This study aimed to identify clinical and biochemical predictors of coronary artery disease (CAD) progression in patients undergoing routine cardiovascular evaluation. A retrospective cohort study was conducted involving 183 patients with confirmed CAD (92 with progression and 91 without progression). Clinical data, echocardiographic parameters, and laboratory biomarkers were collected at baseline. CAD progression was assessed based on repeat coronary angiography after a follow-up period. Multivariate logistic regression was used to identify independent predictors of CAD progression. The predictive accuracy of the model was evaluated using the area under the receiver operating characteristic curve), and model fit was assessed using the Hosmer-Lemeshow test. Elevated interleukin-6 levels (OR = 3.051, 95% confidence interval: 1.164-7.999, P = .023) and triglycerides (approaching significance, odds ratio = 1.126, 95% confidence interval: 0.980-1.293, P = .093) were identified as key predictors of CAD progression. The final model showed good discrimination with an area under the receiver operating characteristic curve of 0.701 and an acceptable fit (Hosmer-Lemeshow test: P = .078). Elevated interleukin-6 and triglycerides levels are significant or near-significant predictors of CAD progression. These findings suggest that inflammatory and lipid biomarkers play critical roles in disease progression and may serve as valuable targets for therapeutic interventions in high-risk patients.

This study aimed to assess the predictive capacity of specialized pro-resolving mediators (SPMs) regarding the complexity and prognosis of coronary heart disease (CHD). Total of 602 CHD patients were included in this study and categorized into low-risk, medium-risk, and high-risk groups based on the Synergy Between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) score. Follow-up was conducted for two years, during which patients were dichotomized into poor and good prognosis groups. Additionally, twenty healthy controls were incorporated. Plasma concentrations of lipoxin A4 (LXA4), resolvin D1 (RvD1), protectin D1 (PD1), C-reactive protein (CRP), interleukin-6 (IL-6), and IL-10 were quantified. Plasma LXA4, RvD1, PD1, and the ratios LXA4/IL-6, RvD1/IL-6, PD1/IL-6 exhibited a gradual decrease across control, low-risk, medium-risk, and high-risk groups and exhibited a negative correlation with the SYNTAX score. Spearman's correlation analysis revealed negative correlations between plasma LXA4, RvD1, PD1, and both CRP and IL-6, and positive correlations with IL-10. Multiple linear regression models demonstrated negative associations between plasma LXA4, RvD1, PD1, and SYNTAX score. Moreover, both univariate and multivariate binary logistic regression analyses identified plasma LXA4, RvD1, and PD1 as protective factors against medium/high-risk SYNTAX score categorization. In the poor prognosis group, plasma PD1 was reduced at short-term follow-up, and the ratios LXA4/IL-6, RvD1/IL-6, PD1/IL-6 were reduced at long-term follow-up. Plasma LXA4, RvD1, and PD1 demonstrated negative correlations with CHD complexity and potentially served as protective factors against CHD. Plasma PD1 provided predictive value for short-term prognosis, while the ratios LXA4/IL-6, RvD1/IL-6, PD1/IL-6 were indicative for long-term prognosis.

Interleukins (ILs), a subset of cytokines, play a critical role in the pathogenesis of coronary heart disease (CHD) by mediating inflammation. This review article summarizes the role of ILs such as IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, and IL-10 in the pathogenesis of CHD. Individuals with mild coronary artery disease (CAD) and angina who have ischemic heart disease have higher serum concentrations of IL-1b. Larger studies are needed to verify the safety and assess the effectiveness of low-dose IL-2 as an anti-inflammatory treatment. IL-3 is found more often in patients receiving coronary angioplasty compared to patients with asymptomatic CAD or without CAD. Serum levels of IL-4 are reliable indicators of CAD. An independent correlation between IL-5 and the incidence of CAD was demonstrated. IL-6 helps serve as a reliable biomarker for the degree of CAD, as determined by the Gensini score, and is a key factor in the development of atherosclerosis. Also, variants of IL-7/7R have been linked to the Han Chinese population's genetic susceptibility to CHD. IL-8 plays a role in the progression of CAD occurrences. By interacting with conventional risk factors for CAD, IL-9 may contribute to the development of CAD and offer an innovative approach to its prevention and management. There was a 34% increased risk of a CHD incident for every standard deviation rise in baseline IL-10 levels.

Despite significant advances in imaging modalities for diagnosing coronary artery disease (CAD), there remains a need for novel diagnostic approaches with high predictive values and fewer limitations. Circulating biomarkers, including cytokines such as interleukin-6 (IL-6) and interleukin-8 (IL-8), cell adhesion molecules such as soluble vascular cell adhesion molecule-1 (sVCAM-1), peptides secreted by endothelial cells such as endothelin-1 (ET-1), and enzymes involved in extracellular matrix remodeling such as a disintegrin and metalloproteinase with thrombospondin motifs-1 (ADAMTS-1) offer a promising alternative. This study aimed to evaluate the correlation between the plasma levels of selected biomarkers and the presence and severity of CAD. We enrolled 40 patients admitted for elective coronary angiography. CAD was defined as having at least one coronary artery stenosis ≥ 50%. The severity of CAD was assessed using the Gensini Score (GS). IL-8 levels were significantly higher in the CAD group, with a mean of 9.78 (SD 0.46) compared to 8.37 (SD 0.40) in the non-CAD group (p = 0.0228). No significant differences were observed for the other biomarkers between the groups. A positive Spearman correlation was found between IL-8 levels and the GS (ρ = 0.39, p = 0.017). These findings suggest that IL-8 may have potential as an additional tool for diagnosing or excluding atherosclerosis. Further studies with larger sample sizes are needed to validate its clinical utility.

Acute coronary syndrome (ACS) is one of the most important cardiovascular diseases. The rupture of atherosclerotic plaques in coronary arteries is considered the underlying pathophysiology of ACS. The interaction between cytokines and leukocytes in the presence of platelets results in platelet-leukocyte aggregate (PLA). Monocytes, neutrophils, and cytokines are prime factors that promote PLA formation, which leads to atherosclerotic plaque progression and subsequent ACS development. This study aimed to investigate PLA (PMA and PNA) formation and cytokine (IL-6 and TNF-α) levels as well as the correlation between them in ACS patient samples to identify diagnostic markers.

A total of 30 patients with ACS and 24 healthy controls participated in this study. Flow cytometry analysis was performed to evaluate PLA formation, and the serum levels of cytokines were assessed by ELISA. The Pearson's correlation coefficient and ROC curve were calculated to investigate the correlation between the parameters and their diagnostic value, respectively.

The results showed that PMA, PNA, and IL-6 levels were significantly higher in ACS patients than in healthy controls. Additionally, TNF-α levels were not significantly increased in the patient group. In addition, the Pearson's correlation coefficient results revealed a direct linear and statistically significant relationship between PMA-IL-6 and PNA-IL-6 as well as a direct linear but statistically nonsignificant relationship between IL-6-TNF-α and PMA-PNA, whereas a convers linear but nonsignificant correlation was shown between PMA and TNF-α and no correlation was detected between PNA and TNF-α. Finally, ROC curve analysis revealed that the PMA, PNA, and IL-6 can have diagnostic value.

In conclusion, the PMA, PNA, and IL-6 can be used as powerful diagnostic markers in ACS patients. Therefore, disrupting PMA and PNA formation and inhibiting cytokine production may be new strategies for the treatment of ACS. However, further investigations are required to explore these parameters in the clinical diagnosis of ACS.

Fibroblast growth factor 21 (FGF21) is a secreted protein that plays an important role in atherosclerosis and pathological cardiac remodeling. However, the correlation between FGF21 and the degree of coronary artery stenosis and its potential role in acute myocardial infarction (AMI) remain unclear. We examined whether changes in FGF21 levels in AMI correlate with the degree of coronary artery stenosis and the levels of inflammatory factors, and preliminarily investigated the effects of FGF21 on inflammatory factor levels and myocardial injury in rats with AMI.

Serum levels of FGF21 and inflammatory factors in the AMI group and control group were measured, and the correlation between FGF21 and clinical indicators and inflammatory factors was analyzed. The effects of FGF21 on cardiac function and inflammatory response were evaluated through echocardiography and measurement of inflammatory factors.

Multivariate logistic regression analysis showed that neutrophil percentage (NEUT%, odds ratio [OR]: 1.232; 95 % confidence interval [CI]: 1.028-1.477; p = 0.024) and FGF21 levels (OR: 2.063; 95 % CI: 1.187-3.586; p = 0.01) had independent effects on AMI. Spearman's rank correlation test showed that FGF21 levels were positively correlated with leukocyte count, NEUT%, neutrophil count, neutrophil to lymphocyte ratio, C-reactive protein, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1) and Gensini scores (p < 0.01), but negatively correlated with lymphocyte count (p < 0.01). FGF21 levels in myocardial tissues and serum levels of FGF21, IL-6, TNF-a, and MCP-1 were significantly higher in AMI rats than in the sham-operated group (p < 0.01). After overexpression of FGF21, serum levels of IL-6, TNF-a, and MCP-1 in rats were significantly decreased (p < 0.01), and cardiac function improved significantly.

FGF21 levels were independently associated with AMI and may be related to the severity of coronary artery stenosis. Overexpression of FGF21 reduced serum inflammatory factor levels and improved cardiac function in AMI rats.

Lesions with thin-cap fibroatheroma (TCFA), small luminal area and large plaque burden (PB) have been considered at high risk of cardiovascular events. Older patients were not represented in studies which demonstrated correlation between clinical outcome and plaque characteristics. This study aims to investigate the prognostic role of high-risk plaque characteristics and long-term outcome in older patients presenting with non-ST elevation acute coronary syndrome (NSTEACS).

This study recruited older patients aged ≥ 75 years with NSTEACS undergoing virtual-histology intravascular ultrasound (VH-IVUS) imaging from the Improve Clinical Outcomes in high-risk patieNts with acute coronary syndrome (ICON-1). Primary endpoint was the composite of major adverse cardiovascular events (MACE) consisting of all-cause mortality, myocardial infarction (MI), and any revascularisation. Every component of MACE and target vessel failure (TVF) including MI and any revascularisation were considered as secondary endpoints.

Eighty-six patients with 225 vessels undergoing VH-IVUS at baseline completed 5-year clinical follow-up. Patients with minimal lumen area (MLA) ≤ 4 mm 2 demonstrated increased risk of MACE (hazard ratio [HR] 2.37, 95% confidence interval [CI] 1.00-5.59, p = 0.048) with a worse event-free survival (Log Rank 4.17, p = 0.041) than patients with MLA > 4 mm 2 . Patients with combination of TCFA, MLA ≤ 4 mm 2 and PB ≥ 70% showed high risk of MI (HR 5.23, 95% CI 1.05-25.9, p = 0.043). Lesions with MLA ≤ 4 mm 2 had 6-fold risk of TVF (HR 6.16, 95% CI 1.24-30.5, p = 0.026).

Small luminal area appears as the major prognostic factor in older patients with NSTEACS at long-term follow-up. Combination of TCFA, MLA ≤ 4 mm 2 and PB ≥ 70% was associated with high risk of MI.

NCT01933581.