Apolipoprotein B/A1 Ratio Is Associated with Severity of Coronary Artery Stenosis in CAD Patients but Not in Non-CAD Patients Undergoing Percutaneous Coronary Intervention

Overview

Journal Dis Markers

Publisher Wiley

Specialty Biochemistry

Date 2021 Dec 28

PMID 34961824

Citations 6

Authors

Rui Hua

Yijun Li

Wenyuan Li

Zhen Wei

Zuyi Yuan

Juan Zhou

Affiliations

Soon will be listed here.

Abstract

Background And Aims: Lipid metabolism plays important roles in atherosclerosis. Several studies have found that lipoprotein is associated with coronary artery disease (CAD) and hyperlipidemia. Although the roles of the apolipoprotein B/A1 ratio (ApoB/A1) were originally thought to be atherosclerotic, few studies have focused on the specific relationship between ApoB/A1 and severity of coronary artery stenosis with or without the presence of CAD.

Methods: A total of 6956 consecutive patients aged 21-98 years with suspected CAD who had undergone coronary angiography were enrolled. The severity of coronary lesions was evaluated using the Gensini score (GS). The relationships between ApoB/A1 and severity of coronary artery stenosis were evaluated.

Results: A total of 1795 non-CAD patients and 5161 CAD patients were included in the observational analysis. Patients with CAD had higher ApoB/A1 than individuals without CAD (0.67 (0.53-0.82) vs. 0.61 (0.49-0.75), < 0.001). In CAD patients, the higher the ApoB/A1 was, the higher the proportion of patients with MI, triple-vessel lesions, and higher Gensini scores. ApoB/A1 was significantly positively correlated with HbA1c and Gensini scores in CAD patients but not in non-CAD patients (all < 0.001). Logistic analyses showed that ApoB/A1 could be a risk factor for multivessel disease (OR: 2.768, 95% CI: 1.868-4.103, < 0.001). ApoB/A1 was found to be significantly positively correlated with the Gensini score in CAD patients.

Conclusions: ApoB/A1 is highly associated with the presence and severity of coronary artery stenosis in patients with CAD but not in non-CAD patients.

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