LncRNA NEAT1/miR-211/IL-10 Axis Regulates Inflammation of Peripheral Blood Mononuclear Cells in Acute Myocardial Infarction.

This study aimed to explore the expression of long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) in patients with acute myocardial infarction (AMI) and its inflammatory regulation mechanism through miR-211/interleukin 10 (IL-10) axis.A total of 75 participants were enrolled in this study: 25 healthy people in the control group, 25 patients with stable angina pectoris (SAP) in the SAP group, and 25 patients with AMI in the AMI group. Real-time qPCR was used to detect mRNA expression levels of NEAT1, miR-211, and IL-10. The interaction between miR-211, NEAT1, and IL-10 was confirmed by dual-luciferase reporter assay, and protein expression was detected using western blot.High expression of NEAT1 in peripheral blood mononuclear cells (PBMCs) of patients with AMI was negatively related to serum creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), IL-6, and IL-1ß and was positively correlated with left ventricular ejection fraction (LVEF). In THP-1 cells, miR-211 was confirmed to target and inhibit IL-10 expression. NEAT1 knockdown and miR-211-mimic markedly decreased IL-10 protein levels, whereas anti-miR-211 markedly increased IL-10 protein levels. Importantly, miR-211 level was negatively related to NEAT1 and IL-10 levels, whereas IL-10 level was positively related to the level of NEAT1 expression in PBMCs of patients with AMI.LncRNA NEAT1 was highly expressed in PBMCs of patients with AMI, and NEAT1 suppressed inflammation via miR-211/IL-10 axis in PBMCs of patients with AMI.

Role of Bone Morphogenetic Protein 4 in the Inflammation of the Myocardium and Vascular Tissue of Obese Mice.

ABSTRACT: Bone morphogenetic protein 4 (BMP4) is a proinflammatory factor. The expression of BMP4 is reduced in the adipose and enhanced in the myocardium and vascular during obesity. It is possibly involved in the process of inflammatory response of the myocardium and vascular. Obesity, often regarded as a risk factor for cardiovascular diseases, is a kind of inflammatory response. This study aimed to investigate the relationship of BMP4 with obesity and cardiovascular disease. Ob/ob mice were used as the experimental group, and C57BL/6 mice were used as the control group. The two groups were further divided into 2 subgroups based on the mice carrying adenovirus-encoding shRNA for BMP4 or Lac Z genes. The messenger RNA and protein levels of BMP4, interleukin-1ß, and interleukin-9 were significantly higher in the myocardial tissue and aorta of ob/ob+ Lac Z shRNA than those in the other 3 groups, whereas the levels in the ob/ob+ BMP4 shRNA group were significantly decreased and comparable with those in the control groups. BMP4 is significantly upregulated in the myocardial tissue and aorta of obese mice, and this suggests that BMP4 is an risk factor involved in the local inflammatory response.

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.

Effects of Melatonin for Delirium in Elderly Acute Heart Failure Patients: A Randomized, Single-Center, Double-Blind, and Placebo-Controlled Trial.

BACKGROUND: Delirium is a common, life-threatening, typical clinical syndrome with the main clinical manifestations of temporary organic mental disorder without specific drug treatment. The aim of the study was to explore the benefits of melatonin for the treatment of delirium after acute heart failure in elderly patients. METHODS: This was a randomized, double-blind, and placebo-controlled trial. This study enrolled patients aged more than 60 years after acute heart failure. A computer-generated randomization sequence (in a 1:1 ratio) was used to randomly assign patients to receive either melatonin (3 mg/day, 7 days) or placebos. The primary endpoint was the incidence of delirium, assessed twice daily with the Confusion Assessment Method during the first 7 days. Analyses were performed by intention-to-treat and safety populations. RESULTS: Between October 2015 and October 2019, 584 patients were assessed. A total of 497 patients randomly were assigned to receive either placebo (N = 249) or melatonin (N = 248). The incidence of delirium was significantly lower in the melatonin group than in the placebo group (27.0% vs. 36.9%, P = 0.021). Regarding safety, the occurrence of rhabdomyolysis and abnormal hepatic function did not differ between the two groups. CONCLUSION: The current study (clinical trial registered number: CHWX-904-201511) suggests that acute melatonin treatment can reduce the incidence of delirium for elderly acute heart failure. It also can reduce the time of hospital stays and hospitalization costs. The therapy was safe and worth spreading.

Angiotensin II-C-C chemokine receptor2/5 axis-dependent monocyte/macrophage recruitment contributes to progression of experimental autoimmune myocarditis.

Angiotensin II (ANG II) plays critical roles in modulation of circulatory homeostasis and activation of innate and adaptive immunity and has also been implicated in several mouse models of autoimmune disease. However, how ANG II regulates macrophages and is involved in development of experimental autoimmune myocarditis (EAM) remains unclear. Therefore, the present study aimed to address the above question and explore possible mechanisms. EAM was induced in BALB/c mice. ANG II was quantitated by ELISA and hematoxylin and eosin staining was employed to analyze pathological changes and macrophage infiltration. The chemotactic ability of ANG II was assessed by using a Transwell system. It was found that ANG II is up-regulated in serum and heart tissues of mice with EAM and that ANG II significantly drives monocyte/macrophage infiltration through the C-C chemokine receptor 2/5 (CCR2/5) axis. CCR2/5 antagonists and ANG II receptor inhibitor could all abrogate monocyte/macrophage infiltration and ameliorate development of EAM. Our results have firstly identified a novel function of ANG II: that it is a critical chemokine for monocyte/macrophage recruitment. Furthermore, our results indicate that ANG II is a potential candidate for treatment of inflammatory diseases.

Relationship between the lymphocyte to C­reactive protein ratio and coronary artery disease severity.

Coronary atherosclerosis is a chronic systemic inflammatory disease. Laboratory parameters such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and systemic immune inflammation index (SII) have been used to assess inflammation degree and coronary artery disease (CAD) severity. The lymphocyte-to-C-reactive protein ratio (LCR) is a new SII. However, its relationship with CAD development and severity is unclear. A total of 1,107 patients (479 in control group, 628 in CAD group) underwent coronary angiography. The routine and biochemical indices of the venous blood of patients were assessed before coronary angiography. LCR, SII, NLR and PLR were calculated and statistical analyses were performed. Propensity score matching (PSM) and a logistic regression model were used to analyze the relationship between LCR and CAD. After the PSM, 384 pairs of patients with or without CAD were successfully matched. After the median binary classification of all indicators, uni- and multivariate logistic regression analyses showed that platelet count was an independent risk factor and LCR was an independent protective factor. Using the same method, in the coronary heart disease severity group, 212 pairs were successfully matched and NLR and PLR were independent risk factors, while LCR was an independent protective factor. In conclusion, LCR is an independent protective factor against CAD development and severity.

Significance of Multiple Lymphocyte-to-C-Reactive Protein Ratios in Predicting Long-Term Major Cardiovascular Adverse Events in Emergency Percutaneous Coronary Intervention Patients with ST-Segment Elevation Myocardial Infarction.

Aim: The high morbidity and mortality associated with ST-segment elevation myocardial infarction (STEMI) are an urgent concern. This study aimed to investigate the ratio of lymphocyte count to C-reactive protein ratio (LCR) in multiple measurements in the perioperative period, exploring dynamic changes as the best predictor of major adverse cardiovascular events (MACE) in STEMI patients. Methods: We enrolled 205 STEMI patients, conducting blood counts at admission, 24 hours post-percutaneous coronary intervention (PCI), and at discharge. Cox proportional risk models evaluated factors independently associated with STEMI prognosis. The receiver operating characteristic (ROC) curve and the De-Long test determined the best predictor. Kaplan-Meier analysis assessed the prognostic value of LCR for STEMI patients. Statistical differences and correlations between LCR at 24 hours post-PCI and cardiovascular disease risk factors were also analyzed. Results: Gensini score (HR, 1.015; 95% CI, 1.007-1.022; P < 0.001), total stent length (HR, 1.015; 95% CI, 1.002-1.029; P=0.025), lipoprotein (a) (HR, 1.001; 95% CI, 1.000-1.002; P=0.043), LCR at admission (HR, 0.995; 95% CI, 0.989-1.000; P=0.002), and LCR at 24 hours post-PCI (HR, 0.587; 95% CI, 0.486-0.708; P < 0.001) were independent risk factors for long-term STEMI prognosis after PCI. LCR at admission (cut-off value, 2.252; 95% CI, 0.040-0.768; P < 0.001) and LCR at 24 hours post-PCI (cut-off value, 2.252; 95% CI, 0.831-0.924; P < 0.001) effectively predicted MACEs occurrence, with the latter exhibiting a superior predictive effect (P<0.001). Kaplan-Meier analysis revealed that patients with LCR at admission ≤ 50.29 and LCR at 24 hours post-PCI ≤ 2.25 had significantly higher risks of developing MACEs (Log-rank P < 0.0001). Conclusion: LCR at 24 hours post-PCI may be a superior marker for long-term MACE prediction in STEMI patients, serving as the best predictor for distant MACE occurrence.

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.

Percutaneous valved stent implantation in the ascending aorta for the treatment of very high-risk aortic regurgitation: an animal study.

PURPOSE: We investigated the effects of percutaneous valved stent implantation in the ascending aorta as an alternative treatment for aortic regurgitation in a canine model. MATERIALS AND METHODS: A total of 16 healthy dogs weighing an average of 18.3 ± 2.1 kg were used for the establishment of animal models of chronic aortic regurgitation by percutaneous aortic valve perforation and balloon dilation. At 2 mo after successful model establishment, all experimental animals underwent valved stent implantation in the ascending aorta and then were followed up for 3 mo. RESULTS: Experimental models of chronic aortic regurgitation were successfully established in 10 dogs. Surviving dogs underwent successful valved stent implantation in the ascending aorta and were subsequently followed up for 3 mo. The level of instantaneous aortic regurgitation at 3-mo follow-up was significantly reduced compared with that before valved stent implantation (2.4 ± 0.9 versus 10.6 ± 2.1 mL/s, P < 0.05). The left ventricular ejection fraction was significantly increased (53.8 ± 4.2% versus 37.8 ± 3.7%, P < 0.05), and the left ventricular end-diastolic volume was also significantly reduced (30.3 ± 2.2 versus 40.1 ± 3.6 mL, P < 0.05). No paravalvular leak, stroke, atrioventricular block, or other complications occurred in dogs undergoing valved stent implantation. CONCLUSIONS: Percutaneous valved stent implantation in the ascending aorta is feasible, effective, and safe as an alternative treatment for very high-risk aortic regurgitation in a canine model.

[Serum parathyroid hormone levels predict hospitalization in outpatients of heart failure: a preliminary study].

OBJECTIVE: To evaluate the predicative value of serum parathyroid hormone (PTH) levels in outpatients of heart failure (HF) for hospitalization. METHODS: A total of 102 consecutive HF outpatients were enrolled. The receiver operating characteristic (ROC) curves demonstrated the optimal cut-off points of PTH levels for hospitalization due to HF. And Logistic regression analysis model was employed to analyze the independent association between PTH and hospitalization for HF. RESULTS: The more advanced grade of New York Heart Association (NYHA), the higher serum level of PTH. The ROC curves showed PTH levels ≥ 56.05 ng/L were the optimal cut-off point for hospitalization for HF with a sensitivity of 90.0%, a specificity of 89.2% and the area under ROC curve of 0.92. After adjustment for predictors for hospitalization due to HF (gender, age, diabetes mellitus, hypertension, left ventricular ejection fraction, estimated glomerular filtration rate and brain natriuretic peptide), PTH levels were associated with hospitalization due to HF (OR = 1.282, 95%CI 1.026-1.362). CONCLUSION: The serum level of PTH in HF outpatients is an independent predicator for hospitalization due to HF.

Preoperative lymphocyte to C-reactive protein ratio: A new prognostic indicator of post-primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction.

BACKGROUND: The lymphocyte-to-C-reactive protein ratio (LCR) is a novel inflammatory biomarker for many diseases. This study aimed to examine the association between LCR and major adverse cardiovascular events (MACEs) in patients with ST-segment elevation myocardial infarction (STEMI) who were undergoing percutaneous coronary intervention. METHODS: A total of 382 patients with STEMI were included in this study; these patients were enrolled from January 2014 to January 2016 at a single center, and the LCR was calculated for each patient. During the in-hospital and long-term follow-up period, MACEs included cardiovascular death, new-onset non-fatal myocardial infarction, heart failure, malignant arrhythmias, revascularization in unstable angina, and new-onset atrial fibrillation. Using receiver operating characteristic curves, we assessed the predictive impact for MACEs using a combination of six inflammatory markers in patients with STEMI and focused on LCR to elucidate its prognostic value. Univariate and multivariate Cox proportional hazard models were used to define the factors associated with MACEs. RESULTS: Among the assessed variables, preoperative LCR showed the highest accuracy in predicting hospitalized (AUC:0.71) and long-term follow-up(AUC:0.602) MACEs in patients with STEMI. Decreased preoperative LCR was significantly associated with the Gensini score (P < 0.05) and no-reflow (P < 0.05). Multivariate Cox analysis showed that a high preoperative LCR (cutoff threshold = 112.4) was an independent protective factor for hospitalized MACEs in patients with STEMI (hazard ratio, 0.409; 95 % confidence interval, 0.283-0.590; P < 0.001). A high preoperative LCR (cutoff threshold = 106.3) was an independent protective factor for long-term follow-up MACEs in patients with STEMI (hazard ratio, 0.552; 95 % confidence interval, 0.369-0.740; P < 0.001). CONCLUSION: Preoperative LCR is a novel and valuable prognostic marker to determine the occurrence of MACEs in hospitals and long-term follow-up after primary percutaneous coronary intervention in patients with STEMI.

Correlation Between GDF11 Serum Levels, Severity of Coronary Artery Lesions, and the Prognosis of Patients with ST-segment Elevation Myocardial Infarction.

We aimed to explore the correlation among serum GDF11, the severity of coronary artery lesions, and the prognosis of patients with ST-segment elevation myocardial infarction (STEMI). A total of 367 patients were enrolled and divided into control (n = 172) and STEMI (n = 195) groups. Serum GDF11 (P < 0.001) was an independent predictor of STEMI and was negatively correlated with SYNTAX score (P < 0.05). ROC curve analysis showed that serum GDF11 could screen patients for major adverse cardiovascular events (MACEs). KM curve analysis showed that patients with lower concentration of GDF11 had a higher incidence of MACEs, and Cox proportional hazards regression analysis showed that the serum GDF11 (P < 0.001) was an independent predictor of MACEs. Serum GDF11 was negatively correlated with the severity of coronary lesions and was also an independent prognostic indicator of MACEs in patients with STEMI.

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.

Corrigendum: A nomogram risk prediction model for no-reflow after primary percutaneous coronary intervention based on rapidly accessible patient data among patients with ST-segment elevation myocardial infarction and its relationship with prognosis.

[This corrects the article DOI: 10.3389/fcvm.2022.966299.].

Slow-Reflow and Prognosis in Patients with High Parathyroid Hormone Levels Undergoing Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction.

We aimed to evaluate the correlation among serum parathyroid hormone (PTH) and slow-reflow during primary percutaneous coronary intervention (PCI) and prognosis in patients with ST-segment elevation myocardial infarction (STEMI). A total of 262 patients were enrolled and divided into a slow-reflow group (n = 61) and a control group (n = 201). PTH was an independent risk factor for slow-reflow (P < 0.05), and the regression model had good discrimination and calibration. ROC curve analysis showed that PTH (≥ 63.65 pg/ml) had a predictive value for slow-reflow (P < 0.001). During the 1-year follow-up, the patients were divided into a PTH-h group (≥ 63.65 pg/ml, n = 100) and a PTH-l group (< 63.65 pg/ml, n = 162). Readmission for HF was independently associated with PTH levels (P < 0.05). KM survival analysis suggested that PTH-h had a predictive value for MACEs, especially for readmission for HF (P < 0.05). PTH levels were associated with slow-reflow during PCI and MACEs during follow-up in patients with STEMI.

PTH Predicts the in-Hospital MACE After Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction.

Objective: To investigate the correlation between serum parathyroid hormone (PTH) levels and in-hospital major adverse cardiovascular events (MACE) in patients with acute ST-segment elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI), and establish a risk prediction model based on parameters such as PTH for in-hospital MACE. Methods: This observational retrospective study consecutively enrolled 340 patients who underwent primary PCI for STEMI between January 2016 and December 2020, divided into a MACE group (n=92) and a control group (n=248). The least absolute shrinkage and selection operator (LASSO) and logistic regression analyses were used to determine the risk factors for MACE after primary PCI. The rms package in R-studio statistical software was used to construct a nomogram, to detect the line chart C-index, and to draw a calibration curve. The decision curve analysis (DCA) method was used to evaluate the clinical application value and net benefit. Results: Correlation analysis revealed that PTH level positively correlated with the occurrence of in-hospital MACE. Receiver operating characteristic curve analyses revealed that PTH had a good predictive value for in-hospital MACE. Multivariate logistic regression analysis indicated that Killip class II-IV, and FBG were independently associated with in-hospital MACE after primary PCI. A nomogram model was constructed using the above parameters. The model C-index was 0.894 and the calibration curve indicated that the model was well calibrated. The DCA curve suggested that the nomogram model was better than TIMI score model in terms of net clinical benefit. Conclusion: Serum PTH levels in patients with STEMI are associated with in-hospital MACE after primary PCI, and the nomogram risk prediction model based on PTH demonstrated good predictive ability with obvious clinical practical value.

A nomogram risk prediction model for no-reflow after primary percutaneous coronary intervention based on rapidly accessible patient data among patients with ST-segment elevation myocardial infarction and its relationship with prognosis.

Background: No-reflow occurring after primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) can increase the incidence of major adverse cardiovascular events (MACE). The present study aimed to construct a nomogram prediction model that can be quickly referred to before surgery to predict the risk for no-reflow after PCI in STEMI patients, and to further explore its prognostic utility in this patient population. Methods: Research subjects included 443 STEMI patients who underwent primary PCI between February 2018 and February 2021. Rapidly available clinical data obtained from emergency admissions were collected. Independent risk factors for no-reflow were analyzed using a multivariate logistic regression model. Subsequently, a nomogram for no-reflow was constructed and verified using bootstrap resampling. A receiver operating characteristic (ROC) curve was plotted to evaluate the discrimination ability of the nomogram model and a calibration curve was used to assess the concentricity between the model probability curve and ideal curve. Finally, the clinical utility of the model was evaluated using decision curve analysis. Results: The incidence of no-reflow was 18% among patients with STEMI. Killip class ≥2 on admission, pre-operative D-dimer and fibrinogen levels, and systemic immune-inflammation index (SII) were independent risk factors for no-reflow. A simple and quickly accessible prediction nomogram for no-reflow after PCI was developed. This nomogram demonstrated good discrimination, with an area under the ROC curve of 0.716. This nomogram was further validated using bootstrapping with 1,000 repetitions; the C-index of the bootstrap model was 0.706. Decision curve analysis revealed that this model demonstrated good fit and calibration and positive net benefits. Kaplan-Meier survival curve analysis revealed that patients with higher model scores were at a higher risk of MACE. Multivariate Cox regression analysis revealed that higher model score(s) was an independent predictor of MACE (hazard ratio 2.062; P = 0.004). Conclusions: A nomogram prediction model that can be quickly referred to before surgery to predict the risk for no-reflow after PCI in STEMI patients was constructed. This novel nomogram may be useful in identifying STEMI patients at higher risk for no-reflow and may predict prognosis in this patient population.

Percutaneous valved stent implantation above the coronary ostia.

BACKGROUND: In recent years, some experimental and clinical studies on transcatheter aortic valve implantation (TAVI) have been conducted. TAVI is indicated in patients with calcified pure or predominant aortic stenosis. The risk of this technique is still high. Aortic valved stent implantation above the coronary ostia might avoid blocking the coronary ostia. METHODS AND RESULTS: Twenty healthy dogs were selected to establish a canine model of acute aortic valve rupture. The dogs were randomly divided into 2 groups: the rupture model group without any treatment and the valved stent group with percutaneous valved stent implantation above the coronary ostia. The 2 groups of animals were followed up for 3 months. Echocardiography and other tests were performed to assess aortic regurgitation and ventricular function. Acute aortic valve rupture models were successfully established in 16 of 20 dogs. In the rupture model group, the mean aortic regurgitation was 6.8 ± 1.9 ml/s; only 3 of 8 animals survived for 3 months. In the valved stent group, the mean aortic regurgitation was 7.0 ± 2.1 ml/s; valved stents were successfully implanted in 8 animals. Instant post-implantation anatomy showed that the stents were located appropriately. Seven dogs survived for 3 months. CONCLUSIONS: Percutaneous valved stent implantation above the coronary ostia is feasible and effective as a transitional treatment for acute aortic valve rupture.

[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.