Work

Layered plaque in patients with chronic coronary syndrome

Year: 2025

Type: article

Abstract: 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). The study aimed to investigate the association between atherothrombotic biomarkers and layered plaque at culprit lesions. 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. 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. The antithrombotic mechanism appears to play a key role in layered plaque formation. • Among four biomarker clusters—antithrombotic, atherogenic, prothrombotic, and inflammatory—only antithrombotic biomarkers (plasminogen and AT3) were significantly associated with layered plaque formation in chronic coronary syndrome (CCS) patients. • The layer index, derived from OCT imaging, increased across tertiles of antithrombotic factor levels, suggesting a protective role of endogenous fibrinolytic mechanisms in plaque healing. • Atherogenic biomarkers correlated with lipid accumulation and macrophage infiltration, but did not influence layered plaque morphology, underscoring distinct biological pathways in plaque progression. • These findings support the hypothesis that plaque healing is actively modulated by antithrombotic mechanisms, offering a potential avenue for preventive strategies in CCS beyond traditional lipid-centric approaches.

Source: Atherosclerosis Plus

DOI: 10.1016/j.athplu.2025.11.002