bluuebunny/crossref_metadata_2025_split huggingface dataset:
The use of allopurinol in prophylaxis against contrast-induced nephropathy in patients undergoing percutaneous coronary intervention
Authors: Mahmoud K , Hasan W , Salah Eldin H , Elramissy D 
Published: October 2024

Abstract

Background
Contrast-induced nephropathy (CIN) is a serious complication after percutaneous coronary intervention (PCI). Inflammation and development of reactive oxygen species are among the postulated mechanisms of CIN. Allopurinol with anti-inflammatory action could be a preventive method of CI-AKI.

Aim of the work
To determine the effect of adding allopurinol to hydration in the prevention of CIN in patients undergoing PCI, with or without hyperuricemia.

Methods
One hundred and seven patients with moderate to high Mehran score undergoing elective PCI were randomly allocated to the allopurinol (n=52) or the control group (n=55). Those in the allopurinol group (hyperuricemic n=25, and normouricemic n= 27) received allopurinol 300 mg one day and one hour before PCI beside intravenous hydration (1 ml/kg/hour) normal saline, a maximum of 100 ml/hour for 12 hours pre and post coronary angiography. Patients in the control group (hyperuricemic n=26 and normouricemic n=29), received the same intravenous hydration only. Serum creatinine and urea were measured before and 48 hours after the procedure while the uric acid level was measured before the procedure only. CIN was defined by a percentage increase in serum creatinine of ≥25% or absolute serum creatinine ≥0.5 mg/dl, 48 hours after PCI.

Results
The mean age of the studied patients was 59.6 ± 9.1 years old, 59% were male. No difference between both groups regarding baseline characteristics or medications. Average Mehran score was 9.0 ± 1.2. CIN was observed in 5 patients in the allopurinol group (9.6%) and 15 patients in the control group (27.3%) (P = 0.017). There was no significant difference between both groups regarding the contrast volume (179.8 ± 68.1 vs. 153.8 ± 57.9 ml, p: 0.052). Hyperuricemia had no significant effect on increasing the incidence of CI-AKI either in patients with or without CKD (p=0.964).

Conclusion
Allopurinol on the top of hydration was found to decrease the incidence of CIN following PCI in patients with moderate to high Mehran score for CIN. The anti-inflammatory action of allopurinol could be the mechanism of this favorable effect, as baseline uric acid didn't affect the results. Further multi-center study with a larger sample size is needed to offer more definite results.
Extracellular vesicle-incorporated long noncoding RNA PUNISHER is increased in coronary artery disease and regulates endothelial cell function
Authors: Hosen D R , Li M E D , Liu M E D , Jansen M E D , Nickenig D R 
Published: October 2024

Abstract

Aims
Long noncoding RNAs (lncRNAs) have emerged as biomarkers and regulators of cardiovascular disease. Circulating lncRNAs can be incorporated into extracellular vesicles (EVs). Our aim was to study the expression pattern of circulating EV-incorporated lncRNAs in patients with and without coronary artery disease (CAD). The regulation of the lncRNA PUNISHER was further assessed as an intercellular messenger in endothelial cell (EC) biology.

Methods and results
Circulating EVs were isolated from the plasma of patients using ultracentrifugation. Electron microscopy, western blot, and NTA were used to determine the size and origin of the EVs. PCR-based human lncRNA array analysis revealed that certain EV-lncRNAs are significantly different in patients with CAD compared to patients without CAD. To validate the lncRNA array results, 60 patients with (n=30) or without (n=30) CAD were prospectively studied. Four atherosclerosis-related lncRNAs (PUNISHER, GAS5, MALAT1, and H19) were quantified in the circulating EVs by using real-time quantitative PCR (RT-qPCR). Among these, PUNISHER (p=0.002) and GAS5 (0.02) were significantly increased in patients with CAD, compared to non-CAD patients. Analysis of RNA degradation revealed that circulating PUNISHER is mainly incorporated within EVs. In vitro, atherosclerotic stimuli consisting of oxLDL or TNF-a treatment caused an upregulation of PUNISHER levels in human coronary artery endothelial cells (HCAEC) and in the corresponding EVs. Labeling of EVs followed by RT-qPCR demonstrated that functional PUNISHER was transported into the recipient ECs, which accelerated cell migration, proliferation, and tube formation. Mechanistically, the RNA-binding protein hnRNPK was identified by an RNA immunoprecipitation (RIP) assay as an interaction partner of PUNISHER, regulating its loading into small EVs. Knockdown of PUNISHER abrogated the EV-mediated effects on EC migration, proliferation, and tube formation. PCR-based gene profiling showed that the expression of VEGF RNA was significantly increased in ECs by treatment with EVs. Protein stability and RNA-immunoprecipitation followed by RT-qPCR analysis indicated that the PUNISHER-hnRNPK axis regulates the stability and binding of VEGFA mRNA to hnRNPK. Knockdown of PUNISHER in EVs abrogated the EV-mediated promotion of VEGFA gene- and protein expression.

Conclusion
The circulating lncRNA PUNISHER is increased in CAD patients. Intercellular transfer of EV-incorporated PUNISHER promotes a pro-angiogenic phenotype via a VEGFA-dependent mechanism.
Early detection of cardiac dysfunction using shear wave imaging: insights into reduced cardiorespiratory fitness in childhood cancer survivors
Authors: Youssef A , Verschueren S , Vanrusselt D , Van Ermengem N , Uyttebroeck A , Hornickx M , Pleysier S , Wouters L , Cools B , D'hooge J , Voigt J U 
Published: October 2024

Abstract

Background
Diastolic dysfunction is thought to be the earliest cardiotoxic sequel after cancer therapy among childhood cancer survivors. Despite many survivors do exhibit reduced cardiorespiratory fitness (CRF) potentially due to cardiotoxicity, current echocardiographic parameters fail to detect hidden diastolic dysfunction early after therapy (1). High frame rate (HFR) shear wave imaging (SWI) is a novel tool that could give insights about myocardial stiffness, which is a key determining factor of diastolic function.

Purpose
We aimed at testing the ability of SWI to detect early alterations in myocardial stiffness among childhood cancer survivors and its relation with the reduced CRF.

Methods
Fifty childhood cancer survivors (mean 20 ±3 years) who received chemo-and/or- radiotherapy (mean time after treatment: 4 ±3 years) and thirty-two matched healthy volunteers (HV) were recruited. Conventional as well as HFR echocardiographic images (ca. 1200 frames/second) were acquired at rest using a modified commercial echocardiography machine. All participants underwent an incremental, symptom-limited cardiopulmonary exercise test on a treadmill measuring peak oxygen consumption (VO2 peak). HFR data were analysed offline. An anatomical M mode was drawn along the ventricular septum, and tissue Doppler acceleration maps were extracted to measure SW velocities after mitral valve closure (MVC) (Figure 1).

Results
Among cancer survivors, left ventricular ejection fraction (LVEF) and global longitudinal strain were significantly lower compared to HV (56 % ±4 vs 59 % ±4, and 17.6 % ±1.6 vs 19.1 % ±1.2, respectively; p &lt;0.001). However, both LVEF and GLS were within the normal range and none of them correlated with the peak VO2 (Figure 2A&B). None of the echocardiographic diastolic parameters (e.g. mitral E, E/e’, left atrial volume or TR jet velocity) showed significant difference between both groups (P &gt; 0.05). The mean SW velocities were significantly higher in cancer survivors compared to HV (3.9 ±0.6 m/s vs 3.2 ±0.3 m/s respectively; p &lt;0.001). Interestingly, SW velocities among cancer survivors showed moderate significant negative correlation with the VO2 peak (r= -0.590, p &lt;0.001) indicating increasing myocardial stiffness as the cardiorespiratory fitness declined (Figure 2C).

Conclusions
Our data indicate that myocardial stiffness in cancer survivors is significantly increased. We hypothesize that this increased stiffness may at least in part explain the significantly reduced cardiorespiratory fitness in this population. Echocardiographic shear wave elastography appears as a promising non-invasive tool for early detection of diastolic dysfunction in follow-up of childhood cancer survivors.Figure 1.Figure 2.
Significant stenosis without thrombus may be the third most common etiology of acute coronary syndrome
Authors: Mori H , Suzuki H , Shinke T 
Published: October 2024

Abstract

Background
Plaque rupture (PR), plaque erosion (PE) and calcified nodule (CN) are known as major etiologies of acute coronary syndrome (ACS). On the other hand, significant stenosis without thrombus (SSWT) can be sometimes observed in culprit plaque of ACS. However, incidence and clinical feature of SSWT in ACS patients are not well known in Japanese.

Method
This is a sub study of TACTICS registry which include ACS patients (n=702) undergoing primary percutaneous coronary intervention (PCI) under optical coherence tomography (OCT) in Japan. Using this registry data, we compared the clinical features and OCT findings of SSWT in ACS patients in comparison with PR, PE and CN. Major adverse cardiac event (MACE) was defined as death, non-fatal myocardial infarction, heart failure, or ischemia-driven revascularization at 1-year.

Results
Plaque rupture (PR: n=411, 61%) and plaque erosion (PE: n=178, 26%) were 2 major etiologies, which was followed by SSWT (n=59, 9%) and calcified nodule (CN: n=28, 4%). Clinical characteristics are shown in table 1. Patients with SSWT was slightly older than PR and PE but younger than CN. Proportion of male was fewer than PR and PE but greater than CN. In terms of traditional coronary risk factors, there were significant differences in prevalences of diabetes, active smoking, and hemodialysis among different etiologies. In SSWT, non-ST elevation myocardial infarction was the main type of ACS followed by unstable angina and ST elevation myocardial infarction (51%, 39% and 10%, respectively), which may be associated with the least CK level and greater TIMI flow. Lesion was less complex with lower proportion of type B2 or C, shorter procedure time, lower proportion of multivessel disease and lower syntax score. OCT findings are shown in table 2. Regarding lipid component and calcification, SSWT showed similar finding as PE. Cholesterol crystal was relatively less as compared to PR and PE. Kaplan-Meier survival curve showing MACE and ischemia driven-TLR are shown in figure 1 and 2. MACE and TLR was the least in SSWT.

Conclusion
SSWT was the third most common etiology of ACS with different feature from PR, PE and CN.
Platelet-large cell ratio predicts no-reflow in patients undergoing primary coronary angioplasty for ST-segment elevation myocardial infarction
Authors: Scridon A , Sus I , Lakatos E K , Demjen Z , Ceamburu A , Fisca C , Cozac D A , Mutu C C , Hadadi L 
Published: October 2024

Abstract

Background
Increased platelet indices have been shown to reflect higher degree of platelet activation and have been related to poorer short- and long-term outcomes in patients presenting with ST-segment elevation myocardial infarction (STEMI).

Purpose
We aimed to evaluate the ability of a validated marker of platelet activation (i.e., the platelet-large cell ratio [P-LCR]) to predict the occurrence of no-reflow in patients undergoing primary percutaneous coronary intervention (pPCI) for STEMI. The ability of P-LCR to predict other markers of thrombotic charge (i.e., use of glycoprotein IIb/IIIa inhibitors and/or thrombus aspiration) was also investigated.

Methods
Use of glycoprotein IIb/IIIa inhibitors and/or thrombus aspiration, occurrence of the ‘no-reflow’ phenomenon and P-LCR values on admission were recorded in 836 consecutive patients treated by pPCI for STEMI. Patients’ demographic data and symptom onset-to-cardiac catheterization laboratory time intervals were also recorded. Correlations between P-LCR values and the presence of thrombotic charge markers were evaluated.

Results
No-reflow occurred in 124 (14.8%) of the study patients; glycoprotein IIb/IIIa inhibitors and thrombus aspiration were used in 228 (27.3%) and in 289 (34.5%) of patients, respectively. Mean P-LCR values were 27.1 ± 7.6%. P-LCR values on admission were significantly higher in patients who presented no-reflow than in those who did not (29.1 ± 5.6% vs. 25.3 ± 5.8%, p = 0.03). Similarly, P-LCR were significantly higher in patients in whom glycoprotein IIb/IIIa inhibitors (29.5 ± 6.1% vs. 25.2 ± 5.3%, p = 0.04) and/or thrombus aspiration (28.4 ± 5.7% vs. 24.8 ± 5.4%, p = 0.03) were used. A P-LCR value ≥26.9% predicted the occurrence of no-reflow with 70.9% sensitivity and 55.4% specificity (p = 0.04).

Conclusions
In the present cohort, P-LCR values on admission predicted the presence of thrombotic charge markers in patients undergoing pPCI for STEMI. Evaluating P-LCR on admission could help identify patients at increased risk of no-reflow, in whom more intensive antiplatelet strategies may be of interest.
Comparison of GRACE and TIMI risk scores in the prediction of in hospital outcome among NSTEMI patients: a single centre study
Authors: Chowdhury M D , Tun-Nessa Malik F , Uddin K , Ahmed N , Badiuzzaman M , Nesaruddin M I R , Banik D , Dutta A , Shahriar Huq T , Habibur Rahman M D 
Published: October 2024

Abstract

Background
Major component of ACS, Non-ST segment elevation myocardial infarction (NSTEMI), has more than twice the incidence compared to ST-segment elevation myocardial infarction (STEMI). GRACE (Global Registry of Acute Coronary Events) and TIMI (Thrombolysis in Myocardial Infarction) risk scores are the two most popular prediction models in ACS due to TIMI’s advantage in its simplicity in clinical application and GRACE’s favorable discriminating power. Nevertheless, limited evidence compared the usefulness of these two major risk scores and their association with in-hospital events.

Purpose
To compare between the predictive ability of GRACE & TIMI risk scores for In hospital outcomes among the NSTEMI patients .

Methods
This prospective observational study was carried out from 8th march 2020 to 7th March 2022. Total 2152 acute NSTEMI patients were included. Both GRACE & TIMI risk score were calculated. For GRACE score, patients who scored ≤108 points were low risk,109-139 points were medium risk, ≥140 points were high risk . For TIMI scores patients with 0-2 scores were low risk , 3-4 scores were medium risk and 5-7 score were High risk. In Hospital outcomes were defined as the in hospital composite events which includes acute left ventricular failure, cardiogenic shock, arrhythmia & mortality.

Results
Among the 2152 patients majority were male (73.5%) with mean age of the study population were 58.33 ± .25 years. Mean Grace score & TIMI score of the study population were 137.81±16.38& 3.29±.97 respectively. Most of the patients were categorized in to Medium risk groups by both GRACE & TIMI risk scores , 70% & 51.3% respectively. However, high risk group percentage were higher in GRACE score group(41.3%) in comparison to TIMI score group(10.3%). GRACE score showed better predictive ability than TIMI score for in-hospital outcomes as evaluated by ROC curve( AUC of GRACE vs TIMI, In hospital ALVF:0.89vs 0.59, P&lt;0.001; Cardiogenic Shock 0.72 vs 0.57, P=0.002; Mortality: 0.75 vs 0.59, P=0.002; arrhythmia 0.72 vs0.63, P=0.003).

Conclusion
GRACE showed better predictive accuracy than TIMI in NSTEMI patients for in-hospital outcomes. The sequential use of TIMI and GRACE scores provide an easy and promising discriminative tool in predicting outcomes in NSTEMI patients , thus improve the identification of high-risk patients.Pic :ROC curve for prediction of ALVFPic: ROC curve for Mortality prediction
Clinical characteristics and outcomes of patients presenting with acute coronary syndromes and suspected plaque erosion
Authors: Di Vito L , Di Giusto F , Bruscoli F , Scalone G , Alfieri M , Panzella F , Delfino D , Silenzi S , Jang I K , Grossi P 
Published: October 2024

Abstract

Background
Plaque erosion (PE) is the second most common pathology of acute coronary events after plaque rupture. PE is characterized by endothelial denudation and formation of neutrophil extracellular traps. Patients with PE may have a different prognosis as compared to those with plaque rupture. Specific clinical and laboratory predictors were validated to suspect PE among acute coronary syndrome (ACS) patients.

Purpose
The objectives of this study were to compare both clinical and laboratory findings, and outcomes of ACS patients with high probability of PE and those with less likely PE.

Methods
Six hundred ninety-six ACS patients were divided into two groups (suspected PE vs less likely PE) based on 5 reported predictors of PE. The predictors were: age &lt;68, anterior ischemia, no diabetes mellitus, hemoglobin &gt;15 g/dL and normal renal function (eGFR&gt; 60 ml/min) as assessed at hospital admission.
Patients with 4 or 5 of these 5 predictors were included in the suspected PE group, while patients with 0 or 1 entered less likely PE group. Baseline clinical features and laboratory analyses at hospital admission were compared between the two groups.
Major adverse cardiac events (MACE), defined as death from any cause, non-fatal myocardial infarction or unplanned revascularization, were compared between the two groups at 20 months after hospital discharge.

Results
Among 696 patients, 283 (41%) composed the suspected PE group, while 413 (59%) entered into less likely PE group.
The suspected PE group had a higher prevalence of current smokers and had a higher BMI. They showed higher values of both LDL cholesterol and triglycerides, while C-reactive protein and fibrinogen levels were significantly lower. The suspected PE group showed a higher frequency of single vessel disease (Table).
The suspected PE group showed a significantly lower rate of MACEs at 20 months (7.4% vs 28.8%, p=0.0001) as well as death from any cause was significantly lower (2.1% vs 24.9%, p=0.0001). The median time from the index ACS episode to recurrent myocardial infarction or unplanned coronary revascularization tended to be longer in the suspected PE group as compared to the less likely PE group (15 months [9-20] vs 9 months [6-13], p=0.062) (Figure).

Conclusions
In a cohort of ACS population, the suspected PE group showed distinctive clinical characteristics with less coronary plaque burden and low grade of systemic inflammation. The suspected PE group had a better prognosis at 20-month follow-up time with a significantly lower rate of death from any cause, and non-fatal coronary events tended to occur later.Table.Baseline characteristicsFigure.Non fatal coronary events
NRF3-mediated mitochondrial superoxide promotes cardiomyocyte apoptosis and impairs cardiac functions by suppressing Pitx2
Authors: Zheng A , Chen Q , Shi Z , Xu X , Yang M , Sun S , Wang L , Wang Y , Xiao Q , Zhang L 
Published: October 2024

Abstract

Background
Myocardial infarction (MI) elicits mitochondria reactive oxygen species (ROS) production and cardiomyocyte apoptosis. Nrf3 (Nuclear factor erythroid 2-related factor 3) has an established role in regulating redox signaling and tissue homeostasis. Herein, we aimed to uncover the exact role and potential mechanism of Nrf3 in injury-induced cardiac remodeling.

Methods
Global (Nrf3-KO) and cardiomyocyte-specific (NRF3△CM) Nrf3 knockout mice were subjected to MI or ischemia/reperfusion (I/R) injury, followed by functional and histopathological analysis. Primary neonatal mice (NMVMs) and rat (NRVMs) ventricular myocytes as well as cardiomyocytes derived from human induced pluripotent stem cells (hiPSC-CMs) were used to detect the possible impact of Nrf3 on cardiomyocyte apoptosis and mitochondrial ROS production. Chromatin immunoprecipitation sequencing and immunoprecipitation–mass spectrometry analysis were used to uncover potential targets of Nrf3. MitoPQ administration and cardiomyocyte-specific AAV vector were used to further confirm the in vivo relevance of the identified signal pathways.

Results
Increased level of Nrf3 was observed in cardiomyocytes within border zone of infarcted human heart and murine cardiac tissues post-MI. Both global and cardiomyocyte-specific Nrf3 knockout significantly decreased injury-induced mitochondrial ROS production and cardiomyocyte apoptosis, consequently improving cardiac functions. Additionally, cardiac-specific Nrf3 overexpression reversed the cardiac phenotypes observed in Nrf3-KO mice. Functional studies showed that Nrf3 promoted NMVM, NRVM and hiPSC-CM apoptosis by increasing mitochondrial ROS production. Critically, restoring mitochondrial ROS using MitoParaquat blunted the beneficial effects of Nrf3 deletion on cardiac functions and remodeling. Mechanistically, the cardiac redox regulator paired-like homeodomain transcription factor 2 (Pitx2) was identified as one of the main target genes of Nrf3. Specifically, Nrf3 binds to Pitx2 gene promoter where it increases Pitx2 gene promoter DNA methylation through recruiting heterogeneous nuclear ribonucleoprotein K and DNA-methyltransferase 1 complex, thereby inhibiting Pitx2 expression. Importantly, cardiomyocyte-specific knockdown of Pitx2 blunted the beneficial effects of Nrf3 deletion on cardiac functions and remodeling.

Conclusions
Nrf3 promotes injury-induced cardiomyocyte apoptosis and deteriorates cardiac functions by increasing mitochondrial ROS production via suppressing Pitx2 expression. Targeting Nrf3-Pitx2-mitochondrial ROS signal axis could represent novel therapeutics for treating MI patients.Graphic Abstract
Shear wave speed, dispersion slope and anisotropy evaluation using cardiac shear wave elastography in patients with Fabry disease
Authors: Cafezeiro C , Alencar A C , Pereira F L , Mathias Jr W , Dabarian A L , Chammas M C , Fernandes F 
Published: October 2024

Abstract

Background
Cardiac shear wave imaging has been proposed to investigate left ventricular myocardial alterations non-invasively. Dispersion slope and anisotropy are fundamental properties that have not been studied in Fabry disease (FD) patients yet.

Purpose
The aim of this study was to determine and compare shear wave propagation speed, dispersion slope and fractional anisotropy in FD patients and healthy controls.

Methods
We prospectively included 20 FD patients and 20 healthy controls (HC). Shear wave speed, dispersion slope and fractional anisotropy were measured non-invasively in anteroseptal basal segment using an ultrasound for cardiac shear wave imaging. Echocardiography, electrocardiogram and laboratory evaluations were performed.

Results
Shear wave propagation speed was higher in FD patients than in HC group (1.46 ± 0.12 m/s and 1.36 ± 0.17 m/s, p = 0.03). No difference was found in dispersion slope (11.4 m/s/kHz in FD group and 11.3 m/s/kHz in HC group, p = 0.6). Fractional anisotropy was 0.05 ± 0.04 in FD group and 0.05 ± 0.04 in HC group, p = 0.4.

Conclusion
Shear wave speed was higher in FD patients compared to control group. Dispersion slope and fractional anisotropy in FD group did not reveal significant difference to the control group.