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Among the patients in the syncope group, the sensitivity of the HUTT was 65.9%, which was significantly higher than a sensitivity of 44.8% for patients in the non-syncope group (P 60 years old), the sensitivities were 74.7%, 67.7%, 45.6%, and 31.2%, respectively. And all gender, age and symptom (whether suffered from a syncope or not) significantly affected the positive responses of HUTT. There were two adverse events and no deaths during the HUTT in this study. Conclusion The direct drug-potentiated HUTT is a safe and highly sensitive tool with which to diagnose VVS. Patients with precursor syncope symptoms without syncope should undergo a HUTT, especially young females presenting with weakness and sweating, which can decrease the probability of a misdiagnosis or a missed diagnosis.Background Tetralogy of Fallot (TOF) is the most common cyanotic heart disease. However, the association of cardiac metabolic reprogramming changes and underlying molecular mechanisms in TOF-related chronic myocardial hypoxia damage are still unclear. Methods In this study, we combined microarray transcriptomics analysis with liquid chromatography tandem-mass spectrometry (LC-MS/MS) spectrum metabolomics analysis to establish the metabolic reprogramming that occurs in response to chronic hypoxia damage. Two Gene Expression Omnibus (GEO) datasets, GSE132176 and GSE141955, were downloaded to analyze the metabolic pathway in TOF. Then, a metabolomics analysis of the clinical samples (right atrial tissue and plasma) was performed. Additionally, an association analysis between differential metabolites and clinical phenotypes was performed. Next, four key genes related to sphingomyelin metabolism were screened and their expression was validated by real-time quantitative PCR (QT-PCR). Results The gene set enrichment analysis (GSEA) showed that sphingolipid metabolism was downregulated in TOF and the metabolomics analysis showed that multiple sphingolipids were dysregulated. Additionally, genes related to sphingomyelin metabolism were identified. We found that four core genes, UDP-Glucose Ceramide Glucosyltransferase (UGCG), Sphingosine-1-Phosphate Phosphatase 2 (SGPP2), Fatty Acid 2-Hydroxylase (FA2H), and Sphingosine-1-Phosphate Phosphatase 1 (SGPP1), were downregulated in TOF. Conclusion Sphingolipid metabolism was downregulated in TOF; however, the detailed mechanism needs further investigation.We reported a case of sitosterolemia, which is a rare genetic disease, characterized by increased plant sterol absorption and great heterogeneity of clinical manifestations. Our patient was initially referred to the lipid clinic due to high cholesterol levels and premature cardiovascular disease. Diagnosis of familial hypercholesterolemia was established in accordance with the Dutch Lipid Clinic Network criteria. Next-generation sequencing was later performed, which revealed a nonsense mutation in the ABCG8 gene, which led to the diagnosis of sitosterolemia. The aim of our report is to demonstrate, how genetic testing helped to make the correct diagnosis and to explain many of the patient's health problems, which etiology remained unclear for many years.Aim Thoracic aortic dissection (TAD) is a high-risk vascular disease. The mortality rate of untreated TADs in 24 h was as high as 50%. Thus, rapid diagnosis of TAD in the emergency department would get patients to the right treatments to save their lives. Methods We profiled the proteome of aortic tissues from TAD patients using a label-free quantification proteomics method. The differentially expressed proteins were screened and subjected to bioinformatics analysis. Candidate biomarkers were selected and validated in independent serum samples using enzyme-linked immunosorbent assays (ELISAs). The diagnostic values were further predicted via receiver operating characteristic (ROC) curve analysis. Results A total of 1,141 differentially expressed proteins were identified in aortic tissues from 17 TAD patients and eight myocardial infarction (MI) patients. Six proteins were selected as candidate biomarkers for ELISAs in an independent training set of 20 serum samples (TAD = 10, MI = 10). Of these proteins, four with a P-value less then 0.01 were further validated in another independent set of 64 serum samples (TAD = 32, MI = 32) via ELISAs. ITGA2, COL2A1, and MIF had P-values less then 0.0001, and their areas under the curve (AUCs) were 0.801 (95% CI 0.691-0.911), 0.773 (95% CI 0.660-0.887), and 0.701 (95% CI 0.574-0.828), respectively. Conclusion ITGA2, COL2A1, and MIF were identified as promising biomarkers for discriminating TAD from emergency patients with severe chest pain. Biomarker-guided emergency triage could further shorten the time for patients to get more effective treatments.Fibromuscular dysplasia (FMD) is the second common cause of renovascular hypertension. With the advent of endovascular therapy, angiography has become a diagnostic gold standard for FMD. Optical coherence tomography (OCT) by reflecting in vivo histology may improve diagnostic and classification accuracy. Renal fractional flow reserve (rFFR), measured by pressure guidewire, may distinguish the patients who may benefit from revascularization by identifying physiologically significant stenoses. However, the role of usage of both OCT and rFFR is not well-studied. We herein report a 17-year-old male with renovascular hypertension due to FMD. Angioplasty of drug-coated balloon (DCB) guided by OCT and FFR favorably achieved blood pressure (BP) control. In conclusion, the utility of both OCT and FFR may be useful for the appropriate selection of patients with renal FMD.

Hypothermic circulatory arrest (HCA) in aortic arch surgery has a significant risk of neurological injury despite the newest protective techniques and strategies. Nitric oxide (NO) could exert a protective role, reduce infarct area and increase cerebral perfusion. This study aims to investigate the possible neuroprotective effects of NO administered in the oxygenator of selective antegrade cerebral perfusion (SCP) during HCA.

Thirty male SD adult rats (450-550 g) underwent cardiopulmonary bypass (CPB), cooling to 22°C body core temperature followed by 30 min of HCA. Rats were randomized to receive SCP or SCP added with NO (20 ppm) administered through the oxygenator (SCP-NO). All animals underwent CPB-assisted rewarming to a target temperature of 35°C in 60 min. At the end of the experiment, rats were sacrificed, and brain collected. Immunofluorescence analysis was performed in blind conditions.

Neuroinflammation assessed by allograft inflammatory factor 1 or ionized calcium-binding adapter molecule 1 expression, a microglia activation marker was lower in SCP-NO compared to SCP (4.11 ± 0.59 vs. SB525334 research buy 6.02 ± 0.18%;

< 0.05). Oxidative stress measured by 8oxodG, was reduced in SCP-NO (0.37 ± 0.01 vs. 1.03 ± 0.16%;

< 0.05). Brain hypoxic area extent, analyzed by thiols oxidation was attenuated in SCP-NO (1.85 ± 0.10 vs. 2.74 ± 0.19%;

< 0.05). Furthermore, the apoptotic marker caspases 3 was significantly reduced in SCP-NO (10.64 ± 0.37 vs. 12.61 ± 0.88%;

< 0.05).

Nitric oxide administration in the oxygenator during SCP and HCA improves neuroprotection by decreasing neuroinflammation, optimizing oxygen delivery by reducing oxidative stress and hypoxic areas, finally decreasing apoptosis.

Nitric oxide administration in the oxygenator during SCP and HCA improves neuroprotection by decreasing neuroinflammation, optimizing oxygen delivery by reducing oxidative stress and hypoxic areas, finally decreasing apoptosis.Background Clinical trials of non-vitamin K antagonist oral anticoagulants (NOACs) in patients with chronic heart failure and atrial fibrillation (AF) have demonstrated reduced risks of stroke and bleeding compared with vitamin K antagonists (VKAs). Here, we aim to assess the clinical efficacy and safety of rivaroxaban, a NOAC, compared with warfarin, a VKA, and the effects of rivaroxaban on cardiovascular biomarkers in patients with acute decompensated heart failure (ADHF) with reduced ejection fraction (≤40%) and AF. Methods Rivaroxaban Once-daily vs. dose-adjusted vitamin K antagonist on biomarkers in Acute Decompensated Heart Failure and Atrial Fibrillation (ROAD HF-AF) is a randomized, open-labeled, controlled, prospective, multicenter pilot study designed to assess cardiovascular biomarkers and the safety of rivaroxaban (20 or 15 mg in patients with creatinine clearance 30-49 mL/min per day) compared with VKA (target international normalized range 2-3) in 150 patients hospitalized with ADHF and AF. The primary endpoint is the change in circulating high-sensitivity cardiac troponin (hsTn) during hospitalization. The secondary endpoints are bleeding, hospital stay duration, in-hospital mortality, and changes in cardiovascular, renal, and thrombosis biomarkers. Patients will be followed for 180 days. Conclusion We hypothesize that rivaroxaban will reduce myocardial injury and hemodynamic stress, as reflected by the biomarker status, within 72 h in patients with ADHF and AF, compared with VKA. We hope to facilitate future biomarker-based, large-scale outcome trials using NOACs in patients with ADHF and AF, based on the results of this multicenter, randomized, controlled study.Purpose There is uncertainty as to which anticoagulant should be used in non-valvular atrial fibrillation (AF) with valvular heart disease. This systematic review and meta-analysis aimed to assess the efficacy and safety of direct-acting oral anticoagulants (DOACs) compared with warfarin in patients with non-valvular AF with valvular heart disease. Methods We performed a comprehensive literature search using PubMed, Scopus, Embase, and Clinicaltrials.gov from the inception of databases up until August 2, 2021, and the search was updated and finalized on October 17, 2021. The intervention group was DOACs and the control group was warfarin. The primary outcome was systemic embolism and stroke (SSE), and the secondary outcome was major bleeding and intracranial hemorrhage. The pooled effect estimate was reported as the hazard ratio (HR) and odds ratio (OR). Results There were 21,185 patients from seven studies included in this systematic review and meta-analysis. Stroke and systemic embolism were lower in patients receiving DOACs [HR 0.76 (95% CI 0.67, 0.87), p less then 0.001; I2 5%] compared with warfarin. The subgroup analysis on RCTs showed the significant reduction of SSE in the DOACs group [HR 0.73 (95% CI 0.60, 0.89), p = 0.002; I2 16%]. There was no significant difference in terms of major bleeding [HR 0.89 (95% CI 0.75, 1.05), p = 0.18; I2 69%]. Intracranial hemorrhage [HR 0.42 (95% CI 0.22, 0.80), p = 0.008; I2 73%] were lower in the DOAC group. Conclusion This meta-analysis indicates that DOACs were associated with a lower risk of SSE and intracranial hemorrhage compared with patients receiving warfarin. There was no significant difference between the two groups in terms of major bleeding.Background During arteriogenesis, outward remodeling of the arterial wall expands luminal diameter to produce increased conductance in developing collaterals. We have previously shown that diameter expansion without loss of internal elastic lamina (IEL) integrity requires both degradation of elastic fibers and LOX-mediated repair. The aim of this study was to investigate the expression of genes involved in remodeling of the extracellular matrix (ECM) using a model of arteriogenesis. Methods Sprague-Dawley rats underwent femoral artery ligation with distal arteriovenous fistula (FAL + AVF) placement. Profunda femoral arteries (PFA) were harvested for analysis at various time points. Serum desmosine, an amino acid found exclusively in elastin, was evaluated with enzyme-linked immunosorbent assay (ELISA) as a marker of tissue elastolysis. Tissue mRNA isolated from FAL + AVF exposed PFAs was compared to the contralateral sham-operated using qPCR. HCAECs were cultured under low shear stress (8 dyn·s/cm 2) for 24 h and then exposed to high shear stress (40 dyn·s/cm 2) for 2-6 h.

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