Purpose of Review In recent years, a family of adiponectin paralogs designated as C1q/TNF-related protein (CTRP) has attracted increasing attention. They are inflammatory adipocytokines mostly secreted from epicardial adipose tissue, which modulate the development and prognosis of coronary artery disease (CAD). This review summarizes the pathophysiological roles of individual members of the CTRP superfamily in the development of CAD. Recent Findings Recent studies have revealed how members of the CTRP family, CTRP1, CTRP3, CTRP5, CTRP9, CTRP12, and CTRP13, can influence both development and progression of CAD by modulating metabolic pathways, influencing immuno-inflammatory response, and regulating cardiovascular functions. Summary Research to date has not been sufficient to answer the specific mechanism of the CTRP family in the occurrence and development of CAD. This review explores the evidence of CTRP superfamily regulating different pathophysiology stages of CAD through the immuno-inflammation, glucose and lipid metabolism, and vascular endothelial function.

Background: The atherogenic index of plasma (AIP), triglyceride-glucose (TyG) index, and monocyte-tolymphocyte ratio (MLR) are strongly associated with atherogenesis of the coronary artery. This study aimed to investigate the association of the AIP, TyG index, and MLR with subclinical coronary artery disease (CAD) and evaluate their ability to predict subclinical CAD.Methods: A total of 697 asymptomatic patients were enrolled in this study and assigned to the subclinical CAD group (n=332) and control group (n=365). The clinical data, coronary artery calci cation score, and calculated AIP, TyG index, and MLR were collected by graduate students in the cardiology division. Multivariate logistic regression models were set up to assess the risk factors for subclinical CAD.Results: The AIP, TyG index and MLR values were higher in the subclinical CAD group than in the control group (all P<0.05). In addition to the classic independent clinical risk factors, increased AIP, TyG index and MLR values were all independent risk factors for subclinical CAD (all P<0.05). The AUCs were higher after combining clinical risk factors than the AIP, TyG index, or MLR alone (all P<0.05).Conclusions: The AIP, TyG index and MLR are independent risk factors for subclinical CAD, which can be useful for improving the diagnosis and prevention of CAD.

Retinol-binding protein-4 (RBP-4) along with the lipid profile plays crucial roles in Acute coronary syndrome (ACS). The study aimed to investigate the correlation of RBP-4, lipoprotein combine index (LCI), and RBP-4 + LCI with ACS. 163 ACS and 77 non-CAD in patients were consecutively enrolled in this study. The serum level of RBP-4 was measured via enzyme-linked immunosorbent assay. LCI was calculated using the formula: total cholesterol × triglyceride × low-density lipoprotein cholesterol/high-density lipoprotein cholesterol. RBP-4 ≥4 ng/ml, LCI ≥16 and LCI ≥16 + RBP-4 ≥4 ng/ml were new independent risk factors of ACS, and OR value of LCI ≥16 + RBP-4 ≥4 ng/ml was higher than that of RBP-4 and LCI combined (all p < 0.05). The AUC for LCI + RBP-4 was higher than that for LCI and RBP-4 individually. The risk of high LCI in 1 lesion vessel was greater than those of 2 or ≥3 lesion vessels (all p < 0.05). In 1 lesion vessel or ≥3 lesion vessels group, the risk associated with LCI and RBP-4 combined was higher than the risk of LCI or RBP-4 alone (all p < 0.05). The risk of hypertension, diabetes mellitus, smoking and history of MI increased with numbers of vessels lesion (all p < 0.05). Increase in RBP-4 and LCI values were found to be independent risk factors for ACS, and the risk of the combined rise in LCI and RBP-4 values was higher than LCI or RBP-4 alone. The combined tests of LCI and RBP-4 might be a potential diagnostic marker for ACS.

Background: Lymphocyte-to-monocyte ratio (LMR) is involved in all stages of coronary atherosclerosis and related to coronary artery disease (CAD). However, the correlation between LMR and the coronary plaque burden of CAD is not clearly elucidated. Therefore, this study aimed to investigate their correlation in patients with CAD. Methods: A total of 1953 consecutive eligible inpatients with suspected CAD were retrospectively included in this study. They were assigned into CAD (n = 564) and non-CAD groups (n = 1389). All patients underwent coronary computed tomographic angiography to evaluate coronary stenosis and coronary artery calcification (CAC). Spearman’s tests were used to analyze the correlation between CAC score and LMR. Multivariate logistic regression models were set up to assess the risk factors of CAD. Results: Patients with CAD had lower LMR value than patients without CAD ( P = 0.001). LMR was negatively correlated with CAC score and was an independent risk factor of CAC score ( P < 0.05). Multivariate logistic regression model showed that LMR ≤4.8 was a newly independent risk factor of CAD (all P < 0.05). Additionally, the new risk score model was compared with the Framingham model and showed that NRI was 4.9%, which proved that the new risk score model improved the prediction capability of CAD. Conclusion: LMR ≤4.8 is a new independent risk factor of CAD. LMR value was negatively correlated with CAC score and could be used as a new marker to evaluate the coronary plaque burden of CAD.