形成前或炎症生物标志物之间的关联。结论抗血栓机制在层状斑块形成中起关键作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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