# Diagnostic and Severity Assessment of Coronary Artery Disease Using ApoB/ApoA-I Ratio: Insights from a Statin-Treated Eastern European Cohort

**Authors:** Raul-Alexandru Jigoranu, Ovidiu Mitu, Alexandru Florinel Oancea, Radu-Stefan Miftode, Ana Maria Buburuz, Amin Bazyani, Radu-Sebastian Gavril, Theodor-Constantin Stamate, Cristina Andreea Adam, Ionela-Larisa Miftode, Antoniu Octavian Petris, Irina-Iuliana Costache Enache, Florin Mitu

PMC · DOI: 10.3390/medicina62020297 · 2026-02-02

## TL;DR

This study shows that the ApoB/ApoA-I ratio is a strong predictor of coronary artery disease severity in patients on statins, outperforming traditional measures like LDL-C.

## Contribution

The study demonstrates that the ApoB/ApoA-I ratio is an independent predictor of significant coronary stenosis and severity in a statin-treated Eastern European cohort.

## Key findings

- The ApoB/ApoA-I ratio was significantly higher in patients with significant CAD compared to those with non-significant CAD.
- The ratio correlated strongly with CAD severity as measured by the Gensini score and predicted high-risk features like three-vessel disease.
- Lipoprotein(a) provided only marginal additional predictive value in multivariate models.

## Abstract

Background and Objectives: Atherosclerosis continues to be a major determinant of the global health burden, with ischemic heart disease representing one of the leading causes of morbidity and mortality worldwide. Although cardiovascular (CV) prevention strategies focus on pro-atherogenic lipoproteins, such as LDL-C, non-HDL-C, and apoB, the balance between atherogenic and anti-atherogenic lipoproteins may better reflect the overall atherogenic burden. Apolipoprotein B (apoB) reflects the total number of circulating atherogenic particles, whereas apolipoprotein A-I (apoA) is the main protein component of HDL, the major anti-atherogenic lipoprotein. Integrating these two parameters into the apoB/apoA ratio results in a composite biomarker that reflects this balance. In this study, we aimed to evaluate whether the apoB/apoA ratio can predict the presence and the severity of coronary artery disease (CAD) in a cohort from an Eastern European hospital, under moderate-intensity statin treatment. Additionally, we assessed whether lipoprotein(a) [Lp(a)] provides any additional diagnostic value. Materials and Methods: We consecutively enrolled 121 statin-treated patients, who presented for elective invasive coronary angiography. Patients with history of coronary revascularization or acute coronary syndrome were excluded. The study cohort was further divided into two groups, according to the severity of coronary stenosis: 69 patients with non-significant CAD (N-CAD) and 52 patients with hemodynamically significant CAD (S-CAD). Apolipoprotein B, apolipoprotein A-I, and lipoprotein(a) were measured using a standardized immunoturbidimetric assay, at the moment of enrollment. The severity of coronary stenosis was measured using Quantitative Coronary Analysis (QCA) software and the total coronary atherosclerotic burden of each patient was quantified using the Gensini score. Results: The apoB/apoA ratio was significantly higher in the S-CAD groups, compared with N-CAD patients (0.53 ± 0.16 vs. 0.73 ± 0.18). Furthermore, in the apoB/apoA-based analysis, the Gensini score increased progressively across the three tertiles (8.55 ± 19.60 vs. 14.57 ± 21.65 vs. 29.8 ± 27.78, p = 0.000) and so did the percentage of patients with three-vessel disease (5% vs. 19.5% vs. 32.5%, p = 0.000) and left main disease (5% vs. 7.3% vs. 20%, p = 0.031). The apoB/apoA ratio showed a significant correlation with the severity of CAD, as expressed by the Gensini score (r = 0.513, p < 0.001, 95% CI: 0.357–0.641). The association between apoB/apoA ratio and the presence and severity of CAD expanded beyond group comparison. In the logistic regression, this biomarker proved to be a valuable predictor for S-CAD (per SD increase: OR 2.509, 95% CI: 1.441–4.369, p = 0.001), three-vessel disease (per SD increase: OR 2.339, 95% CI: 1.427–3.892, p = 0.001), and left main disease (per SD increase: OR 2.771, 95% CI: 1.489–5.156, p = 0.001). The apoB/apoA ratio remained significant after adjusting for other CV risk factors and independent to LDL-C, as shown by the analysis that we performed among the lowest LDL-C tertile patients. Participants with S-CAD showed higher concentrations of Lp(a). However, adding this lipoprotein to the multivariate analysis, resulted only in a marginal improvement in the predictive power. Conclusions: The ApoB/apoA ratio emerged as an independent predictor for hemodynamically significant coronary stenosis and for CAD severity. Additionally, higher apoB/apoA values were associated with anatomical high-risk features, such as three-vessel disease or left main disease. In contrast, Lp(a) did not provide a substantial increase in the predictive power of multivariate models in this stable CAD cohort.

## Linked entities

- **Proteins:** APOB (apolipoprotein B), APOAI (apolipoprotein A-I), LPA (lipoprotein(a))
- **Diseases:** coronary artery disease (MONDO:0005010), ischemic heart disease (MONDO:0024644)

## Full-text entities

- **Genes:** PLG (plasminogen) [NCBI Gene 5340] {aka HAE4}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, LPA (lipoprotein(a)) [NCBI Gene 4018] {aka AK38, APOA, LP}, APOA1 (apolipoprotein A1) [NCBI Gene 335] {aka AMYLD3, HPALP2, apo(a)}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, APOB (apolipoprotein B) [NCBI Gene 338] {aka FCHL2, FLDB, LDLCQ4, apoB-100, apoB-48}
- **Diseases:** calcifications (MESH:D002114), stable angina pectoris (MESH:D060050), neoplasia (MESH:D009369), three-vessel disease (MESH:C536223), aorta (MESH:D000784), diabetes mellitus (MESH:D003920), Endothelial dysfunction (MESH:D014652), chronic kidney disease (MESH:D051436), DM (MESH:D009223), liver cirrhosis (MESH:D008103), metabolic syndrome (MESH:D024821), inflammation (MESH:D007249), disease (MESH:D004194), injury to (MESH:D014947), coronary lesion (MESH:D003327), ACS (MESH:D054058), dyslipidemia (MESH:D050171), stenosis (MESH:D003251), Coronary stenosis (MESH:D023921), thoracic aortic calcification (MESH:C562942), left (MESH:D018487), stroke (MESH:D020521), COPD (MESH:D029424), left man disease (MESH:D016715), transient ischemic stroke (MESH:D002544), COVID-19 (MESH:D000086382), atrial fibrillation (MESH:D001281), ischemic heart disease (MESH:D017202), CV (MESH:D002318), CKD (MESH:D012080), MI (MESH:D009203), stent thrombosis (MESH:D013927), Atherosclerosis (MESH:D050197), cardiac death (MESH:D003643), hypertriglyceridemia (MESH:D015228), TIA (MESH:D002546), PAD (MESH:D058729), coronary artery calcifications (MESH:D003324), S (MESH:D018455)
- **Chemicals:** TG (MESH:D014280), TC (MESH:D013667), cholesterol (MESH:D002784), -HDL-C (-), disulfide (MESH:D004220), Atorvastatin (MESH:D000069059), Rosuvastatin (MESH:D000068718), creatinine (MESH:D003404), lipid (MESH:D008055)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12941951/full.md

---
Source: https://tomesphere.com/paper/PMC12941951