# Neutrophil-Percentage-to-Albumin Ratio as a Predictor of Coronary Artery Ectasia: A Comparative Analysis with Inflammatory Biomarkers

## TL;DR

This study finds that a new inflammation marker called NPAR better predicts coronary artery ectasia compared to existing markers like CRP.

## Contribution

The study introduces NPAR as a novel and superior predictor of coronary artery ectasia compared to traditional inflammatory biomarkers.

## Key findings

- NPAR was significantly higher in patients with coronary artery ectasia compared to controls.
- NPAR outperformed CRP in predicting both presence and severity of coronary artery ectasia.
- NPAR showed a strong correlation with disease severity based on the Markis classification.

## Abstract

Background/Objectives: Coronary artery ectasia (CAE) is characterized by abnormal dilation of the coronary arteries and is associated with adverse cardiovascular events. Inflammation is believed to play a pivotal role in the development and progression of CAE. The neutrophil-percentage-to-albumin ratio (NPAR) has emerged as a novel marker of systemic inflammation and may serve as a useful tool in the evaluation of CAE. This study aimed to assess the association between the NPAR and CAE and compare its predictive value to established inflammatory biomarkers, including highly sensitive C-reactive protein (hsCRP), the neutrophil-to-lymphocyte ratio (NLR), and the platelet-to-lymphocyte ratio (PLR). Methods: A retrospective analysis was conducted on 5212 patients who underwent elective coronary angiography between March 2019 and March 2023. The cohort included 165 patients with isolated CAE and 180 controls with normal coronary anatomy. Inflammatory markers and their correlation with CAE were analyzed using logistic regression models and receiver operating characteristic (ROC) analysis to determine predictive performance. Results: The NPAR was significantly elevated in the CAE group compared to the controls (p < 0.001). Multivariate analysis identified the NPAR (OR: 2.14, p = 0.003) and CRP (OR: 1.53, p = 0.02) as independent predictors of CAE. ROC analysis demonstrated that the NPAR had superior predictive value over CRP (AUC: 0.725 vs. 0.635). Additionally, the NPAR showed a strong correlation with CAE severity based on the Markis classification, with higher NPAR values associated with more advanced disease. Conclusions: The NPAR is an independent predictor of CAE and outperforms CRP in predicting both the presence and severity of the condition. As a cost-effective and accessible biomarker, the NPAR may enhance the clinical assessment of CAE and provide valuable insights into its inflammatory underpinnings. Further prospective studies are warranted to validate these findings and explore the potential of the NPAR in risk stratification and management of CAE patients.