Healed plaque and systemic thrombogenicity in patients with chronic coronary syndrome

Abstract Background The majority of plaque disruptions are silent, followed by healing, resulting in layered plaque formation. Some plaque disruptions result in occlusive thrombosis and acute myocardial infarction. Purpose This study aimed to test the hypothesis that the patients with layered plaque at culprit lesions would have robust endogenous anti-thrombotic defense mechanisms compared to those without layered plaque. Methods A total of 119 patients with chronic coronary syndrome were enrolled. Target lesions were imaged by optical coherence tomography (OCT). Factor analysis determined four groups of biomarkers, (1) anti-thrombotic factors: plasminogen, anti-thrombin 3, (2) atherogenic factors: low-density lipoprotein-cholesterol (LDL-C), malondialdehyde-modified low-density lipoprotein (MDA-LDL), (3) prothrombotic factors: D-dimer, fibrin degradation products (FDP), and (4) inflammatory factors: fibrinogen, and high-sensitive C reactive protein (hs-CRP). Patients were divided into three groups according to the tertiles of each of those four groups, and their association with a layered plaque was investigated. A layered plaque was defined as one or more layers of different optical densities and a clear demarcation from the underlying tissue. The arc of each layered plaque was assessed at 1-mm cross-section intervals. Layered plaque length is measured from a longitudinal view. The layer index, equivalent to layered plaque volume, is defined as mean layer arc × total layer length. Results The layered plaque was more prevalent in patients with higher levels of anti-thrombotic factor levels (p for trend=0.013) (Figure 1). Similarly, the layer index was higher in patients with higher anti-thrombotic factor levels (p for trend=0.006) (Figure 2). In contrast, other factors had no associations with layered plaque and layer index. In multivariable analysis, only the anti-thrombotic factor was associated with a higher layer index after adjusting for confounders. Conclusions The systemic anti-thrombotic factor levels might be more important determinants for layered plaque formation than atherogenic, prothrombotic, or inflammatory factors.Figure 1 Figure 2