Vascular Health and Risk Management最新文献

Purpose: To evaluate the performance and outcomes of the 6-minute magnetic resonance imaging (MRI) protocol in diagnosing stroke within Indonesian healthcare setting compared to computed tomography (CT).

Patients and methods: This retrospective single-center study was conducted at the Universitas Indonesia Hospital in Depok, Indonesia from September 2021 to September 2023. Patients who were diagnosed with acute stroke underwent a clinical evaluation and a 6-minute MRI protocol. The primary objective was to assess the efficiency of the 6-minute MRI protocol in promptly and accurately evaluating acute stroke patients, including determining average MRI time, thrombolysis eligibility, and post-thrombolysis outcomes compared to CT imaging. Exclusions comprised those requiring resuscitation, lack of stroke code activation, or having incomplete documentation.

Results: This study involved 182 stroke patients, 136 of which underwent MRI and 46 had CT scans. Thrombolysis eligibility was similar between the groups (48.9% for MRI vs 47.8% for CT-Scan), but a higher proportion of eligible MRI patients received thrombolysis (70.1% vs 54.5%, p = 0.037). MRI also achieved shorter door-to-imaging times, especially from February to June 2022. Among those treated for ischemic stroke via MRI, 70.3% showed improvement compared to 55% for CT (p=0.016). Door-to-MRI times varied across periods, averaging 88.2 minutes before national healthcare insurance collaboration, 29.1 minutes during transition, and 47.8 minutes afterward.

Conclusion: This study emphasizes the crucial role of the 6-minute MRI protocol for accurately diagnosing stroke types, severity, and determining thrombolysis eligibility. Positive outcomes in thrombolysis patients using this protocol highlight its effectiveness. However, prolonged time-to-MRI indicates the need for further improvement. Optimizing time management and workflow efficiency are critical for improving treatment efficacy and safety.

Purpose: To explore the association between angiopoietin-like protein 2 (Angptl2) and cyclophilin A (CyPA) with acute myocardial infarction (AMI) and the occurrence of in-stent restenosis (ISR) after percutaneous coronary intervention (PCI).

Patients and methods: A single-center retrospective research was conducted. Clinical data from 146 AMI patients who underwent PCI at our hospital were analyzed and designated as the AMI group. Additionally, 56 healthy individuals who underwent medical check-ups during the same period were enrolled as the Control group. Serum levels of Angptl2 and CyPA were compared between the AMI and control groups. Furthermore, based on the presence or absence of in-stent restenosis (ISR) during the follow-up period, the AMI patients were further divided into ISR and NISR groups. Logistic regression analysis was utilized to ascertain the risk factors influencing ISR after PCI in AMI patients. The diagnostic value of serum Angptl2 and CyPA for ISR after PCI was assessed using the receiver operating characteristic (ROC) curve.

Results: Compared with the Control group, the AMI group exhibited significantly elevated levels of Angptl2 and CyPA (P<0.05). Logistic regression analysis identified serum Angptl2 and CyPA are risk factors for occurrence of ISR after PCI in AMI patients. Additionally, the ROC curve analysis demonstrated that the combined use of serum Angptl2 and CyPA achieved an area under the curve (AUC) of 0.895 for predicting ISR in AMI patients after PCI.

Conclusion: Elevated serum levels of Angptl2 and CyPA in AMI patients who developed ISR after PCI suggest that these biomarkers may serve as potential risk indicators for predicting ISR following PCI.

Introduction: Manny evidence indicates that numerous immune cells are linked to the onset and progression of VTE, though the causal relationship remains unclear. To determine the association between immune cells and VTE, we performed a bidirectional two-sample Mendelian randomization (MR) study.

Methods: A comprehensive MR analysis was conducted to ascertain the causal relationship between immune cell signatures and VTE. Leveraging publicly available genetic data, we examined the causal associations between 731 immune cell signatures and the risk of VTE. The analysis encompassed four types of immune signatures, namely median fluorescence intensities, relative cell counts, absolute cell counts, and morphological parameters. We employed the two-sample MR analysis, used the inverse variance-weighted (IVW) approach as the primary analytical method. Rigorous sensitivity analyses were employed to validate the robustness, heterogeneity, and presence of horizontal pleiotropy in the results. Furthermore, the reverse MR analysis was implemented to confirm the existence of reverse causal relationships.

Results: Eighteen immune cell signatures were found to have nominally significant associations with VTE according to the IVW method. The level of CD14 expression on CD14+ CD16+ monocytes (OR 0.95) and ten other phenotypes were identified as protective factors against VTE. Conversely, the percentage of HLA DR+ T cells among lymphocytes (OR 1.03) and six other phenotypes were identified as risk factors associated with an increased likelihood of VTE. The expression level of CX3CR1 on CD14- CD16+ monocytes showed a potential bidirectional causal relationship.

Conclusion: Our study identified 18 types of immune cell signatures that could impact VTE development, offering novel insights for future mechanistic and clinical studies in this field. Further studies to prospectively validate our findings are needed.

Purpose: It is crucial to differentiate critically ill patients exhibiting thrombocytopenia and hemolytic anemia alongside organ damage to enable rapid identification of thrombotic thrombocytopenic purpura (TTP) and TTP-like syndrome, which allows for targeted emergency interventions such as plasma exchange.

Patients and methods: This study retrospectively analyzed clinical data from patients with TTP and TTP-like syndrome to further elucidate the potential differences between these conditions. We also established a new predictive model to facilitate early identification and differentiation between TTP and TTP-like syndrome. A new predictive model for diagnosing TTP was developed using five key indicators: reticulocyte percentage, platelet count, schistocyte percentage, LDH/ULN, and indirect bilirubin. The performance of this new model was compared with the traditional PLASMIC score by evaluating sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV).

Results: Thirty-five patients were diagnosed with TTP and 42 were diagnosed with TTP-like syndrome. TTP is most commonly associated with autoimmune diseases (n=13, 37.14%), while TTP-like syndrome frequently arises from infections (n=23, 54.76%). The ADAMTS13 activity was significantly lower in the TTP group than in the TTP-like syndrome group (Mean 8.30% vs 46.12%). TTP-like syndrome patients had significantly higher levels of inflammatory markers. The new predictive model was developed for TTP with a predictive ability of 96.9%. Overall, 16 patients (20.77%) died, including 3 (8.57%) in the TTP group and 13 (30.95%) in the TTP-like syndrome group. Kaplan-Meier survival analysis showed significant differences in survival between TTP and TTP-like syndrome patients, with a 180-day overall survival (OS) rate of 90.6% vs 60.9% (p=0.009); and plasma exchange improved 180-day OS rate in the TTP group compared to the TTP-like syndrome group (90.6% vs 65.6%) (p=0.054).

Conclusion: This study demonstrates that TTP and TTP-like syndrome are two distinct types of diseases. The new predictive model has shown good efficacy in distinguishing TTP and TTP-like syndrome. Plasma exchange significantly improves survival in TTP patients; however, its effect on TTP-like syndrome is minimal.

Background: Peripheral artery disease (PAD), a common manifestation of systemic atherosclerosis, is linked to high morbidity and mortality. Risk factors such as age, male gender, and hyperlipidemia significantly contribute to PAD. This study aims to estimate the Predictors and associations of peripheral artery diseases in the Abu Dhabi population.

Methods: Cross-sectional analysis of diabetic patients who had ankle brachial index tests in 2018-2019. Data collected from electronic medical records include demographics, treatment history, comorbidities (hypertension, smoking), lab results (HbA1c, renal function, lipid profile), and findings from sudoscan test used to assess the function of small nerve fibers and evaluate autonomic dysfunction. A cohort study from the Abu Dhabi Cardiovascular Risk Study (ADRS), to determine the predictors and relationships associated with peripheral artery disease in Abu Dhabi. Data were analyzed using Statistical Package for the Social Sciences (SPSS) version 26.

Results: Among the 359 patients from the cross-sectional study, 65.5% had normal ABI, 14.2% had low abnormal ABI, and 20.3% had high abnormal ABI. The average age was 65.3 years, with 66.3% females and 75.49% United Arab Emirates (UAE) nationals. Most patients (65.2%) were on non-insulin treatments, and 75.8% had hypertension. The mean HbA1c level was 7.3%. Regarding renal function, 51.5% had stage 1 estimated glomerular filtration rate (eGFR), and 9.2% had abnormal eye grading. Ulcers were present in 95.8%, and 9.7% had vascular referrals. Multivariate analysis showed no significant predictors of abnormal ABI (p > 0.05). In the cohort study of 8699 patients, PAD prevalence was highest among those aged 40-59, with significant associations with age, smoking, and diabetes.

Conclusion: Abnormal ABI was present in 34.5% of patients, with no significant association with various risk factors. However, the cohort study showed that age, smoking, and diabetes are significantly related to PAD development.

Purpose: Aquaporin 1 (AQP1), a transmembrane water channel protein, has been implicated in the regulation of necroptosis. However, its specific role in atherosclerotic plaque stability through the modulation of necroptosis remains unclear. Therefore, in this study, we aim to investigate whether AQP1 influences necroptosis in atherosclerosis by binding to receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and decreasing the expression of receptor-interacting serine/threonine-protein kinase 3 (RIPK3) and mixed lineage kinase domain-like pseudokinase (MLKL).

Patients and methods: The gene expression of AQP1 and necroptosis-associated genes significantly differ between atherosclerosis and normal groups. Genes linked to necroptosis were screened to influence the AS identified by weighted gene coexpression network analysis (WGCNA). Then we collected femoral atherosclerosis and normal aortic samples, further conducted single-cell sequencing and spatial transcriptomic methods to confirm the potential function and pathway of AQP1 in endothelial cells. Meanwhile, we overexpressed AQP1 in ox-LDL-treated endothelial cells in vitro.

Results: Firstly, via single-sample Gene Set Enrichment Analysis (ssGSEA) scores, we found that necroptosis plays the most important role among all ways of programmed cell death in two kinds of atherosclerosis. AQP1, RIPK1, RIPK3 and MLKL express differently in normal and atherosclerosis tissue by differentially expressed gene (DEG) analysis and Western Blot (WB). WGCNA analysis indicates that AQP1, MLKL and RIPK3 were significantly related to the AS. The area under the curve of the above hub genes was greater than 0.8 (AQP1 0.946, RIPK1 0.908, RIPK3 0.988, MLKL 0.863). We found AQP1 highly enriched in endothelial cells (ECs) by single-cell analysis. We sequenced the samples by spatial transcriptome and found that AQP1 was also mainly enriched in ECs both in expression and spatial location. With AQP1 overexpression in ECs, it significantly inhibited the expression of MLKL and RIPK3 and stimulated EC proliferation.

Conclusion: Our study identified that AQP1 suppresses atherosclerotic necroptosis by inhibiting the expression of RIPK3 and MLKL in ECs which might indicates that AQP1 plays a role in atherosclerosis. This new mechanism contributes to improving the diagnostic, prognostic, and therapeutic outcomes of atherosclerosis.

Background: Aerobic training has been considered beneficial for determining the detrimental alterations in blood vessels caused by aging.

Objective: Evaluate the relationship between the preventive effects of aerobic exercise and time of practice on cardiovascular health, in aged Wistar rats.

Methods: Wistar rats (16 months) were divided into 3 groups: (1) sedentary (AGED); (2) long-term trained61 weeks (LTT); and (3) short-term trainedfinal 8 weeks of life (STT). Body weight, maximum physical capacity, systolic blood pressure (SBP), pulse wave velocity (PWV), plasma nitrite (NO), oxidative stress (TBARS), wall thickness, the wall-to-lumen ratio, and collagen of the thoracic aorta, carotid, and femoral arteries were measured.

Results: Both trained groups showed an increase in physical capacity when compared to the AGED group (p=<0.001 for LTT and p=0.011 for STT), and the LTT group demonstrated higher values when compared to the STT group (p= 0.004). The LTT group presented attenuation of PWV (p= 0.002) and a reduction in the wall thickness and wall-to-lumen ratio of the thoracic aorta (p=0.032 and 0.008, respectively) and carotid arteries (p=0.019 and 0.012, respectively) when compared to the AGED group. The STT group presented a reduction in TBARS compared to the AGED group (p=0.046). Additionally, both trained groups (LTT and STT) presented a reduction in the percentage of arterial collagen compared to the AGED group in the thoracic aorta (p=<0.001 and p=0.001 respectively) and carotid arteries (p= <0.008 and p= 0.041 respectively).

Conclusion: This study demonstrated that long-term training decreased the level of collagen, PWV values, wall thickness, and the wall-to-lumen ratio of the aorta and carotid arteries compared to the AGED group. Moreover, short-term training reduced TBARS and collagen percentage in the aorta and carotid arteries compared to the AGED group.

Background: Hypertension (HT) is a major risk factor for adult morbidity and mortality in low- and middle-income countries and little is known regarding the distribution of HT risk and treatment access within urban areas.

Patients and methods: We used data from the Vientiane Multi-Generational Birth Cohort in urban Lao PDR to assess the prevalence of loss and retention across five stages of HT care for 40+ year old adults: i) prevalence of hypertension, ii) hypertensives who ever had their BP measured by a health care professional, iii) hypertensives ever diagnosed with HT by a professional, iv) patients currently treated with HT medication, and v) patients with currently controlled BP. We estimated associations between sociodemographic and lifestyle predictors and the proportion of participants who reached each care cascade step using mutually adjusted Poisson regression modeling.

Results: Among the 3196 participants aged 40 to 99 years, the overall prevalence of HT was 16.3%, with higher rates for women, people over 60 years, peripheral district residents, low educated, widowed, and obese. Among people with HT, 90.2% ever had their BP measured by a health care professional, 69.3% ever received a HT diagnosis, 60.9% HT were currently on (drug) treatment, and 39.5% had currently controlled BP. The largest cascade of care losses occurred at the diagnosis and control stages with better outcomes for women. While central districts showed higher rates of diagnosis, control levels were lower than in peripheral districts, but there these differences appeared to be explained by adjusting for sociodemographic and lifestyle factors.

Conclusion: While HT prevalence in Lao PDR is lower than reported for other LMICs, more than 16% over the age of 40 years suffer from HT, and 60% of these cases are currently not controlled. Major policy efforts are needed to support this population and to prevent HT-driven excess mortality.

Background: Kawasaki disease (KD), also known as mucocutaneous lymph node syndrome, is a systemic immune vasculitis with an unclear etiology. It is often complicated by coronary artery disease. This study uses bidirectional Mendelian randomization (MR) to investigate the interaction between KD and circulating inflammatory factors, providing insights into their causal relationships.

Methods: We conducted a two-way pooled MR analysis to examine the causal links between 41 circulating inflammatory regulators and the risk of KD. Genetic data related to inflammation were sourced from three genome-wide association studies (GWASs) involving CRP, PCT, and cytokines, while KD data were derived from other studies. Inverse-variance weighting (IVW) was the primary MR method, with sensitivity analyses performed using MR‒Egger, weighted median, weighted mode, and MR-PRESSO to ensure robustness.

Results: Forward MR analyses showed no significant relationship between inflammatory factors and KD outcomes. In contrast, reverse MR, with KD as the exposure factor, revealed that interleukin-2 (IL-2) and interleukin-8 (IL-8) were significantly associated with KD (IL-2: OR=1.0085, P=0.037; IL-8: OR=1.0099, P=0.014). Borderline significant associations were observed for factors such as B_NGF, EOTAXIN, HGF, and IL_12_P70 in MR‒Egger and weighted median analyses.

Conclusion: This bidirectional MR study highlights the role of circulating inflammatory modulators in KD risk, offering insights into KD pathogenesis and potential therapeutic targets.