Impact of serum iron levels on in-hospital mortality and clinical outcomes in patients with ST segment elevation myocardial infarction undergoing emergency percutaneous coronary intervention: a retrospective analysis.

BACKGROUND: Despite advances in percutaneous coronary intervention (PCI) for ST segment elevation myocardial infarction (STEMI), in-hospital mortality remains a concern, highlighting the need for the identification of additional risk factors such as serum iron levels. OBJECTIVE: This study aims to assess the relationship between serum iron levels and in-hospital mortality among patients with STEMI undergoing emergency PCI. METHODS: A total of 685 patients diagnosed with STEMI, treated with emergency PCI between January 2020 and June 2023, were included in this retrospective observational study. Participants were categorized based on serum iron levels into a low serum iron group (Fe <7.8 µmol/L) and a control group (Fe ≥7.8 µmol/L). Clinical and biochemical variables were compared between the groups. Univariate and multivariate logistic regression analyses were performed to identify independent risk factors for in-hospital mortality. RESULTS: The low serum iron group demonstrated significantly higher in-hospital mortality rates (9.3 vs. 1.0%, P < 0.05) compared with the control group. Multivariate logistic regression revealed that a left ventricular ejection fraction less than 40% upon admission [odds ratio (OR), 8.01; 95% confidence interval (CI), 1.230-52.173; P = 0.029], the occurrence of no-reflow during PCI (OR, 7.13; 95% CI, 1.311-38.784; P = 0.023), and serum iron levels below 7.8 µmol/L (OR, 11.32; 95% CI, 2.345-54.640; P = 0.003) were independent risk factors for in-hospital mortality. CONCLUSION: Low serum iron levels are associated with increased in-hospital mortality in patients with STEMI undergoing emergency PCI. Serum iron levels may serve as an independent prognostic marker and could inform risk stratification and therapeutic targeting in this patient population.

Predictive value of the neutrophil percentage-to-albumin ratio for coronary atherosclerosis severity in patients with CKD.

BACKGROUND: The neutrophil percentage-to-albumin ratio (NPAR), which is defined as the percentage of neutrophils divided by the concentration of albumin, is a cost-effective and readily available biomarker of inflammation. This study aimed to evaluate the association between the NPAR and the severity of coronary atherosclerosis in patients with chronic kidney disease (CKD). METHODS: A total of 280 CKD patients who underwent coronary angiography were retrospectively enrolled in this study. The severity of coronary atherosclerosis was evaluated using the Gensini score (GS). Patients were divided into low-, medium- and high-NPAR groups according to the tertiles of the NPAR values. Logistic regression analysis was conducted to analyze the relationship between the NPAR and the GS. The cutoff points for the sensitivity and specificity of the NPAR in predicting the GS were estimated via receiver operating characteristic (ROC) analysis. RESULTS: There was a higher prevalence of coronary artery disease (CAD) among CKD patients with higher NPARs (P =0.041). More patients in the high-NPAR group had complex CAD (triple-vessel disease and/or left main coronary artery stenosis) and chronic total occlusion lesions, and more of these patients required revascularization therapy (P<0.05). Multivariate logistic regression analysis revealed a significant positive correlation between the NPAR and the severity of coronary stenosis (adjusted OR 2.68, 95% CI 1.25-5.76, p=0.012), particularly among female and older (age ≥65) patients. The ROC analysis indicated that the optimal cutoff value for the NPAR in predicting severe coronary artery stenosis (GS>60) in CKD patients was 1.91 (sensitivity 0.495, specificity 0.749), with an area under the curve (AUC) of 0.650 (95% CI 0.581-0.719, P<0.001). A subgroup analysis according to sex revealed that the NPAR exhibited stronger predictive value in female patients (AUC 0.730, 95% CI 0.643-0.817) than in male patients (AUC 0.565, 95% CI 0.460-0.670) (P<0.001), and the optimal cutoff value for the NPAR in female patients was 1.80 (sensitivity 0.667, specificity 0.705). CONCLUSIONS: Our study demonstrated that the NPAR is independently associated with the severity of coronary atherosclerosis in CKD patients, especially in female and elderly patients (≥65 years old). Moreover, the NPAR can effectively predict the severity of coronary atherosclerosis, exhibiting greater predictive value in females than in males.

The Relationship and Clinical Significance of Hepc-20, LpPLA2, PTX3, and Acute Myocardial Infarction in Patients with Varying Degrees of Coronary Artery Disease.

Objective: This study aimed to investigate the association between hepcidin-20 (Hepc-20), lipoprotein-associated phospholipase A2 (LpPLA2), pentraxin 3 (PTX3), acute myocardial infarction (AMI) occurrence, the severity of coronary artery lesions, and their predictive effectiveness. Methods: A total of 100 patients diagnosed and treated for AMI at our hospital between January 2021 and January 2022 were included in the AMI group. Based on the severity of coronary artery lesions determined by the Gensini score, patients were divided into the mild group and the moderate-to-severe group. Additionally, 100 healthy individuals were selected as control samples and included in the normal group. Serum levels of Hepc-20, LpPLA2, and PTX3 were compared, and receiver operating characteristic curves (ROC curves) were constructed to analyze the predictive efficacy of these biomarkers for AMI occurrence and the degree of coronary artery disease. Results: Compared to the normal group, the AMI group exhibited significantly increased serum levels of Hepc-20, LpPLA2, and PTX3 (P < .05). The sensitivity and specificity of serum Hepc-20, LpPLA2, and PTX3 in predicting AMI occurrence and the severity of coronary artery lesions were >60.00%, and the Area Under Curve (AUC) was >0.70. Moreover, compared to the mild group, the moderate-to-severe group showed significantly higher serum levels of Hepc-20, LpPLA2, and PTX3 (P < .05). Hepc-20, LpPLA2, and PTX3 demonstrated positive correlations with the severity of coronary artery lesions (P < .05). Conclusions: The levels of Hepc-20, LpPLA2, and PTX3 are elevated abnormally in AMI patients and positively associated with the degree of coronary artery disease. Hepc-20, LpPLA2, and PTX3 have the potential to serve as sensitive and accurate predictors of AMI occurrence and the severity of coronary artery disease, thereby warranting their clinical application.

The predictive value of the nomogram model of clinical risk factors for ischemia-reperfusion injury after primary percutaneous coronary intervention.

Ischemia-reperfusion injury is a risk factor for poor clinical prognosis in patients with ST-segment elevation myocardial infarction (STEMI). However, due to the inability to predict the risk of its occurrence early, the effect of intervention measures is still being determined. This study intends to construct a nomogram prediction model and evaluate its value in predicting the risk of ischemia-reperfusion injury (IRI) after primary percutaneous coronary intervention (PCI). The clinical admission data of 386 STEMI patients who underwent primary PCI were retrospectively analyzed. According to the degree of ST-segment resolution (STR), the patients were divided into the STR < 70% group (n = 197) and the STR > 70 group (n = 187). The least absolute shrinkage and selection operator (LASSO) regression method was used to screen out IRI's admission-related clinical risk factors. The R language software was used to construct and verify the IRI nomogram prediction model based on the above indicators. The peak troponin level and the incidence of in-hospital death in the STR < 70% group were significantly higher than those in the STR > 70% group (p < 0.01), and the left ventricular ejection fraction was significantly lower than that in the STR > 70% group (p < 0.01). Combined with the results of LASSO regression and receiver operating characteristic curve comparison analysis, we constructed a six-dimensional nomogram predictive model: hypertension, anterior myocardial infarction, culprit vessel, proximal occlusion, C-reactive protein (CRP) > 3.85 mg/L, white blood cell count, neutrophil cell count, and lymphocyte count. The area under the nomogram's receiver operating characteristic (ROC) curve was 0.779. The clinical decision curve found that the nomogram had good clinical applicability when the occurrence probability of IRI was between 0.23 and 0.95. The nomogram prediction model constructed based on six clinical factors at admission has good prediction efficiency and clinical applicability regarding the risk of IRI after primary PCI in patients with acute myocardial infarction.

Effects of Doxorubicin on Heme Biosynthesis and Metabolism in Cardiomyocyte. / Os Efeitos da Doxorrubicina na Biossíntese e no Metabolismo do Heme em Cardiomiócitos.

BACKGROUND: Doxorubicin is associated with cardiotoxicity and late cardiac morbidity. Heme is related to cellular oxidative stress. However, its specific regulation in cardiomyocytes under doxorubicin effects has not yet been documented. OBJECTIVE: This study seeks to evaluate the changing profiles of rate-limiting enzymes in the heme metabolism pathway under the effect of doxorubicin. METHODS: H9c2 cardiomyocytes were incubated with doxorubicin at different concentrations (1,2,5,10µM respectively). The real-time PCR and Western Blot were used to determine the mRNA and protein expression for four pivotal enzymes (ALAS1, ALAS2, HOX-1, and HOX-2) regulating cellular heme metabolism, as well as the levels of heme were detected by ELISA. p<0.01 was considered significant. RESULTS: This study observed a dose-dependent changing pattern in heme levels in H9c2 cells with the highest level at the 5µM concentration for doxorubicin, which occurred synchronously with the highest upregulation level of ALAS1, as well as the degradative enzymes, HOX-1, and HOX-2 in mRNA and protein expression. By contrast, ALAS2, contrary to the increasing concentrations of doxorubicin, was found to be progressively down-regulated. CONCLUSION: The increase in ALAS1 expression may play a potential role in the heme level elevation when H9c2 cardiomyocyte was exposed to doxorubicin and may be a potential therapeutic target for doxorubicin-induced myocardial toxicity. (Arq Bras Cardiol. 2021; 116(2):315-322).

FUNDAMENTO: A doxorrubicina está associada à cardiotoxicidade e à morbidade cardíaca tardia. O heme está relacionado ao stress oxidativo celular. Entretanto, sua regulação específica em cardiomiócitos sob os efeitos de doxorrubicina ainda não foi documentada. OBJETIVO: Nosso objetivo é avaliar as alterações de enzimas limitantes de velocidade no caminho metabólico do heme sob o efeito de doxorrubicina. MÉTODOS: Cardiomiócitos H9c2 com doxorrubicina em concentrações diferentes (1, 2, 5, 10µM respectivamente). Os testes de PCR em tempo real e Western Blot foram usados para determinar a expressão de proteína e mRNA para quatro enzimas cruciais (ALAS1, ALAS2, HOX-1, e HOX-2) que regulam o metabolismo do heme celular, e os níveis de heme foram detectados por ELISA. Um p<0,01 foi considerado significativo. RESULTADOS: Observamos um padrão com alteração dependendo da dose nos níveis de heme nas células H9c2 com o nível mais alto na concentração de 5µM de doxorrubicina, o que ocorreu sincronicamente com o nível mais alto de regulação para cima de ALAS1, bem como as enzimas degenerativas HOX-1 e HOX-2 na expressão de proteína e mRNA. Em contraste, observamos que a ALAS2 foi regulada para baixo gradualmente, inversamente proporcional às concentrações de doxorrubicina. CONCLUSÃO: O aumento da expressão de ALAS1 pode ter um papel na elevação do nível do heme quando o cardiomiócito H9c2 for exposto à doxorrubicina, e pode ser um alvo terapêutico para a toxicidade miocárdica induzida por doxorrubicina. (Arq Bras Cardiol. 2021; 116(2):315-322).

Schizandrin B attenuates hypoxia/reoxygenation injury in H9c2 cells by activating the AMPK/Nrf2 signaling pathway.

Schizandrin B exhibits prominent antioxidant and anti-inflammatory effects, and plays an important role in ameliorating myocardial ischemia/reperfusion injury. However, the underlying protective mechanisms remain to be elucidated. The aim of the present study was to explore the cardioprotective effects of schizandrin B against hypoxia/reoxygenation (H/R)-induced H9c2 cell injury, focusing on the role of the adenosine monophosphate-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in this process. The results showed that schizandrin B attenuated the H/R-induced decrease in cell viability and the increase in lactate dehydrogenase release, as well as the apoptosis rate in H9c2 cells. Schizandrin B also mitigated H/R-induced oxidative stress, as illustrated by the decrease in intracellular reactive oxygen species generation, malondialdehyde content and NADPH oxidase 2 expression, and the increase in antioxidant enzyme superoxide dismutase and glutathione peroxidase activities. In addition, schizandrin B reversed the H/R-induced upregulation of pro-inflammatory cytokines [interleukin (IL)-1ß (IL-1ß) tumor necrosis factor-α, IL-6 and IL-8] and the downregulation of anti-inflammatory cytokines (transforming growth factor-ß and IL-10) in the culture supernatant. Notably, schizandrin B increased the expression of Nrf2, NAD(P)H: Quinone oxidoreductase (NQO-1) and heme oxygenase-1 (HO-1) in H/R-treated H9c2 cells, activating the Nrf2 signaling pathway. The cardioprotection of schizandrin B against H/R injury was inhibited by Nrf2 knockdown induced byNrf-2-specific small interfering RNA (siRNA; si-Nrf2) transfection. Furthermore, schizandrin B enhanced phosphorylated (p)-AMPK expression, while AMPK knockdown induced by AMPK-specific siRNA(si-AMPK) transfection remarkably eliminated schizandrin B-induced cardioprotection and reduced Nrf2 expression in H/R-treated H9c2 cells. Taken together, these results suggested that schizandrin B exerts cardioprotection on H/R injury in H9c2 cells due to its antioxidant and anti-inflammatory activities via activation of the AMPK/Nrf2 pathway.

Os Efeitos da Doxorrubicina na Biossíntese e no Metabolismo do Heme em Cardiomiócitos / Effects of Doxorubicin on Heme Biosynthesis and Metabolism in Cardiomyocyte

Resumo Fundamento A doxorrubicina está associada à cardiotoxicidade e à morbidade cardíaca tardia. O heme está relacionado ao stress oxidativo celular. Entretanto, sua regulação específica em cardiomiócitos sob os efeitos de doxorrubicina ainda não foi documentada. Objetivo Nosso objetivo é avaliar as alterações de enzimas limitantes de velocidade no caminho metabólico do heme sob o efeito de doxorrubicina. Métodos Cardiomiócitos H9c2 com doxorrubicina em concentrações diferentes (1, 2, 5, 10μM respectivamente). Os testes de PCR em tempo real e Western Blot foram usados para determinar a expressão de proteína e mRNA para quatro enzimas cruciais (ALAS1, ALAS2, HOX-1, e HOX-2) que regulam o metabolismo do heme celular, e os níveis de heme foram detectados por ELISA. Um p<0,01 foi considerado significativo. Resultados Observamos um padrão com alteração dependendo da dose nos níveis de heme nas células H9c2 com o nível mais alto na concentração de 5μM de doxorrubicina, o que ocorreu sincronicamente com o nível mais alto de regulação para cima de ALAS1, bem como as enzimas degenerativas HOX-1 e HOX-2 na expressão de proteína e mRNA. Em contraste, observamos que a ALAS2 foi regulada para baixo gradualmente, inversamente proporcional às concentrações de doxorrubicina. Conclusão O aumento da expressão de ALAS1 pode ter um papel na elevação do nível do heme quando o cardiomiócito H9c2 for exposto à doxorrubicina, e pode ser um alvo terapêutico para a toxicidade miocárdica induzida por doxorrubicina. (Arq Bras Cardiol. 2021; 116(2):315-322)

Abstract Background Doxorubicin is associated with cardiotoxicity and late cardiac morbidity. Heme is related to cellular oxidative stress. However, its specific regulation in cardiomyocytes under doxorubicin effects has not yet been documented. Objective This study seeks to evaluate the changing profiles of rate-limiting enzymes in the heme metabolism pathway under the effect of doxorubicin. Methods H9c2 cardiomyocytes were incubated with doxorubicin at different concentrations (1,2,5,10μM respectively). The real-time PCR and Western Blot were used to determine the mRNA and protein expression for four pivotal enzymes (ALAS1, ALAS2, HOX-1, and HOX-2) regulating cellular heme metabolism, as well as the levels of heme were detected by ELISA. p<0.01 was considered significant. Results This study observed a dose-dependent changing pattern in heme levels in H9c2 cells with the highest level at the 5μM concentration for doxorubicin, which occurred synchronously with the highest upregulation level of ALAS1, as well as the degradative enzymes, HOX-1, and HOX-2 in mRNA and protein expression. By contrast, ALAS2, contrary to the increasing concentrations of doxorubicin, was found to be progressively down-regulated. Conclusion The increase in ALAS1 expression may play a potential role in the heme level elevation when H9c2 cardiomyocyte was exposed to doxorubicin and may be a potential therapeutic target for doxorubicin-induced myocardial toxicity. (Arq Bras Cardiol. 2021; 116(2):315-322)

Pitavastatin Combined with Ezetimibe Treatment was an Effective Approach to Non-IRA Lesion of ST-segment Elevation Myocardial Infarction Patients with Primary Percutaneous Coronary Intervention.

OBJECTIVE: ST-Segment Elevation Myocardial Infarction (STEMI) patients with the multivessel disease have distinctive plaque characteristics in non-IRA lesions. Intensive statin therapy was a potential approach to treat STEMI patients with the non-IRA disease. However, there is still poor evidence about the therapeutic effect. In this study, we have evaluated the detailed therapeutic effect of statin plus ezetimibe intensive therapy. METHODS: For STEMI patients with non-IRA disease undergoing primary Percutaneous Coronary Intervention (PCI), 183 control STEMI patients without non-IRA disease undergoing primary PCI, and 200 STEMI patients with non-IRA disease undergoing primary PCI were introduced into this study. 200 STEMI patients with non-IRA disease undergoing primary PCI were divided into Normal group, Intensive group, Normal & Combined group, and Intensive & Combined group. The baseline information for each participant was recorded. Meanwhile, the physiological and biochemical indicators of each member with different treatments were collected after one-year follow-up. RESULTS: For STEMI patients with non-IRA disease undergoing primary PCI, no differences could be detected in multiple indexes such as OCT examination results, age, stroke, etc. However, diabetes mellitus, smoking, and coronary Gensini score were different between different groups (P<0.05). After one year follow-up, cholesterol, low-density lipoprotein, coronary Gensini score, thin-cap fibroatheroma, length of non-infarcted arterial lesions, non-infarct artery lesion range, myocardial infarction again, and revascularization again were significantly different between different groups (P<0.05). CONCLUSION: The results mentioned above suggested that pitavastatin combined with ezetimibe was an effective approach for STEMI patients with non-IRA disease undergoing primary PCI. The results obtained in this study have provided a novel method for the treatment of STEMI patients with non-IRA disease undergoing primary PCI.

CircMACF1 Attenuates Acute Myocardial Infarction Through miR-500b-5p-EMP1 Axis.

It is widely accepted that circular RNA (circRNA) plays an important role in cardiovascular diseases. Therefore, this experiment aimed to investigate the pathogenesis of circMACF1 in acute myocardial infarction (AMI). qRT-PCR and immunoblotting were used to detect the expression levels of circMACF1, miR-500b-5p, and epithelial membrane protein 1 (EMP1). The role of circMACF1, miR-500b-5p, and EMP1 in cardiomyocyte apoptosis was assessed using annexin V-FITC/PI. Echocardiographic assessment, serum creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH), myocardial infarct size, and TUNEL staining were applied in our research. In the MI group, the expression levels of circMACF1 and EMP1 were decreased with the increasing expression level of miR-500b-5p. CircMACF1 upregulated the expression of EMP1 as a sponge of miR-500b-5p, and circMACF1 was a direct target of miR-500b-5p. CircMACF1 impaired the progression of AMI by modulating the miR-500b-5p/EMP1 axis. CircMACF1 may be a potential therapeutic target for treating AMI. Graphical Abstract CircMACF1 upregulated EMP1 expression by sponge miR-500b-5p.

Association of Monocyte Count on Admission with the Angiographic Thrombus Burden in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention / Associação da Contagem de Monócitos na Internação com a Carga Trombótica Angiográfica em Pacientes com Infarto com Supradesnivelamento do Segmento ST Submetidos à Intervenção Coronária Percutânea Primária

Abstract Background: The intracoronary high-thrombus burden during the primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction (STEMI) can lead to poor outcomes. Monocytes have been described to play an important role in thrombotic disorders. Objectives: This study aimed to investigate the relationship between admission monocyte count and angiographic intracoronary thrombus burden in patients receiving primary percutaneous coronary intervention (PPCI). Methods: A total of 273 patients with acute STEMI who underwent PPCI were enrolled. The patients were divided into two groups according to the thrombolysis in myocardial infarction (TIMI) thrombus grade: low-thrombus burden group with a grade of 0-2 and high-thrombus burden group with a grade of 3-4. The monocyte count and other laboratory parameters were measured on admission before PPCI. P-value < 0.05 was considered significant. Results: There were 95 patients (34.8%) in the high-thrombus burden group, and 178 patients (65.2%) in the low-thrombus burden group. Patients with high-thrombus burden had significantly higher admission monocyte count (0.61 ± 0.29×109/L vs. 0.53 ± 0.24×109/L, p = 0.021). In multivariate analysis, monocyte count was the independent predictor of angiographic high-thrombus burden (odds ratio 3.107, 95% confidence interval [CI] 1.199-7.052, p = 0.020). For the prediction of angiographic high-thrombus burden, admission monocyte count at a cut-off value of 0.48×109/L yielded 0.59 ROC-AUC (71.9% sensitivity, 46.9% specificity). Conclusions: Monocyte count on admission was an independent clinical predictor of high-thrombus burden in patients with STEMI undergoing PPCI. Our findings suggest that admission monocyte count may be available for early risk stratification of high-thrombus burden in acute STEMI patients and might allow the optimization of antithrombotic therapy to improve the outcomes of PPCI.

Resumo Fundamento: A carga trombótica intracoronária durante a intervenção coronária percutânea primária em pacientes com Infarto com Supradesnivelamento do Segmento ST (STEMI) pode levar a resultados negativos.Os monócitos foram descritos para desempenhar um papel importante nos distúrbios trombóticos. Objetivos: Este estudo investigou a relação entre a contagem de monócitos no momento da internação e a carga trombótica angiográfica intracoronária em pacientes submetidos à intervenção coronária percutânea primária (ICPP). Métodos: Um total de 273 pacientes com STEMI agudo submetidos à ICPP participaram. Os pacientes se dividiram em dois grupos de acordo com o grau trombótico na trombólise do infarto do miocárdio (TIMI): grupo baixa carga trombótica, com graus de 0-2, e grupo alta carga trombótica, com graus de 3-4. A contagem de monócitos e outros parâmetros laboratoriais foram medidos na internação antes da ICPP. Consideramos o valor de p < 0,05 significativo. Resultados: Havia 95 pacientes (34,8%) no grupo alta carga trombótica, e 178 pacientes (65,2%) no grupo baixa carga trombótica. Pacientes com alta carga trombótica apresentaram contagem de monócitos no momento da internação mais alta (0,61 ± 0,29×109/L vs. 0,53 ± 0,24×109/L, p = 0,021). Na análise multivariada, a contagem de monócitos foi o indicador independente da alta carga trombótica angiográfica (odds ratio 3,107, intervalo de confiança de 95% [IC] 1,199-7,052, p = 0,020). Para a previsão da alta carga trombótica angiográfica, a contagem de monócitos na internação tinha ponto de corte de 0,48×109/L, chegou a 0.59 ROC-AUC (71,9% sensibilidade, 46,9% especificidade). Conclusões: a contagem de monócitos na internação foi um indicador clínico independente da alta carga trombótica em pacientes com STEMI submetidos à ICPP. Nossos achados sugerem que a contagem de monócitos na internação pode estar disponível para a estratificação de risco precoce da alta carga trombótica em pacientes com STEMI agudo, e podem levar à otimização da terapia antitrombótica para melhorar os resultados da ICPP.

Association of Monocyte Count on Admission with the Angiographic Thrombus Burden in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

BACKGROUND: The intracoronary high-thrombus burden during the primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction (STEMI) can lead to poor outcomes. Monocytes have been described to play an important role in thrombotic disorders. OBJECTIVES: This study aimed to investigate the relationship between admission monocyte count and angiographic intracoronary thrombus burden in patients receiving primary percutaneous coronary intervention (PPCI). METHODS: A total of 273 patients with acute STEMI who underwent PPCI were enrolled. The patients were divided into two groups according to the thrombolysis in myocardial infarction (TIMI) thrombus grade: low-thrombus burden group with a grade of 0-2 and high-thrombus burden group with a grade of 3-4. The monocyte count and other laboratory parameters were measured on admission before PPCI. P-value < 0.05 was considered significant. RESULTS: There were 95 patients (34.8%) in the high-thrombus burden group, and 178 patients (65.2%) in the low-thrombus burden group. Patients with high-thrombus burden had significantly higher admission monocyte count (0.61 ± 0.29×109/L vs. 0.53 ± 0.24×109/L, p = 0.021). In multivariate analysis, monocyte count was the independent predictor of angiographic high-thrombus burden (odds ratio 3.107, 95% confidence interval [CI] 1.199-7.052, p = 0.020). For the prediction of angiographic high-thrombus burden, admission monocyte count at a cut-off value of 0.48×109/L yielded 0.59 ROC-AUC (71.9% sensitivity, 46.9% specificity). CONCLUSIONS: Monocyte count on admission was an independent clinical predictor of high-thrombus burden in patients with STEMI undergoing PPCI. Our findings suggest that admission monocyte count may be available for early risk stratification of high-thrombus burden in acute STEMI patients and might allow the optimization of antithrombotic therapy to improve the outcomes of PPCI.

Utility of Hematological Parameters in Predicting No-Reflow Phenomenon After Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction.

OBJECTIVE: Because the no-reflow phenomenon in patients with ST- segment elevation myocardial infarction can lead to poor outcomes and early identification of patients at high risk may alter the clinical outcome, we aimed to study possible differences in the predictive utility among hematological parameters for early identification of patients at high risk of the no-reflow phenomenon during the primary percutaneous coronary intervention. METHODS: A total of 612 patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention were enrolled. The patients were divided into 2 groups: no-reflow and normal reflow. Hematological parameters were measured on admission. Sensitivity, specificity, positive and negative predictive values, and receiver-operating characteristic areas under the curve were determined to evaluate the predictive values of these parameters. RESULTS: The patients in the no-reflow group had a significantly higher neutrophil count, neutrophil-lymphocyte ratio, platelet-lymphocyte ratio, and mean platelet volume-to-lymphocyte ratio when compared to the normal reflow patients. We identified mean platelet volume-to-lymphocyte ratio to have a moderate predictive value and high specificity (66.8%) for the no-reflow phenomenon. Neutrophil-lymphocyte ratio provided the largest area under the curve for predicting no reflow. Regarding the predictive utility for no reflow, the comparison showed no statically significant differences among evaluated hematological parameters. CONCLUSION: For the prediction of no reflow, mean platelet volume-to-lymphocyte ratio yielded moderate performance. No hematological parameter on admission had persuasive superior capacities to predict no-reflow in patients receiving the primary percutaneous coronary intervention.

The relationship between post-procedural platelet count and left ventricular aneurysm in patients with acute anterior ST-segment elevation myocardial infarction following primary percutaneous coronary intervention.

BACKGROUND: Left ventricular aneurysm (LVA) relates to worse prognosis in patients with myocardial infarction despite successful reperfusion treatment. There is no evidence that early detectable biomarkers can predict the risk for the future development of LVA. AIM: The aim of our study was to investigate the possible predictive value of periprocedural haematological parameters for LVA. METHODS: A total of 281 patients with acute anterior ST-segment elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (pPCI) were enrolled. Haematological parameters were measured on admission before pPCI and between 8 and 12 h after pPCI, separately. The development of LVA was evaluated at one-year follow-up. The patients were then divided into two groups: an LVA group and a non-LVA group. Univariate and multivariate logistic regression analyses were performed to find the predictors of LVA. RESULTS: A total of 34 (12.1%) patients developed LVA at one-year follow-up after pPCI. Multivariate analyses revealed that a 10 × 109/L increase in platelet count 12 h after pPCI (odds ratio [OR] 1.092, 95% confidence interval [CI] 1.015-1.188, p = 0.039), peak cardiac troponin I (OR 1.107, 95% CI 1.003-1.215, p = 0.000), and left ventricular ejection fraction (OR 0.853, 95% CI 0.772-0.943, p = 0.002) were independent risk factors for LVA. For the prediction of LVA, platelet count 12 h after pPCI at a cut-off value > 197 × 109/L yielded a receiver operating characteristic-area under the curve (ROC-AUC) of 0.635 (82.3% sensitivity, 44.1% specificity). CONCLUSIONS: Platelet count after pPCI was significantly associated with the development of LVA in anterior STEMI patients and may be available for early risk stratification of future LVA formation.

Hypotonic contrast media is more toxic than isotonic contrast media on endothelial cells in vivo and in vitro.

The aim of the current study was to investigate the cytotoxic effects of hypotonic (iopamidol) and isotonic (iodixanol) contract media (CMs) in vitro and in vivo. A total of 60 Wistar rats were included and were randomly divided into three groups (20 rats per group). Iodixanol (4 g iodine/kg), iopamidol (4 g iodine/kg) or equal volume of normal saline was injected via tail vein. HUVEC and H5V cell viability was determined by Cell Counting Kit­8 agents. Western blotting was performed to detect ATP­binding cassette subfamily G member 1 (ABCG1) expression. For histological analysis, hematoxylin and eosin staining was performed. Plasma endothelin, von Willebrand factor, tissue type plasminogen activator, plasminogen activator inhibitor, D­Dimer, fibrinogen, anti­thrombin III, plasminogen and nitric oxide synthase (NOS) were measured by using ELISA. Both iopamidol and iodixanol treatments deceased cell viability and increased apoptosis of HUVEC and H5V cells, along with downregulated NOS and ABCG1. The injection of iopamidol or iodixanol into rats changed the endothelium­related plasma levels of biomarkers, including endothelin, von Willebrand factor, tissue type plasminogen activator, plasminogen activator inhibitor, D­Dimer, fibrinogen and anti­thrombin III. However, endothelia isolated from rat abdominal aorta in the iodixanol group retained their normal structure, whereas endothelial structure in the iopamidol group was injured and disrupted. The findings in the present study suggested that both hypotonic and isotonic CMs may lead to endothelial dysfunction and thrombin and fibrinolytic system disorder. However, hypotonic CMs may be more toxic than isotonic CMs. Therefore, additional cautions should be taken when selecting hypotonic CMs and their dosages during cardioangiography.

Association of monocyte count on admission with angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction.

BACKGROUND: The no-reflow phenomenon during primary percutaneous coronary intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI) can lead to poor outcomes. It has been shown that the monocytes may be involved in the pathogenesis of coronary artery disease and associated with high risk of myocardial infarction. AIM: To assess the relation between admission monocyte count and angiographic no-reflow after pPCI. METHODS: A total of 236 patients with acute STEMI, who underwent pPCI, were enrolled. The patients were divided into two groups (no-reflow and normal reflow) based on post-pPCI Thrombolysis in Myocardial Infarction (TIMI) flow grade. No reflow was defined as TIMI flow grades ≤ 2, and normal reflow was defined as TIMI 3 flow grade. The monocyte count and other laboratory parameters were measured on admission before pPCI. RESULTS: There were 43 (18.2%) patients in the no-reflow group and 193 (81.8%) patients in the normal-reflow group. Patients with no-reflow had significantly higher admission monocyte count (0.76 ± 0.48 × 109/L vs. 0.55 ± 0.29 × 109/L, p = 0.004). Also, white blood cell and neutrophil counts were significantly higher while haemoglobin was significantly lower in the no-reflow group. In multivariate analysis, monocyte count remained an independent predictor of angiographic no-reflow phenomenon (odds ratio [OR] 2.665, 95% confidence interwal [CI] 1.102-6.445, p = 0.030) together with low haemoglobin concentration (OR 0.978, 95% CI 0.961-0.995, p = 0.013). CONCLUSIONS: Monocyte count on admission and low haemoglobin concentration were independent clinical predictors of no-reflow following pPCI in patients with STEMI. Our findings suggest that admission monocyte count may be available for early risk stratification of no-reflow after pPCI and might allow the improvement of strategies to prevent this phenomenon.

The relationship between neutrophil counts on admission and angiographic no-reflow after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction.

BACKGROUND: The no-reflow phenomenon during primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction (STEMI) can lead to poor outcomes. Increased neutrophil counts have been associated with an increased risk of adverse clinical events after acute myocardial infarction (AMI). The aim of this study was to assess the relation between admission neutrophil counts and angiographic no-reflow after PPCI. METHODS: A total of 217 patients with acute STEMI who underwent PPCI, were enrolled. The patients were divided into two groups: no-reflow and normal-reflow. The neutrophil counts and other laboratory parameters were measured on admission before PPCI. RESULTS: There were 41 patients (18.9%) in the no-reflow group and 176 patients in the normal-reflow group. Patients with no-reflow were older (68.0 ± 11.7 years vs 60.7 ± 13.2 years, P = 0.019) and had significantly higher admission neutrophil counts (9.02 ± 3.97 × 109/L vs 7.57 ± 2.82 × 109/L, P = 0.007). Also, high-sensitivity C-reactive protein (hsCRP), white blood counts, monocyte counts were significantly higher while haemoglobin values were significantly lower in the no-reflow group. In multivariate analysis, neutrophil counts remained a strong independent predictor of angiographic no-reflow (odds ratio 1,200, 95% confidence interval 1.073-1.342, P = 0.001) together with age (odds ratio 1.041, 95% confidence interval 1.012-1.071, P = 0.005). CONCLUSIONS: Neutrophil counts on admission and age were independent clinical predictors of no-reflow following primary PCI in patients with STEMI. Our findings suggest that admission neutrophil counts may be available for early risk stratification of no-reflow after primary PCI and might allow the improvement of strategies to prevent this phenomenon.

Conservative pharmacotherapy vs. staged percutaneous coronary intervention for non-culprit vessels in patients with ST-segment elevation myocardial infarction.

The present study aimed to compare the effect of conservative pharmacotherapy (CP) and staged percutaneous coronary intervention (SPCI) on significant non-culprit vessels in patients with ST-segment elevation myocardial infarction (STEMI). A total of 266 male and 40 female patients were divided into two groups following their first successful PCI treatment: i) Patients in the complete revascularization (CR) group undergoing SPCI; and ii) patients in the CP group undergoing CP. Follow-up data were collected at 180 or 360 days after surgery to compare the rates of major adverse cardiovascular events (MACE), recurrent myocardial infarction, recurrent angina pectoris and MACE-free survival rates between the two groups. The rate of MACE in the CP group was higher compared with that in the CR group at the 360-day follow-up (6.1 vs. 12.7%; P=0.05), and the same was reflected in the rate of recurrent myocardial infarction (10.1 vs. 4.1%; P=0.04). The rate of recurrent angina pectoris in the CP group was significantly higher compared with that in CR group at the 180-day (13.9 vs. 5.4%; P=0.012) and 360-day follow-up (18.4 vs. 8.1%; P=0.009). The MACE-free survival rate of patients was significantly higher in the CR group compared with that in the CP group at the 360-day follow-up (93.9% vs. 87.3%, P<0.05). In conclusion, the SPCI of non-culprit vessels in patients with STEMI is associated with better clinical outcomes than CP.

[Effects of rosuvastatin on arterial stiffness in hyperlipidemia patients].

OBJECTIVE: To evaluate the effects of rosuvastatin on arterial stiffness in hyperlipidemia patient without hypertension. METHODS: A total of 60 patients without hypertension received rosuvastatin (10 mg, n = 60) daily for 12 weeks while another 60 subjects used no statins. Brachial-ankle pulse wave velocity (ba-PWV), radial artery augmentation index of reflected wave (rAI) and metabolic index were measured before and after treatment. RESULTS: There were no significant change before and after non-statin treatment. Total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) levels decreased dramatically after resuvastin treatment [TC: (4.0 ± 1.0) vs (5.8 ± 1.1) mmol/L; LDL-C: (2.1 ± 0.7) vs (3.8 ± 0.7) mmol/L, both P < 0.01]. In rosuvastatin group, ba-PWV and rAI decreased significantly [ba-PWV: (1 340 ± 177) vs (1 477 ± 159) cm/s; rAI: (44 ± 13) % vs (57 ± 15) %, P < 0.01 and P < 0.05). CONCLUSION: Atherosclerosis may be improved by rosuvastatin treatment in hyerlipidemia patient without hypertension.

[High-dose tirofiban in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention].

OBJECTIVE: To evaluate the clinical outcomes of high-dose tirofiban in patients with ST-elevation myocardial infarction (ASTEMI) undergoing primary percutaneous coronary intervention (PCI). METHODS: A total of 104 consecutive ASTEMI patients undergoing primary PCI were enrolled from January 2010 to February 2011. They were randomized into the high-dose tirofiban group (n = 52) and the normal-dose tirofiban group (n = 52). We measured the sumST-segment resolution of ECG post-PCI respectively and left ventricular ejective fraction (LVEF) at Day 90 post-PCI. RESULTS: After PCI, the sumST-segment resolution of ECG of the high-dose tirofiban group significantly improved than that of the normal-dose tirofiban group (38% ± 12% vs 34% ± 13%, P < 0.05). Before PCI, LVEF of two groups is 50.2% ± 1.4% vs 49.6% ± 1.1% (P > 0.05), but at day 90 post-PCI, LVEF had significant difference between two groups (60.1% ± 1.1% vs 56.0% ± 1.2%, P < 0.05). The rates of major and moderate hemorrhage did not differ significantly between two groups. CONCLUSION: High-dose tirofiban improves myocardial reperfusion and clinical outcome. It re-emphasizes the importance of further platelet aggregation inhibition in ASTEMI patients undergoing primary PCI.