The value of D-dimer to lymphocyte ratio in predicting clinical outcomes after percutaneous coronary intervention in ST-segment elevation myocardial infarction patients: A retrospective study.

BACKGROUND: D-dimer to lymphocyte ratio (DLR) is a novel composite metric. This study investigated the association between DLR and major adverse cardiovascular events (MACEs) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention. MATERIALS AND METHODS: This retrospective study included 683 STEMI cases treated between January 2018 and June 2021 at a single center. DLR was calculated for each patient. Receiver operating characteristic curves assessed the predictive value of in-hospital and long-term MACEs, with calculated AUC. Based on the optimal DLR cutoff value, the population was categorized into groups for clinical characteristic analysis. Multivariate logistic and COX regression analyses determined factors independently associated with MACEs. Kaplan-Meier estimation method and log-rank tests assessed event-free survival among different DLR groups. Spearman's test explored the correlation between DLR and Gensini score. RESULTS: DLR demonstrated an AUC of 0.792 for predicting in-hospital MACEs and 0.708 for long-term MACEs in patients with STEMI. Multivariate logistic regression analysis revealed that a high DLR (cutoff value, 0.47) independently increased the risk of MACEs during hospitalization in patients with STEMI (P = 0.003; odds ratio: 3.015; 95 % CI: 1.438-6.321). Multivariate COX regression showed that a high DLR (cutoff value, 0.34) independently predicted MACEs during long-term follow-up in patients with STEMI (P = 0.011; hazard ratio: 1.724; 95 % CI: 1.135-2.619). Furthermore, DLR exhibited a positive correlation with the Gensini score (P < 0.001). CONCLUSIONS: DLR is a valuable predictor for MACEs occurrence in patients with STEMI during hospitalization and long-term follow-up after PCI.

Association of Systemic Inflammatory Response Index and Pan-Immune-Inflammation-Value with Long-Term Adverse Cardiovascular Events in ST-Segment Elevation Myocardial Infarction Patients After Primary Percutaneous Coronary Intervention.

Aim: Reducing the high morbidity and mortality of ST-segment elevation myocardial infarction (STEMI) and improving patient prognosis remains a major global challenge. This study aimed to explore whether dynamic fluctuations in biomarkers are valuable predictors of prognosis in patients with STEMI. Methods: This study included 216 patients with STEMI. Blood routine tests were performed on admission, 12 h after percutaneous coronary intervention (PCI), and at discharge. Systemic immune-inflammation index (SII), systemic inflammatory response index (SIRI), and pan-immune-inflammation-value (PIV) serum immune-inflammatory markers were calculated. The Cox proportional hazard model was used to assess the factors independently associated with the prognosis of STEMI. The optimal cutoff values for the inflammatory markers were calculated. Results: Eighty-five (39.35%) of the 216 patients had major adverse cardiovascular events (MACEs) during the 1-year follow-up. Most were male (81.18%) with a median age of 64 years (interquartile, 55-69.5). Killip class ≥ II on admission (hazard ratio [HR], 1.859; 95% CI, 1.169-2.957; P = 0.009), total stent length (HR, 1.016; 95% CI, 1.003-1.029; P = 0.019), values of SIRI at 12 h after PCI (HR, 1.079; 95% CI, 1.050-1.108; P < 0.001), and the Gensini score (HR, 1.014; 95% CI, 1.007-1.022; P < 0.001) were independently associated with an increased risk of MACEs. Compared with SII, SIRI and PIV calculated at various time points and dynamically fluctuating changes, SIRI (cutoff value, 4.15; 95% CI, 0.701-0.819; P < 0.001) and PIV (cutoff value, 622.71; 95% CI, 0.674-0.796; P < 0.001) at 12 h after PCI showed the best efficacy for the prognosis of STEMI. Conclusion: Our study provides relevant evidence to the notion that SIRI or PIV at 12 h after PCI may be more accurate and economical predictors of long-term adverse prognosis in patients with STEMI.

GDF11 Is a Novel Protective Factor Against Vascular Calcification.

ABSTRACT: Vascular calcification (VC) occurs via an active cell-mediated process, which involves osteogenic differentiation, apoptosis, and phenotypic transformation of vascular smooth muscle cells (VSMCs). As a member of the transforming growth factor-ß family, growth differentiation factor 11 (GDF11) can inhibit apoptosis and osteogenic differentiation and maintain the stability of atherosclerotic plaques. In this study, coronary artery calcium score (CACS) of participants with GDF11 measurements was measured using computed tomography angiography and was scored according to the Agatston score. ß-glycerophosphate (10 mM), dexamethasone (100 nM), and l -ascorbic acid (50 µg/mL) [osteogenic medium (OM)] were used to induce calcification of human aortic smooth muscle cells. We found that CACS was negatively correlated with serum GDF11 levels in patients and GDF11 was a strong predictor of elevated CACS (OR = 0.967, 95% CI: 0.945-0.991; P = 0.006), followed by age (OR = 1.151, 95% CI: 1.029-1.286; P = 0.014), triglycerides (OR = 4.743, 95% CI: 1.170-19.236; P = 0.029), C-reactive protein (OR = 1.230, 95% CI: 1.010-1.498; P = 0.04), and hypertension (OR = 7.264, 95% CI: 1.099-48.002; P = 0.04). Furthermore, exogenous GDF11 inhibited OM-induced calcification by inhibiting osteogenic differentiation, the phenotypic transformation and apoptosis of human aortic smooth muscle cells. Our study demonstrates that GDF11 plays a crucial role in reducing vascular calcification and serves as a potential intervention target to vascular calcification.

CircSamd4: A novel biomarker for predicting vascular calcification.

BACKGROUND: Vascular calcification (VC) is usually associated with cardiovascular diseases (CVDs), which are one of the main causes of mortality in the world. This study aimed to analyze the expression of circular RNAs (circRNAs) in patients with VC and to evaluate biomarkers for the diagnosis of VC. METHODS: Calcified human aortic endothelial cells (HAECs) and the calcification in mouse aorta were detected by qRT-PCR. Subsequently, this was verified in the plasma of patients with coronary artery calcification (CAC). The plasma of 40 patients in the control group and 31 patients in the calcified group were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) to detect the level of circSamd4a in the blood. The diagnostic value was evaluated by logistic regression analysis and the working characteristics of subjects. RESULTS: In the HAECs, the qRT-PCR showed a significant decrease in the level of circSamd4a expression in the calcification group compared to the control group (p < 0.05). The calcified mouse aorta showed the same trend for circSamd4a expression, wherein the difference was statistically significant (p < 0.05); the expression of circSamd4a was significantly downregulated in the plasma of patients with VC (p < 0.01). The receiver operating characteristic (ROC) curves of circSamd4a in patients with VC and control group showed that the area under the curve (AUC) was 0.81 (95% CI: 0.707-0.913; p < 0.001). CONCLUSION: CircSamd4a showed a stable downward trend in different specimens, and had significant advantages as a biomarker for diagnosis of VC.

[Knockdown of PCSK9 inhibits endothelial-to-mesenchymal transition of human aortic endothelial cells].

Objective To investigate the protective effect of proprotein convertase subtilisin/kexin type 9 (PCSK9) knockdown on endothelial-to-mesenchymal transition (EndoMT) induced by ß glycerophosphate, dexamethasone, and L-ascorbic acid in human aortic endothelial cells (HAECs). Methods EndoMT model was established by inducing HAECs with (0, 10, 30, 50) mmol/L of ß glycerophosphate combined with 100 nmol/L of dexamethasone and 50 µg/mL of L-ascorbic acid. HAECs were transfected with specific small interfering RNA of PCSK9 (si-PCSK9), and the mRNA and protein expression levels of PCSK9 in HAECs were detected by real-time quantitative PCR and Western blotting. HAECs were randomized into blank group, EndoMT group, EndoMT group transfected with negative control small interfering RNA (si-NC), and EndoMT group transfected with si-PCSK9. The mRNA levels of α-smooth muscle actin (α-SMA), fibroblast-specific protein 1 (FSP1), and vascular endothelial cadherin (VE-cadherin) were detected by real-time quantitative PCR, the protein levels of α-SMA and VE-cadherin were detected by Western blotting, and the expression of α-SMA was detected by immunofluorescence staining. Results 30 mmol/L of ß glycerophosphate had the best effect in inducing EndoMT, and the expression of PCSK9 mRNA and protein was up-regulated when EndoMT occurred. After PCSK9 knockdown, the expressions of α-SMA and FSP1 were down-regulated, while the expression of VE cadherin was up-regulated. Conclusion Knockdown of PCSK9 inhibits the EndoMT of HAECs.

Systemic immune-inflammation index predicts the severity of coronary stenosis in patients with coronary heart disease.

BACKGROUND: Coronary atherosclerosis is a systemic chronic inflammatory disease with variable occurrence and progression. Some laboratory parameters, such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and C-reactive protein (CRP) level, are used to evaluate the degree of inflammation and the severity of coronary artery disease (CAD). The neutrophil*platelet/lymphocyte is a novel systemic immune-inflammation index (SII), and its relationship with the development and severity of CAD is unclear. OBJECTIVE: To investigate the association between the SII and the severity of CAD. METHODS: Three-hundred and ninety-five patients who underwent coronary angiography were enrolled; among whom, 285 patients were included in the CAD group and 110 patients were included in the non-CAD group according to the WHO guidelines. Patients with CAD were further divided according to the Gensini score into the severe coronary stenosis group and the mild coronary stenosis group. The SII was calculated using the following formula: neutrophil*platelet/lymphocyte. RESULTS: When the cutoff value of the SII was set at 439.44, the predictive power of CAD was the highest, with a sensitivity and specificity of 64.6 and 68.2%, respectively. When the cutoff value of the SII was set at 652.83, the predictive power of severe coronary stenosis was the highest, with a sensitivity and specificity of 71.0 and 86.0%, respectively. The area under the curve of the SII in predicting severe coronary stenosis was greater than that of the NLR, PLR and CRP level. CONCLUSION: The SII is an independent risk factor for the occurrence and severity of CAD.