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 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.

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.

Intracoronary Near-Infrared Spectroscopy to Predict No-Reflow Phenomenon During Percutaneous Coronary Intervention in Acute Coronary Syndrome.

Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) can identify the lipid-rich lesions, described as high lipid-core burden index (LCBI). The aim of this study was to investigate the relation between lipid-core plaque (LCP) in the infarct-related lesion detected using NIRS-IVUS and no-reflow phenomenon during percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS). We investigated 371 patients with ACS who underwent NIRS-IVUS in the infarct-related lesions before PCI. The extent of LCP in the infarct-related lesion was calculated as the maximum LCBI for each of the 4-mm longitudinal segments (maxLCBI4mm) measured by NIRS-IVUS. The patients were divided into 2 groups using a maxLCBI4mm cut-off value of 400. The overall incidence of no-reflow phenomenon was 53 of 371 (14.3%). No-reflow phenomenon more frequently occurred in patients with maxLCBI4mm ≥400 compared with those with maxLCBI4mm<400 (17.5% vs 2.5%, p <0.001). After propensity score matching, multivariable logistic regression analysis demonstrated that maxLCBI4mm (odds ratio: 1.008; 95% confidence interval: 1.005 to 1.012, p <0.001) was independently associated with the no-reflow phenomenon. The maxLCBI4mm of 719 in the infarct-related lesion had the highest combined sensitivity (69.8%) and specificity (72.1%) for the identification of no-reflow phenomenon. In conclusion, in patients with ACS, maxLCBI4mm in the infarct-related lesion assessed by NIRS-IVUS was independently associated with the no-reflow phenomenon during PCI.

The predictive value of the HALP score for no-reflow phenomenon and short-term mortality in patients with ST-elevation myocardial infarction.

OBJECTIVE: ST-elevation myocardial infarction (STEMI) is a medical emergency demanding immediate intervention, and primary percutaneous coronary intervention (pPCI) is the standard of care for this condition. While PCI has proven highly effective, a subset of patients experience the devastating no-reflow phenomenon, and some face increased short-term mortality. The Hemoglobin, Albumin, Lymphocyte, and Platelet (HALP) score, a novel biomarker-based tool, has recently surfaced as an innovative predictor of these adverse outcomes. This study aims to investigate the groundbreaking findings that designate a low HALP score as a robust risk factor for no-reflow and short-term mortality in STEMI patients. METHODS: 1817 consecutive STEMI patients who underwent pPCI were included in this retrospective study, and the patients were divided into two groups according to whether no-reflow developed or not, and the HALP scores of the groups were compared. In addition, short-term mortality was compared between the study groups according to their HALP score values. The predictive ability of the HALP score for no-reflow was evaluated using a receiver operating characteristic curve. RESULTS: No-reflow developed in 198 (10.1%) of the patients included in the study. HALP score value was found to be significantly lower in the no-reflow group (27 ± 13 vs 47 ± 24, p < 0.001). After multivariable adjustment, the HALP score was an independent predictor of no-reflow (OR, 0.923, 95% CI, 0.910-0.935, p < 0.001). Furthermore, the HALP score showed good discrimination for no-reflow (AUC, 0.771, 95% CI, 0.737-0.805, p < 0.001). In addition, HALP score was determined to be an independent predictor for short-term mortality (HR, 0.955, 95% CI, 0.945-0.966, p < 0.001). CONCLUSIONS: HALP score can independently predict the development of no-reflow and short-term mortality in STEMI patients undergoing pPCI.

The predictive value of laboratory parameters for no-reflow phenomenon in patients with ST-elevation myocardial infarction following primary percutaneous coronary intervention: A meta-analysis.

To date, the predictive role of laboratory indicators for the phenomenon of no flow is unclear. Hence, our objective was to conduct a meta-analysis to investigate the association between laboratory parameters and the risk of the no-reflow phenomenon in patients with ST-elevation myocardial infarction (STEMI) following primary percutaneous coronary intervention (PCI). This, in turn, aims to offer valuable insights for early clinical prediction of no-reflow. We searched Pubmed, Embase, and Cochrane Library from the establishment of the database to October 2023. We included case-control or cohort study that patients with STEMI following primary PCI. We excluded repeated publication, research without full text, incomplete information or inability to conduct data extraction and animal experiments, reviews, and systematic reviews. STATA 15.1 was used to analyze the data. The pooled results indicated that elevated white blood cell (WBC) count (odds ratio [OR] = 1.061, 95% confidence interval [CI]: 1.013-1.112), neutrophil count (OR = 1.324, 95% CI: 1.128-1.553), platelet (PLT) (OR = 1.002, 95% CI: 1.000-1.005), blood glucose (OR = 1.005, 95% CI: 1.002-1.009), creatinine (OR = 1.290, 95% CI: 1.070-1.555), total cholesterol (TC) (OR = 1.022, 95% CI: 1.012-1.032), d-dimer (OR = 1.002, 95% CI: 1.001-1.004), and fibrinogen (OR = 1.010, 95% CI: 1.005-1.015) were significantly associated with increased risk of no-reflow. However, elevated hemoglobin was significantly associated with decreased risk of no-reflow. In conclusion, our comprehensive analysis highlights the predictive potential of various parameters in assessing the risk of no-reflow among STEMI patients undergoing PCI. Specifically, WBC count, neutrophil count, PLT, blood glucose, hemoglobin, creatinine, TC,  d-dimer, and fibrinogen emerged as significant predictors. This refined risk prediction may guide clinical decision-making, allowing for more targeted and effective preventive measures to mitigate the occurrence of no-reflow in this patient population.

The non-HDL-C/HDL-C ratio is a strong and independent predictor of the no-reflow phenomenon in patients with ST-elevation myocardial infarction.

BACKGROUND: No-reflow (NR) is the inability to achieve adequate myocardial perfusion despite successful restoration of attegrade blood flow in the infarct-related artery after primary percutaneous coronary intervention. The non-HDL-C/HDL-C ratio has been shown to be superior to conventional lipid markers in predicting most cardiovascular diseases. In this study, we wanted to reveal the predictive value of the NR by comparing the Non-HDL-C/HDL-C ratio with traditional and non-traditional lipid markers in patients who underwent primary percutaneous coronary intervention (pPCI) due to ST-elevation myocardial infarction (STEMI). METHODS: A total of 1284 consecutive patients who underwent pPCI for STEMI were included in this study. Traditional lipid profiles were detected and non-traditional lipid indices were calculated. Patients were classified as groups with and without NR and compared in terms of lipid profiles. RESULTS: No-reflow was seen in 18.8% of the patients. SYNTAX score, maximal stent length, high thrombus burden, atherogenic index of plasma and non-HDL-C/HDL-C ratio were determined as independent predictors for NR (p < 0.05, for all). The non-HDL-C/HDL-C ratio predicts the development of NR in STEMI patients with 71% sensitivity and 67% specificity at the best cut-off value. In ROC curve analysis, the non-HDL-C/HDL-C ratio was superior to traditional and non-traditional lipid markers in predicting NR (p < 0.05, for all). CONCLUSION: The non-HDL-C/HDL-C ratio can be a strong and independent predictor of NR in STEMI patients and and therefore non-HDL-C/HDL-C ratio may be a useful lipid-based biomarker that can be used in clinical practice to improve the accuracy of risk assessment in patients with STEMI.

The stress hyperglycemic ratio can predict the no-reflow phenomenon following saphenous vein graft intervention in patients with acute coronary syndrome.

AIMS: The no-reflow phenomenon (NRP) is a common complication of saphenous vein graft (SVG) interventions. The aim of this study was to investigate the effect of the stress hyperglycemia ratio (SHR) on the development of NRP in patients with acute coronary syndrome (ACS) undergoing percutaneous SVG intervention. METHODS: The study included 223 patients who presented at our center with ACS, had a history of coronary artery bypass graft and underwent a saphenous graft procedure. The relationship between SHR calculated at the time of presentation from glucose and HbA1c values, and the development of NRP evaluated after the procedure with angiography was determined with univariate and multivariate binary regression analysis. RESULT: The study population was separated into two groups as those who developed and did not develop NRP. Mean age was determined to be significantly higher in the group that did not develop NRP compared to the group with NRP (p: 0.004). Angiographically, the thrombus burden was determined to be significantly higher in the group that developed NRP (p < 0.001). Patients were separated into 3 tertiles according to the SHR level (T1, T2, T3), and the rate of NRP development was determined at a significantly higher rate in the T3 group (p < 0.001). CONCLUSIONS: This study showed that SHR, a parameter that can be easily calculated noninvasively, is an independent predictor of NRP development in ACS patients undergoing saphenous interventions. In addition, high thrombus burden and predilatation before stenting were also found to be factors that increase the likelihood of developing NRP.

A retrospective study: Association of C-reactive protein and uric acid to albumin ratio with the no-reflow phenomenon in patients with ST elevation myocardial infarction.

BACKGROUND: The no-reflow phenomenon increases mortality and morbidity in patients with ST-segment elevation myocardial infarction (STEMI). Inflammation, endothelial dysfunction, and oxidative stress play important role in its pathophysiology. We aim to evaluate the relationship between the no-reflow phenomenon and C-reactive protein (CRP) and uric acid (UA) to albumin ratio (CUAR), which is a new marker indicating all these pathophysiological mechanisms. METHODS AND RESULTS: Study population were divided into two groups as no-reflow and reflow; according to the post-procedural thrombolysis in myocardial infarction flows and myocardial blush grade. A1:4 propensity score matching was performed.CUAR was calculated by using the following formula: log10 (CRP x UA /Albumin). CUAR levels were significantly higher in patients with no-reflow than in those with reflow (P < 0.001). CUAR levels above 1.28 predicted no-reflow with higher sensitivity of 74% and specificity of 71% than all including CRP, UA and albumin (AUC = 0.80 [95%CI: 0.76-0.83], P < 0.001). In multivariate logistic regression analysis, CUAR levels above 1.28 (OR: 4.43 [3.04-6.46], 95% CI; P < 0.001) wereindependently associated with no-reflow phenomenon. CONCLUSION: Our results showed that CUAR could be a basic and available marker to predict no-reflow in patients with STEMI who underwent primary percutaneous coronary intervention.

No reflow phenomenon in CAD patients after percutaneous coronary intervention: A prospective hospital based observational study.

The present study assessed incidence, risk factors, in-hospital and short-term outcomes associated with no-reflow in patients undergoing percutaneous coronary intervention (PCI) in STEMI, NSTEMI, unstable angina and stable angina. Out of 449 patients, 42 (9.3%) developed no-reflow. Hypertension, dyslipidemia, obesity and smoking were significant risk factors. There was significant association of no-reflow with left main disease, multiple stents, target lesion length≥ 20 mm and higher thrombus grade. Interestingly, 93 patients (23.4%) of normal flow had myocardial perfusion grade (MPG) of 0/1 with mortality in 9 (10%) patients. No-reflow is associated with poor in-hospital and short-term outcomes with higher incidence of death, cardiogenic shock, heart failure and MACE. Knowledge of risk factors of no-reflow portends a more meticulous approach to improve final outcomes. MPG could be better predictor of outcomes in these patients.

Efficacy and safety of intracoronary epinephrine for the management of the no-reflow phenomenon following percutaneous coronary interventions: a systematic-review study.

BACKGROUND: Currently, no pharmacological or device-based intervention has been fully proven to reverse the no-reflow phenomenon. OBJECTIVES: To assess the efficacy and safety of intracoronary (IC) epinephrine in the management of no-reflow phenomenon following percutaneous coronary intervention (PCI), either as first-line treatment or after the failure of conventional agents. DESIGN: Systematic review. DATA SOURCES AND METHODS: PubMed and Scopus databases were systematically searched up to 28 May 2022, with additional manual search on the Google Scholar and review of the reference lists of the relevant studies to identify all published studies. Cohort studies, case series, and interventional studies written in English which evaluated the efficacy and safety of IC epinephrine in patients with no-flow phenomenon were included in our review. RESULTS: Six of the 646 articles identified in the initial search met our inclusion criteria. IC epinephrine was used either as a first-line treatment [two randomized clinical trials (RCTs)] or after the failure of conventional agents (two cohort studies and two case series) for restoring the coronary flow, mainly after primary PCI. As first-line therapy, IC epinephrine successfully restored coronary flow in over 90% of patients in both RCTs, which significantly outperformed IC adenosine (78%) but lagged behind combination of verapamil and tirofiban (100%) in this regard. In the refractory no-flow phenomenon, successful reperfusion [thrombolysis in myocardial infarction (TIMI) flow grade = 3] was achieved in three out of four patients after the administration of IC epinephrine based on the results from both case series. Their findings were confirmed by a recent cohort study that further compared IC epinephrine with IC adenosine and found significant differences between them in terms of efficacy [% TIMI flow grade 3: (69.1% versus 52.7%, respectively; p value = 0.04)] and 1-year major adverse cardiac event (MACE) outcomes (11.3% versus 26.7%, respectively; p value ⩽ 0.01). Overall, malignant ventricular arrhythmias were reported in none of the patients treated with IC epinephrine. CONCLUSION: Results from available evidence suggest that IC epinephrine might be an effective and safe agent in managing the no-reflow phenomenon.

Evaluation of Coronary Flow Level with Mots-C in Patients with STEMI Undergoing Primary PCI. / Avaliação do Nível de Fluxo Coronário com MOTS-C em Pacientes com IAMCSST Submetidos à ICP Primária.

BACKGROUND: The protective effects of mitochondrial open reading frame of the 12S rRNA-c (MOTS-C) on cardiovascular diseases have been shown in numerous studies. However, there is little documentation of the relationship between MOTS-C and coronary blood flow in ST-segment elevation myocardial infarction (STEMI). OBJECTIVE: We aimed to investigate the role of MOTS-C, which is known to have cytoprotective properties in the pathogenesis of the no-reflow phenomenon, by comparing the coronary flow rate and MOTS-C levels in patients with STEMI submitted to primary PCI. METHODS: 52 patients with STEMI and 42 patients without stenosis >50% in the coronary arteries were included in the study. The STEMI group was divided into two groups according to post-PCI TIMI (Thrombolysis In Myocardial Infarction) flow grade:(i) No-reflow: grade 0, 1, and 2 and (ii) grade 3(angiographic success). A p value of <0.05 was considered significant. RESULTS: MOTS-C levels were significantly lower in the STEMI group compared to the control group (91.9 ± 8.9 pg/mL vs. 171.8±12.5 pg/mL, p<0.001). In addition, the Receiver Operating Characteristics (ROC) curve analysis indicated that serum MOTS-C levels had a diagnostic value in predicting no-reflow (Area Under the ROC curve [AUC]:0.95, 95% CI:0.856-0.993, p<0.001). A MOTS-C ≥84.15 pg/mL measured at admission was shown to have 95.3% sensitivity and 88.9% specificity in predicting no-reflow. CONCLUSION: MOTS-C is a strong and independent predictor of no-reflow and in-hospital MACE in patients with STEMI. It was also noted that low MOTS-C levels may be an important prognostic marker of and may have a role in the pathogenesis of STEMI.

FUNDAMENTOS: Os efeitos protetores da fase de leitura aberta mitocondrial do 12S rRNA-c (MOTS-C) em doenças cardiovasculares foram demonstrados em vários estudos. Entretanto, há pouca documentação da relação entre MOTS-C e fluxo sanguíneo coronariano no infarto do miocárdio com supradesnivelamento do segmento ST (IAMCSST). OBJETIVO: Nosso objetivo foi investigar o papel do MOTS-C, que é conhecido por ter propriedades citoprotetoras na patogênese do fenômeno de no-reflow, comparando a taxa de fluxo coronariano e os níveis de MOTS-C em pacientes com IAMCSST submetidos à ICP primária. MÉTODOS: 52 pacientes com IAMCSST e 42 pacientes sem estenose >50% nas artérias coronárias foram incluídos no estudo. O grupo IAMCSST foi dividido em dois grupos de acordo com o grau de fluxo TIMI (do inglês Thrombolysis In Myocardial Infarction) pós-ICP: (i) No-reflow: graus 0, 1 e 2 e (ii) grau 3 (sucesso angiográfico). Um valor de p <0,05 foi considerado significante. RESULTADOS: Os níveis de MOTS-C foram significativamente menores no grupo IAMCSST em comparação ao grupo controle (91,9 ± 8,9 pg/mL vs. 171,8±12,5 pg/mL, p<0,001). Além disso, a análise da curva Receiver Operating Characteristics (ROC) indicou que os níveis séricos de MOTS-C tinham um valor diagnóstico na previsão de no-reflow (Área sob a curva ROC [AUC]: 0,95, IC95%: 0,856-0,993, p < 0,001). Um valor de MOTS-C ≥84,15 pg/mL medido na hospitalização mostrou ter sensibilidade de 95,3% e especificidade de 88,9% na previsão de no-reflow. CONCLUSÃO: MOTS-C é um preditor forte e independente de no-reflow e eventos cardiovasculares adversos maiores (ECAM) intra-hospitalar em pacientes com IAMCSST. Também foi observado que baixos níveis de MOTS-C podem ser um importante marcador prognóstico e podem ter um papel na patogênese do IAMCSST.

Association between kaolin-induced maximum amplitude and slow-flow/no-reflow in ST elevation myocardial infarction patients treated with primary percutaneous coronary intervention.

BACKGROUND: ST-segment elevation myocardial infarction (STEMI) patients with a high thrombus burden have a relatively high slow-flow/no-reflow risk. However, the association between kaolin-induced maximum amplitude (MAthrombin) and slow-flow/no-reflow has been scarcely explored. METHODS: STEMI patients treated with primary percutaneous coronary intervention (PCI) were retrospectively enrolled from January 2015 to December 2019 at China-Japan Friendship Hospital. MAthrombin levels were measured using thromboelastography before the PCI procedure. The patients were divided into two groups according to thrombolysis in myocardial infarction (TIMI) flow grade after primary PCI: the normal flow group (TIMI flow grade = 3) and slow-flow/no-reflow (TIMI flow grade ≤ 2). The logistic regression model and restricted cubic spline regression (RCS) were used to analyze the predictive value of MAthrombin for slow-flow/no-reflow. All patients were followed up after discharge and observed the adverse cardiovascular events between the two groups. RESULTS: A total of 690 patients were enrolled, with 108(15.7%) having slow-flow/no-reflow. The multivariate logistic regression model analysis showed that MAthrombin level was an independent risk factor for slow-flow/no-reflow. The RCS analysis showed a nonlinear relationship between MAthrombin levels and slow-flow/no-reflow. The cut-off value of MAthrombin levels for predicting slow-flow/no-reflow was 68 mm. During a median follow-up time of 4.4 years, slow-flow/no-reflow (hazard ratio 1.93, 95% confidence interval 1.27-2.93, P = 0.002) and MAthrombin levels (hazard ratio 1.06, 95% confidence interval 1.03-1.08, P < 0.001) were independent risk factors for predicting the long-term of adverse clinical cardiovascular events. CONCLUSION: MAthrombin was an independent risk factor for predicting slow-flow/ no-reflow in STEMI patients who underwent primary PCI.

Administration of intracoronary adenosine before stenting for the prevention of no-reflow in patients with ST-elevation myocardial infarction.

Objectives: No-reflow phenomenon during the primary percutaneous intervention (PCI) for ST-elevation myocardial infarction (STEMI) is accompanied by a poor clinical outcome and mortality. We aimed to determine the effect of intracoronary adenosine in preventing the no-reflow phenomenon, as detected by three different methods, in patients who underwent primary (PCI). Design. In this single-blinded randomized controlled trial, patients with acute STEMI who presented to our center and underwent primary PCI were randomized to the intervention group who received intracoronary adenosine before stenting or the control group who received the standard treatment. No-reflow phenomenon was detected using thrombolysis in myocardial infarction (TIMI) flow grade, TIMI frame count, and myocardial blush grade (MBG). The incidence of the no-reflow phenomenon was then compared between the intervention and control groups. Results. The adenosine group consisted of 110 patients (age = 57 ± 11 years; 92 (84%) male) while 118 patients were in the control group (age = 59 ± 12 years; 89 (75%) male). There was no difference between the study groups in baseline characteristics. The frequency of no-reflow phenomenon was lower in the adenosine group as assessed by TIMI flow grade (15 [14%] vs. 41 [35%]), MBG (23 [21%] vs. 63 [53%]) and TIMI frame count (16 [14%] vs. 50 [42%]) (p < .001 for all). This effect remained significant after adjustment for confounding variables. Conclusion. Intracoronary adenosine could effectively prevent the no-reflow phenomenon in STEMI patients who underwent primary PCI.

LncRNA MALAT1 functions as a biomarker of no-reflow phenomenon in ST-segment elevation myocardial infarction patients receiving primary percutaneous coronary intervention.

MALAT1 was reported to sponge miR-30e, miR-126 and miR-155 in the pathogenesis of many diseases. Plasma miR-30e can indicate the risk of no-reflow during primary percutaneous coronary intervention (pPCI), while miR-126 can be used as a predictor of coronary slow flow phenomenon. In this study, we compared the diagnostic value of above genes in the prediction of no-reflow phenomenon in ST-segment elevation myocardial infarction (STEMI) subjects receiving pPCI. Quantitative real-time PCR, ELISA, Western blot and luciferase assays were performed to explore the regulatory relationship of MALAT1/miR-30e, MALAT1/miR-126, MALAT1/miR-155, miR-126/HPSE, and miR-155/EDN1. ROC analysis was carried out to evaluate the potential value of MALAT1, miRNAs and target genes in differentiating normal reflow and no-reflow in STEMI patients receiving pPCI. Elevated MALAT1, CRP, HPSE, and EDN1 expression and suppressed miR-30e, miR-155 and miR-126 expression was found in the plasma of STEMI patients receiving pPCI who were diagnosed with no-reflow phenomenon. ROC analysis showed that the expression of MALAT1, miR-30e, miR-126 and CRP could be used as predictive biomarkers to differentiate normal reflow and no-reflow in STEMI patients receiving pPCI. MALAT1 was found to suppress the expression of miR-30e, miR-126 and miR-155, and HPSE and EDN1 were respectively targeted by miR-126 and miR-155. This study demonstrated that MALAT1 could respectively sponge the expression of miR-30e, miR-126 and miR-155. And miR-30e, miR-126 and miR-155 respectively targeted CRP, HPSE and EDN1 negatively. Moreover, MALAT1 could function as an effective biomarker of no-reflow phenomenon in STEMI patients receiving pPCI.

MELD-XI score predict no-reflow phenomenon and short-term mortality in patient with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

INTRODUCTION: No-reflow phenomenon (NRP) is one of the complications that mostly occur during percutaneous coronary intervention (PCI). In this study, we comprehensively examined the relationship between the model for end-stage liver disease-XI (MELD-XI) score and NRP. Moreover, we discussed whether the MELD-XI score could be considered as an accurate risk assessment score of patients with ST-segment elevation myocardial infarction (STEMI) who are candidates for PCI. METHODS: This retrospective study involved 693 patients with acute STEMI and who underwent an emergency PCI. They were divided into a normal reflow group or a no-reflow group on the basis of the flow rate of post-interventional thrombolysis in myocardial infarction. Univariate, multivariate logistic regression, and Cox regression analyses were performed to identify the independent predictors of NRP in both groups. Receiver operator characteristic (ROC) curves and Kaplan-Meier curves were plotted to estimate the predictive values of the MELD-XI score. RESULTS: MELD-XI score was found to be an independent indicator of NRP (odds ratio: 1.247, 95% CI: 1.144-1.360, P < 0.001). Multivariate Cox regression analysis also revealed that the MELD-XI score is an independent prognostic factor for 30-day all-cause mortality (hazard ratio: 1.155, 95% CI: 1.077-1.239, P < 0.001). Moreover, according to the ROC curves, the cutoff value of the MELD-XI score to predict NRP was 9.47 (area under ROC curve: 0.739, P < 0.001). The Kaplan-Meier curves for 30-day all-cause mortality revealed lower survival rate in the group with a MELD-XI score of > 9.78 (P < 0.001). CONCLUSION: The MELD-XI score can be used to predict NRP and the 30-day prognosis in patients with STEMI who are candidates for primary PCI. It could be adopted as an inexpensive and a readily available tool for risk stratification.