The triglyceride-glucose index as a predictive marker for coronary slow flow phenomenon.

OBJECTIVE: The triglyceride-glucose index (TyG) has been proposed as a marker of insulin resistance (IR) and has shown associations with cardiovascular diseases. This study aimed to investigate the relationship between the TyG and the coronary slow flow phenomenon (CSFP) and explore the index's potential as a predictor of this condition. PATIENTS AND METHODS: A total of 187 patients who underwent coronary angiography were included; of these, 91 patients were diagnosed with CSFP, and 96 patients with normal coronary flow served as a control group. The TyG was calculated using fasting triglyceride and glucose levels. RESULTS: The results showed that the TyG was significantly higher in the CSFP group compared with the control group (p < 0.001). Additionally, the TyG exhibited a moderate positive correlation with the thrombolysis-in-myocardial-infarction frame count in coronary arteries (p < 0.001). A multivariate logistic regression analysis revealed that the TyG, along with gender, ejection fraction, and uric acid, remained significant predictors of CSFP (p < 0.05). CONCLUSIONS: This study's findings suggest that the TyG may serve as a useful marker for identifying individuals at risk of CSFP and provide insights into the potential role of IR in its pathophysiology.

FGF-21: a novel biomarker predicting no-reflow in ST-segment elevation myocardial infarction.

OBJECTIVE: Primary percutaneous coronary intervention (pPCI) is the most effective reperfusion therapy in the treatment of ST-elevation myocardial infarction (STEMI). Although the infarct-related artery of STEMI patients is effectively revascularized during pPCI, effective reperfusion in the myocardial tissue may not be achieved. This condition is called the no-reflow (NR) phenomenon. FGF-21 is a circulating hormone-like molecule primarily secreted by the liver and has been proven to be the main metabolic regulator of glucolipid metabolism and insulin sensitivity. The aim of this study was to investigate the predictive effect of FGF-21 on the development of the NR phenomenon in STEMI patients undergoing pPCI. PATIENTS AND METHODS: This study included 91 patients with acute STEMI who underwent pPCI and 45 healthy participants. Patients with acute STEMI were split into two groups: 46 patients in the NR phenomenon group and 45 patients in the non-NR phenomenon group. Serum levels of FGF-21 were measured in all study groups. RESULTS: Serum FGF-21, white blood cell count, and high-sensitivity C-reactive protein (hs-CRP) values were considerably different amongst the groups (p = 0.001, p = 0.001, and p = 0.003, respectively). In comparison to patients without NR and the control group, STEMI patients with NR had considerably higher FGF-21 levels. In addition, the FGF-21 level of STEMI patients without NR was significantly higher than that of the control group. In multivariate logistic regression analysis, hs-CRP [odds ratio (OR) 2.106% 95% confidence interval (CI) (0.002-0.069) p = 0.038], age [OR 2.147; 95% (CI) (0.001-0.015); p = 0.0035], and serum FGF-21 levels [OR 4.644; 95% CI (0.003-0.006); p < 0.001] were independent predictors of NR formation. For FGF-21 ≥ 92.2 pg/Ml, 87% sensitivity and 88% specificity were found in predicting NR formation (area under the curve: 0.897, 95% CI: 0.841-0.954; p < 0.001). CONCLUSIONS: Our study demonstrates a strong association between the NR phenomenon, a key indicator of poor prognosis in acute STEMI patients, and an elevated FGF-21 level. These findings indicate FGF-21 as a novel and potent predictor of NR development in STEMI patients.

The Predictive Value of the Inflammatory Prognostic Index for Detecting No-Reflow in ST-Elevation Myocardial Infarction Patients. / O Valor Preditivo do Índice Prognóstico Inflamatório para Detecção de No-Reflow em Pacientes com Infarto do Miocárdio com Supradesnivelamento do Segmento ST.

BACKGROUND: No-reflow (NR) is characterized by an acute reduction in coronary flow that is not accompanied by coronary spasm, thrombosis, or dissection. Inflammatory prognostic index (IPI) is a novel marker that was reported to have a prognostic role in cancer patients and is calculated by neutrophil/lymphocyte ratio (NLR) multiplied by C-reactive protein/albumin ratio. OBJECTIVE: We aimed to investigate the relationship between IPI and NR in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (pPCI). METHODS: A total of 1541 patients were enrolled in this study (178 with NR and 1363 with reflow). Lasso panelized shrinkage was used for variable selection. A nomogram was created based on IPI for detecting the risk of NR development. Internal validation with Bootstrap resampling was used for model reproducibility. A two-sided p-value <0.05 was accepted as a significance level for statistical analyses. RESULTS: IPI was higher in patients with NR than in patients with reflow. IPI was non-linearly associated with NR. IPI had a higher discriminative ability than the systemic immune-inflammation index, NLR, and CRP/albumin ratio. Adding IPI to the baseline multivariable logistic regression model improved the discrimination and net-clinical benefit effect of the model for detecting NR patients, and IPI was the most prominent variable in the full model. A nomogram was created based on IPI to predict the risk of NR. Bootstrap internal validation of nomogram showed a good calibration and discrimination ability. CONCLUSION: This is the first study that shows the association of IPI with NR in STEMI patients who undergo pPCI.

FUNDAMENTO: O no-reflow (NR) é caracterizado por uma redução aguda no fluxo coronário que não é acompanhada por espasmo coronário, trombose ou dissecção. O índice prognóstico inflamatório (IPI) é um novo marcador que foi relatado como tendo um papel prognóstico em pacientes com câncer e é calculado pela razão neutrófilos/linfócitos (NLR) multiplicada pela razão proteína C reativa/albumina. OBJETIVO: Nosso objetivo foi investigar a relação entre IPI e NR em pacientes com infarto do miocárdio com supradesnivelamento do segmento ST (IAMCSST) submetidos a intervenção coronária percutânea primária (ICPp). MÉTODOS: Um total de 1.541 pacientes foram incluídos neste estudo (178 com NR e 1.363 com refluxo). A regressão penalizada LASSO (Least Absolute Shrinkage and Select Operator) foi usada para seleção de variáveis. Foi criado um nomograma baseado no IPI para detecção do risco de desenvolvimento de NR. A validação interna com reamostragem Bootstrap foi utilizada para reprodutibilidade do modelo. Um valor de p bilateral <0,05 foi aceito como nível de significância para análises estatísticas. RESULTADOS: O IPI foi maior em pacientes com NR do que em pacientes com refluxo. O IPI esteve associado de forma não linear com a NR. O IPI apresentou maior capacidade discriminativa do que o índice de imunoinflamação sistêmica, NLR e relação PCR/albumina. A adição do IPI ao modelo de regressão logística multivariável de base melhorou a discriminação e o efeito do benefício clínico líquido do modelo para detecção de pacientes com NR, e o IPI foi a variável mais proeminente no modelo completo. Foi criado um nomograma baseado no IPI para prever o risco de NR. A validação interna do nomograma Bootstrap mostrou uma boa capacidade de calibração e discriminação. CONCLUSÃO: Este é o primeiro estudo que mostra a associação de IPI com NR em pacientes com IAMCSST submetidos a ICPp.

Analysis of correlative factors of female coronary slow-flow phenomenon: A retrospective study.

The coronary slow-flow phenomenon (CSFP) is a manifestation of coronary artery disease wherein coronary angiography reveals no apparent stenosis; however, there is a delay in blood flow perfusion. Given its increased occurrence in male patients, with the majority of subjects in previous studies being male, this study aimed to explore whether distinct risk factors are present in female patients with CSFP. This single-center retrospective study focused on female patients diagnosed with CSFP by using coronary angiography. Eligible patients meeting the predefined inclusion and exclusion criteria were divided into the study group (presenting with CSFP) and control group (displaying normal epicardial coronary arteries). Comparative analyses of clinical and diagnostic data were performed. Ninety-two patients with CSFP and an equal number of controls were enrolled in this study. Patients with CSFP exhibited a higher prevalence of smokers (P = .017) and a heightened incidence of diabetes mellitus (DM) (P = .007). Significantly elevated levels of total cholesterol (TC) (P = .034) and free fatty acids (FFA) (P = .016) were observed in the CSFP group compared to those in the control group. Additionally, patients with CSFP displayed lower levels of apolipoprotein E (ApoE) (P = .092), free thyroxine (FT4) (P = .001), and total thyroxine (TT4) (P = .025). Logistic regression analysis indicated that smoking (P = .019), FFA (P < .001), ApoE (P = .015), and FT4 (P < .001) were independent risk factors for CSFP, accounting for confounding factors. Additionally, the area under the ROC curve (AUC) of the combined effect of smoking, ApoE, FT4, and FFA on CSFP was 0.793 (95% CI: 0.729-0.857, P < .01). In addition to the established risk factors for smoking, diabetes, and hyperlipidemia, female patients with CSFP exhibited significant differences in apoE, FFA, FT4, and TT4 levels compared to the control group. Smoking, FFA, and FT4 levels emerged as independent risk factors for CSFP.

Could Pan-Immune-Inflammation Value be a Marker for the Diagnosis of Coronary Slow Flow Phenomenon?

Inflammation plays a key role in the pathogenesis of the coronary slow flow phenomenon (CSFP). The newly developed inflammatory marker, pan-immune-inflammation value (PIV), is associated with adverse cardiovascular events. This study investigated the predictive value of PIV for diagnosing CSFP in comparison to other inflammation-based markers. A total of 214 patients, 109 in the CSFP group and 105 in the normal coronary flow (NCF) group, were retrospectively included in the study. Coronary flow was calculated using the Thrombolysis in Myocardial Infarction frame count method. In addition to PIV, other inflammatory markers such as neutrophil-lymphocyte ratio, platelet-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) were calculated for the patients. The average age of patients was 50.3 ± 8.4, with a male ratio of 55.1%. Compared to the NCF group, patients in the CSFP group had higher levels of hyperlipidemia, glucose, triglyceride, NLR, PLR, SII, and PIV, while their high-density lipoprotein cholesterol (HDL-C), was lower (p < 0.05). Logistic regression analysis demonstrated that HDL-C, glucose, triglyceride, and PIV were independent predictor factors for CSFP (p < 0.05). PIV is a strong and independent predictor factor for CSFP and superior in predicting CSFP compared to other inflammatory markers.

Asymmetric Dimethylarginine Is Associated with the Phenomenon of Coronary Slow Flow in Patients with Nonvalvular Atrial Fibrillation.

INTRODUCTION: Coronary slow flow phenomena (CSFP) are associated with endothelial and blood component abnormalities in coronary arteries. Asymmetric dimethylarginine (ADMA) can damage the endothelium of the heart or blood vessels in patients with non-valvular atrial fibrillation (NVAF), causing changes in levels of biological indicators. Our aim was to analyze the relationship between ADMA and CSFP in NVAF patients. METHODS: We consecutively enrolled 134 patients diagnosed with NVAF and underwent coronary angiography, 50 control patients without a history of atrial fibrillation and with normal coronary angiographic flow were included at the same time. Based on the corrected TIMI frame count (CTFC), the NVAF patients were categorized into two groups, CTFC ≤27 frames and CTFC >27 frames. Plasma ADMA, P-selectin (p-sel), von Willebrand factor (vWF), D-dimer (D-Di), plasminogen activator inhibitor 1 (PAI-1), and nitric oxide (NO) were detected by ELISA in the different groups. RESULTS: We found that plasma ADMA levels were significantly higher among NVAF patients in the CTFC >27 grade group compared with the control or CTFC ≤27 group. In addition, the levels of blood cells and endothelium-related biomarkers (NO, P-selectin, vWF, D-Di, and PAI-1) were significantly altered and correlated with ADMA levels. Multifactorial analysis showed that plasma ADMA (odd ratio [OR; 95% CI]: 1.65 [1.21-2.43], p < 0.001) and left atrial internal diameter (OR [95% CI]: 1.04 [1.02, 1.1], p < 0.001) could be used as independent risk factors for the development of CSFP in patients with NVAF. The ROC curves of ADMA can predict the development of CSFP in NVAF patients. The minimum diagnostic concentration for the development of CSFP in patients was 2.31 µmol/L. CONCLUSION: Our study demonstrated that CSFP in NVAF patients was associated with high levels of ADMA and left atrial internal diameter. Therefore, aggressive preoperative detection and evaluation of ADMA and left atrial internal diameter can help deal with the intraoperative presence of CSFP.

Can plasma TWEAK levels predict coronary slow flow in patients with chronic kidney disease?

BACKGROUND: The tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is one of the inflammatory mediators contributing to the atherosclerotic process. TWEAK has been studied in patients with chronic kidney disease (CKD), and it has demonstrated that its level declines as estimated glomerular filtration rate (eGFR) decreases. Most studies have found that the decreased TWEAK levels were seen in atherosclerosis and associated with plaque calcification. The objective of this prospective study was to clarify any relationship between coronary slow-flow (CSF) and TWEAK levels in patients with CKD under conservative treatment. METHODS: This prospective study included 93 consecutive patients with CKD (mean creatinine level was 1.8±0.4 mg/dL) undergoing invasive coronary angiography (ICA) for any reason except for acute coronary syndromes from May 2019 to March 2020. A total of 93 patients were divided into two groups concerning having CSF (n=35) or no-CSF (n=58). RESULTS: Patients with CSF had higher TWEAK levels than those without CSF (695.2± 225.2 vs. 465.8±157.6, p<0.001). As the number of coronary arteries with slow flow increased, TWEAK levels increased statistically significantly (r:0.635/ p<0.001). Receiver operating characteristic (ROC) analysis showed that TWEAK levels of 516 pg/mL could predict CSF in patients with CKD. CONCLUSIONS: Our study has shown that plasma TWEAK levels were an independent predictor for CSF in patients with CKD. In addition, our study has found that elevated TWEAK levels may not reflect the healthy arteries as it was hypothesized in the past.

Post-occlusive reactive hyperemia and skeletal muscle capillary hemodynamics.

Post-occlusive reactive hyperemia (PORH) is an accepted diagnostic tool for assessing peripheral macrovascular function. While conduit artery hemodynamics have been well defined, the impact of PORH on capillary hemodynamics remains unknown, despite the microvasculature being the dominant site of vascular control. Therefore, the purpose of this investigation was to determine the effects of 5 min of feed artery occlusion on capillary hemodynamics in skeletal muscle. We tested the hypothesis that, upon release of arterial occlusion, there would be: 1) an increased red blood cell flux (fRBC) and red blood cell velocity (VRBC), and 2) a decreased proportion of capillaries supporting RBC flow compared to the pre-occlusion condition. METHODS: In female Sprague-Dawley rats (n = 6), the spinotrapezius muscle was exteriorized for evaluation of capillary hemodynamics pre-occlusion, 5 min of feed artery occlusion (Occ), and 5 min of reperfusion (Post-Occ). RESULTS: There were no differences in mean arterial pressure (MAP) or capillary diameter (Dc) between pre-occlusion and post-occlusion (P > 0.05). During 30 s of PORH, capillary fRBC was increased (pre: 59 ± 4 vs. 30 s-post: 77 ± 2 cells/s; P < 0.05) and VRBC was not changed (pre: 300 ± 24 vs. 30 s post: 322 ± 25 µm/s; P > 0.05). Capillary hematocrit (Hctcap) was unchanged across the pre- to post-occlusion conditions (P > 0.05). Following occlusion, there was a 20-30% decrease in the number of capillaries supporting RBC flow at 30 s and 300 s-post occlusion (pre: 92 ± 2%; 30 s-post: 66 ± 3%; 300 s-post: 72 ± 6%; both P < 0.05). CONCLUSION: Short-term feed artery occlusion (i.e. 5 min) resulted in a more heterogeneous capillary flow profile with the presence of capillary no-reflow, decreasing the percentage of capillaries supporting RBC flow. A complex interaction between myogenic and metabolic mechanisms at the arteriolar level may play a role in the capillary no-reflow with PORH. Measurements at the level of the conduit artery mask significant alterations in blood flow distribution in the microcirculation.

Predictive value of N-terminal pro-B-type natriuretic peptide (NT-pro BNP) combined with D-dimer for no-reflow phenomenon in patients with acute coronary syndrome after emergency of percutaneous coronary intervention.

Acute coronary syndrome (ACS) is a critical illness in cardiovascular disease. The purpose of this study was to investigate the value of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and D-dimer in predicting the occurrence of no reflow in emergency percutaneous coronary intervention (PCI) in patients with ACS. One hundred and sixty-eight ACS patients were recruited, including 88 patients with normal reflow and 80 patients with no reflow after emergency PCI. The levels of serum NT-proBNP and D-dimer in the patients were detected before PCI, immediately after PCI, 2 hours, and 6 months after PCI. The ROC curve was used to evaluate the predictive value of NT-proBNP and D-dimer in no-reflow phenomenon. Logistic regression model was used to analyze the independent influencing factors of no reflow phenomenon. Logistic regression analysis confirmed that NT-proBNP and D-dimer were independent predictors of the occurrence of no reflow in the total population. The ROC curve showed that the AUC value was 0.909 when NT-proBNP combined with D-dimer. The detection of NT-proBNP combined with D-dimer was helpful to predict the occurrence of no-reflow phenomenon after emergency PCI in ACS patients.

Vitamin D level predicts angiographic no-reflow phenomenon after percutaneous coronary intervention in patients with ST segment elevation myocardial infarction.

Aim: No-reflow phenomenon (NRP) is an undesirable result of coronary interventions, and usually occurred during the primary percutaneous coronary intervention (PPCI). On the other hand, there is growing evidence of epidemiological studies suggest that serum 25 hydroxy-vitamin D (25(OH)D3) level is significantly associated with cardiovascular mortality and morbidity. Objective: To investigate whether there is a relationship between admission serum 25(OH)D3 levels and NRP in patients with ST elevation myocardial infarction (STEMI). Methods: This study consisted of 496 consecutive acute STEMI patients who underwent PPCI. After the restoration of antegrade flow, the patients were divided into the normal flow and no-reflow groups. No-reflow defined as; thrombosis in myocardial infarction (TIMI) flow grade ≤2, or a TIMI flow grade = 3 with a myocardial perfusion grade ≤1. Results: Angiographic no-reflow occurred 18.2% of all study patients. Serum 25(OH)D3 levels were significantly lower when compared with the normal flow group (14.6 ± 7.3 vs 22.6 ± 9.6 ng/ml; p < 0.001). 25(OH)D3 level was significantly negatively correlated with Neutrophil/lymphocyte (N/L) ratio. In multivariate analysis, 25(OH)D3 level on admission (OR: 0.738; 95% CI: 0.584-0.878; p = 0.001) was found an independent predictor of NRP together with N/L ratio, N-Terminal-proBNP, balloon pre dilatation and syntax score I. On receiver operating curve analysis (ROC), the cut-off value of admission 25(OH)D3 level was 10.5 ng/ml for the prediction of NRP with a sensitivity of 93% and specificity of 68%. The area under the ROC curve (AUC) was 0.772 (95% CI: 0.697-0.846; p < 0.001). Conclusion: We have shown that lower 25(OH)D3 level on admission is associated with higher NRP frequency and may be used as a predictor for NRP in STEMI patients undergoing PPCI.

Predictors of no-reflow phenomenon following percutaneous coronary intervention for ST-segment elevation myocardial infarction.

OBJECTIVES: No reflow during percutaneous coronary intervention (PCI) is a complex issue with serious outcomes. Multiple studies have studied predictors of no-reflow during primary PCI, but data on patients with the late presentation is sparse, which constitutes the majority of patients in peripheral centers. This study aimed to determine predictors of no-reflow during PCI in patients with ST-segment elevation myocardial infarction (STEMI) in 7 days. METHODS: It was a single-center prospective case-control study performed at a tertiary care center and included 958 patients with STEMI who underwent PCI within 7 days of symptom onset. Baseline and angiographic data of patients undergoing PCI were recorded and patients divided into reflow and no-reflow group. RESULTS: Of 958 who underwent PCI, 182 (18.9%) showed no-reflow by myocardial blush grade (MBG)<2. No-reflow group had a higher mean age (66.46±10.71 vs. 61.36±9.94 years), lower systolic blood pressure (SBP) on admission (100.61±26.66 vs. 112.23±24.35, P<0.0001), a higher level of peak Troponin I level (9.37±2.81 vs. 7.66±3.11ng/dL, P<0.0001), low left ventricular ejection fraction (36.71±3.89 vs. 39.58±4.28% respectively P<0.0001). Among angiographic data and procedural features, multivariable logistic regression analysis identified that advanced age, reperfusion time>6hours, SBP<100mmHg on admission, functional status of Killip class for heart failure≥3, lower EF (≤35%), low initial myocardial blush grade (≤1) before PCI, long target lesion length, larger reference diameter of vessel (>3.5mm) and high thrombus burden on angiography were found to be independent predictors of no-reflow (P<0.05). CONCLUSION: No-reflow phenomenon after PCI for STEMI is complex and multifactorial and can be identified by simple clinical, angiographic, and procedural features. Preprocedural characters of the lesion and early perfusion decides the fate of the outcome.

Relationship between blood viscosity and no-reflow phenomenon in ST-segment elevation myocardial infarction performed in primary percutaneous coronary interventions.

Background: This study aimed to analyze the associations between no-reflow (NR) phenomenon development and whole-blood viscosity in patients with ST-elevated myocardial infarction. Methods: A total of 217 patients with ST-elevated myocardial infarction were included. whole-blood viscosity values were assessed using hematocrit and total protein values, and low shear rate (LSR) and high shear rate (HSR) were calculated. Results: The average LSR and HSR values of the study group were significantly higher than the control group (p < 0.001). Multivariate logistic regression analysis showed that both HSR (odds ratio: 4.957; p < 0.001) and LSR (odds ratio: 1.114; p < 0.001) were independent predictors for NR development. Conclusion: This study found that increased blood viscosity was an independent predictor for NR development.

Lay abstract Following a heart attack, surgeons can attempt to repair the damage using a procedure called a percutaneous coronary intervention. In some cases, blood flow does not return to the heart tissue as expected ('failure of reperfusion') after this procedure, which is known as the no-reflow (NR) phenomenon. In this study, the researchers investigated whether there was a link between patients who had experienced a type of heart attack called an ST-elevated myocardial infarction (STEMI) and developed NR, and the viscosity (thickness) of their blood. The researchers looked at the viscosity of whole-blood samples from 98 STEMI patients with NR and 119 control individuals matched for age and gender. They found that whole-blood samples could be used to predict the likelihood of a STEMI patient experiencing NR.

Clinical characteristics in patients with coronary slow flow phenomenon: A retrospective study.

ABSTRACT: Coronary slow flow phenomenon (CSFP) is a coronary artery disease in which coronary angiography shows no obvious stenosis, but there is a delay in blood flow perfusion. The etiopathogenic mechanisms of CSFP are still unclear. The aim of the present study was to investigate the role of clinical characteristics in patients with CSFP, and to provide a reference for exploring the potential mechanisms of CSFP. Patients with angiographically normal epicardial arteries were enrolled (145 patients with CSFP and 145 normal controls). Collected clinical information and laboratory indexes, which measured by peripheral venous blood samples before coronary angiography. Logistic regression analysis was performed for statistical analysis. The present study found 19 clinical and laboratory indexes with statistical differences between the two groups in univariate analysis. Multivariate analysis showed that monocyte count, haemoglobin, serum creatinine and globulin were independent predictors of CSFP. Moreover, the monocyte count, haemoglobin, creatinine and globulin levels were significantly higher in the CSFP patients than the controls, with positive associations between these parameters and the extent of CSFP. In addition, ROC analysis showed the diagnostic value of the above indexes for CSFP.

Plasma calprotectin was associated with platelet activation and no-reflow phenomenon in acute coronary syndrome.

BACKGROUND: No-reflow occurs in 3-4% of all percutaneous coronary interventions (PCIs) and has a strong negative impact on clinical outcomes of acute coronary syndrome (ACS). Therefore, the discovery of a biomarker that can early predict the occurrence of no-reflow has great clinical significance. Multiple factors including platelet activation are relevant to no-reflow. Calprotectin is found to be a biomarker of plaque instability and is identified to be a novel diagnostic and prognostic biomarker of cardiovascular diseases. The association of plasma calprotectin with platelet activation and no-reflow phenomenon in ACS is not clear. METHODS: In this prospective study performed at Yantai Yuhuangding Hospital from 2017 to 2018, a total of 176 Chinese patients with ACS who had undergone PCIs were recruited consecutively, aged from 30 to 88 years. Angiographic no-reflow was defined as thrombolysis in myocardial infarction grade less than 3. Blood samples were collected immediately at admission for the detection of plasma calprotectin and platelet-monocyte aggregates formation. Statistical analysis was performed for the variable's comparisons between groups and the prediction value of plasma calprotectin for no-reflow. RESULTS: The mean age of the 176 included ACS patients were 64(±11) years and acute ST-segment elevation myocardial infarction (STEMI) was present in 41.5% of patients. Twenty-two patients had no-reflow during the PCI procedures and the prevalence was 12.5%. Patients with higher plasma calprotectin had a higher level of platelet-monocyte aggregates (PMA) and a higher prevalence of no-reflow (p < 0.001). The multivariate regression showed that plasma calprotectin and admission hs-cTnI were independently associated with PMA, while plasma calprotectin and serum LDL-c were independent predictors of no-reflow (p < 0.001 and p = 0.017). AUC of calprotectin for predicting no-reflow were 0.898. The cut-off value of plasma calprotectin for no-reflow was 4748.77 ng/mL with a sensitivity of 0.95 and a specificity of 0.77. CONCLUSION: Plasma calprotectin was associated with platelet activation and may act as an early predictive biomarker of no-reflow in patients with acute coronary syndrome.

Platelet-Derived Thrombogenicity Measured by Total Thrombus-Formation Analysis System in Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

BACKGROUND: Prompt and potent antiplatelet effects are important aspects of management of ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI). We evaluated the association between platelet-derived thrombogenicity during PPCI and enzymatic infarct size in STEMI patients.Methods and Results:Platelet-derived thrombogenicity was assessed in 127 STEMI patients undergoing PPCI by: (1) the area under the flow-pressure curve for the PL-chip (PL18-AUC10) using the total thrombus-formation analysis system (T-TAS); and (2) P2Y12reaction units (PRU) using the VerifyNow system. Patients were divided into 2 groups (High and Low) based on median PL18-AUC10during PPCI. PRU levels during PPCI were suboptimal in both the High and Low PL18-AUC10groups (median [interquartile range] 266 [231-311] vs. 272 [217-317], respectively; P=0.95). The percentage of final Thrombolysis in Myocardial Infarction (TIMI) 3 flow was lower in the High PL18-AUC10group (75% vs. 90%; P=0.021), whereas corrected TIMI frame count (31.3±2.5 vs. 21.0±2.6; P=0.005) and the incidence of slow-flow/no-reflow phenomenon (31% vs. 11%, P=0.0055) were higher. The area under the curve for creatine kinase (AUCCK) was greater in the High PL18-AUC10group (95,231±7,275 IU/L h vs. 62,239±7,333 IU/L h; P=0.0018). Multivariate regression analysis identified high PL18-AUC10during PPCI (ß=0.29, P=0.0006) and poor initial TIMI flow (ß=0.37, P<0.0001) as independent determinants of AUCCK. CONCLUSIONS: T-TAS-based high platelet-derived thrombogenicity during PPCI was associated with enzymatic infarct size in patients with STEMI.

Inflammatory and Hematological Indices as Simple, Practical Severity Predictors of Microdysfunction Following Coronary Intervention: A Systematic Review and Meta-Analysis.

C-reactive protein (CRP) and high-sensitivity CRP (hsCRP), along with a series of hematological indices, platelet to lymphocyte ratio (PLR), neutrophil to lymphocyte ratio (NLR), mean platelet volume (MPV), platelet distribution width (PDW), and red blood cell distribution width (RDW), are regarded to be related to the incidence of no-reflow or slow flow. Clinical studies were retrieved from the electronic databases of PubMed, EMBASE, Google Scholar, Clinical Trials, and science direct from their inception to August 24, 2019. A total of 21 studies involving 7403 patients were included in the meta-analysis. Pooled analysis results revealed patients with higher hsCRP (odds ratio [OR] = 1.03, 95% confidence interval [CI], 1.01-1.05, P = .006), hsCRP (OR = 1.04, 95% CI: 1.0-1.08, P = .012), NLR (OR = 1.23, 95% CI: 1.11-1.37, P < .0001), PLR (OR = 1.13, 95% CI: 1.07-1.20, P < .0001), and MPV (OR = 2.13, 95% CI: 1.57-2.90, P < .0001) all exhibited significantly higher no-reflow incidence, but there was no significant association between no-reflow risk and RDW or PDW. Patients with higher CRP/hsCRP also performed higher rate of slow flow (OR = 1.06, 95% CI: 1.01-1.11, P = .018). Preangiographic CRP/hsCRP could independently predict no-reflow and slow flow. Moreover, some hematological indices are associated with no-flow.

Predictive accuracy of lymphocyte-to-monocyte ratio and monocyte-to-high-density-lipoprotein-cholesterol ratio in determining the slow flow/no-reflow phenomenon in patients with non-ST-elevated myocardial infarction.

OBJECTIVE: To investigate whether inflammation based scores including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte to monocyte ratio (LMR) and monocyte to high-density lipoprotein cholesterol (HDL-C) ratio (MHR) predict the slow flow (SF)/no-reflow (NR) phenomenon comparatively in patients with non-ST-elevated Myocardial Infarction (NSTEMI) undergoing percutaneous coronary intervention (PCI). METHODS: Current study is retrospective designed and includes 426 NSTEMI patients (mean age of 56.8 ± 11.4 years). The patients were grouped into non slow flow/no-reflow and slow flow/no-reflow groups according to postintervention thrombolysis in myocardial infarction flow grade. RESULTS: The slow flow/no-reflow group had significantly higher MHR and lower LMR values than the non slow flow/no-reflow group (P < 0.01 and P < 0.01, respectively). Lower LMR [odds ratio (OR): 0.659, P < 0.01] and higher MHR (OR: 1.174, P = 0.04) were independent predictors of slow flow/no-reflow phenomenon in model 1 and 2 multivariate analyses, respectively. Furthermore, left ventricular ejection fraction (LVEF) (OR: 0.934, P = 0.01; OR: 0.930, P < 0.01), smoking (OR: 2.279, P = 0.03; OR: 2.118, P = 0.04), Syntax score (1.038, P = 0.04; 1.046, P = 0.01) and high thrombus grade (OR: 7.839, P < 0.01; OR: 8.269, P < 0.01), independently predicted the slow flow/no-reflow development in both multivariate analysis models, respectively. The predictive performance of LMR and MHR was not different (P = 0.88), but both predictive powers were superior to NLR (P < 0.01 and P = 0.03, respectively). CONCLUSION: The MHR and LMR may be useful inflammatory biomarkers for identifying high-risk individuals for the development of slow flow/no reflow in NSTEMI patients who underwent PCI.

Association between impaired cutaneous microvascular endothelial function and lectin-like oxidized low-density lipoprotein receptor-1 in patients with coronary slow flow.

OBJECTIVE: Although increasing studies indicate coronary slow flow (CSF) is a systemic microvascular disorder, whether there is impaired cutaneous microvascular endothelial function in CSF patients remains unclear. This study was designed to test the hypothesis that the cutaneous microvascular endothelial function of CSF patients is impaired and correlates with lectin-like oxidized low-density lipoprotein receptor-1(LOX-1). METHODS: 39 patients with CSF and 45 controls with normal coronary flow were enrolled. Velocity of coronary flow was quantitatively identified by thrombolysis in myocardial infarction frame count (TFC) method. LSCI system was used to assess subjects' cutaneous blood flow at rest and during PORH. Serum soluble LOX-1(sLOX-1) level was measured in all study subjects. RESULTS: PORH-induced vasodilation was significantly reduced in CSF group in comparison with control group (0.26 ± 0.10 vs 0.35 ± 0.07 APU/mmHg, P < 0.001) and negatively correlated with the mean TFC for three coronary arteries (r = -0.385, P = 0.016). Serum sLOX-1 level in CSF group was significantly increased (582.93 ± 74.89 vs 483.64 ± 51.38 pg/ml, P < 0.001) and positively correlated with mean TFC(r = 0.467, P = 0.003).PORH response amplitudes had a significantly negative relationship with serum sLOX-1 level in CSF patients (r = -0.588, P < 0.001). CONCLUSION: These data suggest that cutaneous microvascular endothelial function is impaired in patients with CSF, which is closely associated with increased LOX-1 expression.

Prognostic Value of Pre-Infarction Angina Combined with Mean Platelet Volume to Lymphocyte Count Ratio for No-Reflow and Short-Term Mortality in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention.

BACKGROUND The aim of the present study was to investigate the clinical predictive value of pre-infarction angina (PIA) combined with mean platelet volume to lymphocyte count ratio (MPVLR) for no-reflow phenomenon and short-term mortality in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). MATERIAL AND METHODS A total of 1009 STEMI patients who had undergone PCI were enrolled and subdivided into 4 groups based on the occurrence of PIA and the presence of MPVLR above or below the cutoff value. Analysis of the predictors of the no-reflow phenomenon and 90-day mortality was conducted. Further, evaluation and comparison of the clinical predictive value of PIA, MPVLR, and their combination were done. RESULTS Both MPVLR (odds ratio [OR]=1.476, 95% confidence interval [CI]: 1.401 to 1.756, P<0.001; hazard ratio [HR]=1.430, 95% CI: 1.287 to 1.643, P<0.001) and PIA (OR=0.905, 95% CI: 0.783 to 0.986, P<0.001; HR=0.878, 95% CI: 0.796 to 0.948, P<0.001) were independent predictors of no-reflow phenomenon and 90-day mortality. Spearman's rank correlation test revealed that MPVLR (r=-0.297, P<0.001), monocyte to lymphocyte count ratio (MLR) (r=-0.211, P<0.001) and neutrophil to lymphocyte count ratio (NLR) (r=-0.389, P<0.001) in peripheral blood were significantly negatively correlated with postoperative left ventricular ejection fraction (LVEF). Upon comparing the area under curve (AUC), the MPVLR combined with PIA achieved better performance in differentiating no-reflow phenomenon (AUC=0.847, 95% CI: 0.821 to 0.874) and 90-day mortality (AUC=0.790, 95% CI: 0.725 to 0.855), than the GRACE score, MPVLR and PIA alone, and had similar performance to all other pairwise combinations of the GRACE score, MPVLR and PIA. CONCLUSIONS High MPVLR and PIA were independent predictors of the no-reflow phenomenon and 90-day mortality in patients with STEMI after PCI. Moreover, Combined application of MPVLR and PIA can effectively predict the occurrence of the no-reflow phenomenon and 90-day mortality.

Serum magnesium concentration may predict no-reflow phenomenon in primary angioplasty for ST-elevation myocardial infarction.

No-reflow phenomenon is a serious complication of percutaneous coronary intervention. Magnesium may play a role in pathogenesis of no-reflow phenomenon since it interacts with processes like platelet inhibition and endothelial-dependent vasodilatation. Relationship of serum magnesium concentration at admission and angiographic no-reflow phenomenon in ST elevation myocardial infarction patients undergoing primary percutaneous coronary intervention is investigated in the present study. A total of 2.248 consecutive patients with ST elevation myocardial infarction who underwent primary percutaneous coronary intervention were analyzed. After reopening of the infarct related artery, a TIMI flow rate ≤ 2 was defined as no-reflow. No-reflow phenomenon developed in 386 (17.1 %) patients. Serum magnesium concentration was significantly lower in no-reflow group (1.87 ± 0.25 vs. 2.07 ± 0.33 mg/dL, p<0.001). ROC curve analysis showed that Mg at a cut-point of 1.92 has 71.4% sensitivity and 75.2% specificity in detecting no-reflow phenomenon. In multivariate logistic regression analysis, age, serum magnesium concentration, and stent length were found as independent predictors of no-reflow phenomenon. Serum magnesium concentration is associated with no-reflow phenomenon in ST elevation myocardial infarction patients who underwent primary PCI.