Association of Neutrophil to Lymphocyte Ratio With Plaque Rupture in Acute Coronary Syndrome Patients With Only Intermediate Coronary Artery Lesions Assessed by Optical Coherence Tomography.

Jintong Jiang,Jun Gu,Yang Zhuo,Junfeng Zhang,Huili Zhang,Huasu Zeng,Changqian Wang

doi:10.3389/fcvm.2022.770760

Abstract

ObjectivesPlaque vulnerability and rupture rather than plaque size are the major cause of clinical events in patients with intermediate coronary lesions. Therefore, the present study was aimed to explore potential markers associated with plaque rupture in acute coronary syndrome (ACS) patients with intermediate coronary lesions.MethodsA total of 82 ACS patients presenting with only intermediate coronary lesions (40–70% stenosis demonstrated by quantitative coronary angiography) and no severe stenosis in other main coronary arteries [median age 63 years, 53 male and 29 female] were enrolled. Plaque morphology were assessed by optical coherence tomography (OCT). Hematological indices were assayed by automated hematological analyzer.ResultsPlaque rupture was identified in 14 patients by OCT. Neutrophil to lymphocyte ratio (NLR) in patients with plaque rupture (n = 14) was significantly higher than that in patients with non-plaque rupture (n = 68) [3.85 (3.28, 4.77) vs. 2.13 (1.40, 2.81), p < 0.001]. Multivariate logistic regression analysis revealed that NLR was one of the independent risk factors for plaque rupture in intermediate coronary artery lesions (odds ratio 1.64, 95% confidence intervals 1.18–2.29, p = 0.003). ROC curve analysis found a cutoff point of NLR > 2.94 for plaque rupture with 93.8% sensitivity and 77.9% specificity.ConclusionNLR, an inflammatory biomarker, is closely associated with plaque rupture in intermediate coronary artery lesions. Monitoring NLR may be useful in risk stratification and management for intermediate coronary artery lesions.

Highlights

Intermediate coronary artery stenosis is defined as an angiographic stenosis of 40–70% [1, 2]
The Optical coherence tomography (OCT) findings were described as follow: 35.7% (45/124) fibrous plaques, 22.6% (28/124) fibroatheroma, 8.1% (10/124) fibrocalcific plaques, 16.9% (21/124) mixed plaque, 11.3% (14/124) plaque rupture, 1.6% (2/124) spasm, 1.6% (2/124) dissection, 0.81% (1/124) intimal ulceration/erosion, and 0.81% (1/124) calcified nodule
After follow-up for a median of 35 months [18.0, 45.5], an obvious difference was observed in the incidence of Major adverse cardiac events (MACE) between rupture and non-rupture group (3/14 vs. 3/68, p = 0.026)

Summary

Introduction

Intermediate coronary artery stenosis is defined as an angiographic stenosis of 40–70% [1, 2]. It may account for up to 25% of patients undergoing coronary angiography [3]. Numerous studies have shown that plaque vulnerability and rupture rather than plaque size and stenosis severity are the major cause of cardiovascular events in patients with coronary artery disease (CAD) [4, 5]. The process of plaque rupture may be attributed to neutrophil infiltration and subsequent neutrophil-platelet adhesion. Neutrophil infiltration in disrupted plaques and tissue damage caused by neutrophil elastase were directly visualized by immunohistochemistry in the arteries of the circle of Willis from human autopsy cases [6]. Animal studies suggest that infiltrated neutrophils make plaques prone to rupture by releasing proteolytic enzymes, superoxide radicals and inflammatory mediators [7, 8]

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