-
Annals of Vascular Surgery Jun 2024Assess subsequent cardiovascular events and all-cause mortality in patients with intact AAA treated by EVAR according to the existence of isolated EL at 1 year after...
OBJECTIVE
Assess subsequent cardiovascular events and all-cause mortality in patients with intact AAA treated by EVAR according to the existence of isolated EL at 1 year after EVAR implantation.
METHODS
This retrospective, single-centre study included patients treated with EVAR between 2010 and 2017 in the vascular surgery department of the University Hospital of Lyon with a infrarenal AAA > 50 mm. The baseline clinical characteristics collected just before EVAR were retrieved from electronic patient records of our institution. AAA characteristics, procedure and the one-year post-operative CTA were reported. Study endpoints, major adverse cardiovascular events (MACE), major adverse lower extremity events (MALE) and all-cause mortality, were recorded during follow-up. Patients were divided into 2 groups according to the presence of isolated EL (EL +) or absence (EL -) of any endoleak on CTA at 1 year. MACE, MALE and all-cause mortality were compared between both groups.
RESULTS
During the study period, 589 patients were treated by endovascular surgery and 207 were included. According to the CTA results at 1 year, 60 patients (29%) were included in the EL + group, and 147 patients (71%) in the EL - group. A total of 109 patients (53%) experienced a MACE or MALE; significantly fewer patients in the EL + than in the EL - group did so (p = .009). There were 47 patients (23%) who experienced at least one MALE, and the frequency was significantly lower in the EL + group (p = .017).
CONCLUSION
Patients with AAA treated by EVAR who did not develop EL at one year, were at higher risk of MALE during follow-up. This might be explained by more frequent symptomatic LEPAD at baseline in this group. These patients therefore require a closer follow-up and strict control of cardiovascular risk factors to prevent cardiovascular morbi-mortality.
PubMed: 38942363
DOI: 10.1016/j.avsg.2024.06.001 -
Computer Methods and Programs in... Jun 2024In this work, the analysis of the importance of hemodynamic updates on a mechanobiological model of atheroma plaque formation is proposed.
BACKGROUND AND OBJECTIVE
In this work, the analysis of the importance of hemodynamic updates on a mechanobiological model of atheroma plaque formation is proposed.
METHODS
For that, we use an idealized and axisymmetric model of carotid artery. In addition, the behavior of endothelial cells depending on hemodynamical changes is analyzed too. A total of three computational simulations are carried out and their results are compared: an uncoupled model and two models that consider the opposite behavior of endothelial cells caused by hemodynamic changes. The model considers transient blood flow using the Navier-Stokes equation. Plasma flow across the endothelium is determined with Darcy's law and the Kedem-Katchalsky equations, considering the three-pore model, which is also employed for the flow of substances across the endothelium. The behavior of the considered substances in the arterial wall is modeled with convection-diffusion-reaction equations, and the arterial wall is modeled as a hyperelastic Yeoh's material.
RESULTS
Significant variations are noted in both the morphology and stenosis ratio of the plaques when comparing the uncoupled model to the two models incorporating updates for geometry and hemodynamic stimuli. Besides, the phenomenon of double-stenosis is naturally reproduced in the models that consider both geometric and hemodynamical changes due to plaque growth, whereas it cannot be predicted in the uncoupled model.
CONCLUSIONS
The findings indicate that integrating the plaque growth model with geometric and hemodynamic settings is essential in determining the ultimate shape and dimensions of the carotid plaque.
PubMed: 38941860
DOI: 10.1016/j.cmpb.2024.108296 -
European Journal of Preventive... Jun 2024
PubMed: 38941268
DOI: 10.1093/eurjpc/zwae206 -
Cardiovascular Drugs and Therapy Jun 2024Heme oxygenase-1 (HO-1) is a crucial enzyme in heme metabolism, facilitating the breakdown of heme into biliverdin, carbon monoxide, and free iron. Renowned for its... (Review)
Review
PURPOSE
Heme oxygenase-1 (HO-1) is a crucial enzyme in heme metabolism, facilitating the breakdown of heme into biliverdin, carbon monoxide, and free iron. Renowned for its potent cytoprotective properties, HO-1 showcases notable antioxidant, anti-inflammatory, and anti-apoptotic effects. In this review, the authors aim to explore the profound impact of HO-1 on cardiac senescence and its potential implications in myocardial infarction (MI).
RESULTS
Recent research has unveiled the intricate role of HO-1 in cellular senescence, characterized by irreversible growth arrest and functional decline. Notably, cardiac senescence has emerged as a pivotal factor in the development of various cardiovascular conditions, including MI. Notably, cardiac senescence has emerged as an important factor in the development of various cardiovascular conditions, including myocardial infarction (MI). The accumulation of senescent cells, spanning vascular endothelial cells, vascular smooth muscle cells, cardiomyocytes, and progenitor cells, poses a significant risk for cardiovascular diseases such as vascular aging, atherosclerosis, myocardial infarction, and ventricular remodeling. Inhibition of cardiomyocyte senescence not only reduces senescence-associated inflammation but also impacts other myocardial lineages, hinting at a broader mechanism of propagation in pathological remodeling. HO-1 has been shown to improve heart function and mitigate cardiomyocyte senescence induced by ischemic injury and aging. Furthermore, HO-1 induction has been found to alleviate HO-induced cardiomyocyte senescence. As we grow in our understanding of antiproliferative, antiangiogenic, anti-aging, and vascular effects of HO-1, we see the potential to exploit potential links between individual susceptibility to cardiac senescence and myocardial infarction.
CONCLUSIONS
This review investigates strategies for upregulating HO-1, including gene targeting and pharmacological agents, as potential therapeutic approaches. By synthesizing compelling evidence from diverse experimental models and clinical investigations, this study elucidates the therapeutic potential of targeting HO-1 as an innovative strategy to mitigate cardiac senescence and improve outcomes in myocardial infarction, emphasizing the need for further research in this field.
PubMed: 38940935
DOI: 10.1007/s10557-024-07590-0 -
Turkish Journal of Ophthalmology Jun 2024The triglyceride-glucose (TyG) index is a sign of atherosclerosis in cardiovascular diseases. The TyG index is thought to have clinical significance for the assessment... (Observational Study)
Observational Study
OBJECTIVES
The triglyceride-glucose (TyG) index is a sign of atherosclerosis in cardiovascular diseases. The TyG index is thought to have clinical significance for the assessment of vascular damage. In this study we aimed to demonstrate the connection between the TyG index and retinal vein occlusion (RVO).
MATERIALS AND METHODS
This case-control observational study involved 492 participants aged 40-90, admitted to the ophthalmology outpatient clinic of our hospital. TyG index was calculated using the formula: ln(fasting TG [mg/dL] × fasting plasma glucose [mg/dL]/2).
RESULTS
The RVO group included 387 patients (181 women and 206 men) and the control group included 115 patients (61 women and 54 men). The average patient age was 62.9±11.1 years in the RVO group and 56.7±8.7 years in the control group. The TyG index was higher in the RVO group (8.9±0.7) than in the control group (8.8±0.6). This difference was statistically significant (p=0.04). The correlation was statistically significant when evaluated according to age and sex by multivariate logistic regression analysis (odds ratio: 1.45, confidence interval: 1.03- 2.02, p=0.03).
CONCLUSION
The TyG index is a novel atherogenicity index that is derived from routine blood tests and can be used to determine the risk of RVO in at-risk individuals with a simple calculation. Therefore, the TyG index could help as a reliable guide to identify individuals at RVO with high risk and initiate early intervention.
Topics: Humans; Female; Male; Middle Aged; Retinal Vein Occlusion; Triglycerides; Aged; Blood Glucose; Atherosclerosis; Adult; Case-Control Studies; Risk Factors; Biomarkers; Aged, 80 and over; Retrospective Studies
PubMed: 38940357
DOI: 10.4274/tjo.galenos.2024.69841 -
ACS Applied Materials & Interfaces Jun 2024Natural products have been widely recognized in clinical treatment because of their low toxicity and high activity. It is worth paying attention to modifying the...
Natural products have been widely recognized in clinical treatment because of their low toxicity and high activity. It is worth paying attention to modifying the biopolymer into nanostructures to give natural active ingredients additional targeting effects. In this study, based on the multifunctional modification of β-cyclodextrin (β-CD), a nanoplatform encapsulating the unstable drug (-)-epicatechin gallate (ECG) was designed to deliver to atherosclerotic plaques. Acetalization cyclodextrin (PH-CD), which responds to low-pH environments, and hyaluronic acid cyclodextrin, which targets the CD44 receptor on macrophage membranes, were synthesized from β-CD and hyaluronic acid using acetalization and transesterification, respectively. The resulting dual-carrier nanoparticles (Double-NPs) loaded with ECG were prepared using a solvent evaporation method. The Double-NPs effectively scavenged reactive oxygen species, promoted macrophage migration, inhibited macrophage apoptosis, and suppressed abnormal proliferation and migration of vascular smooth muscle cells. Furthermore, the Double-NPs actively accumulated in atherosclerotic plaques in ApoE mice fed with a high-fat diet, leading to a reduced plaque area, inflammatory infiltration, and plaque instability. Our findings demonstrate that the newly developed ECG nanopreparation represents an effective and safe nanotherapy for diseases such as atherosclerosis.
PubMed: 38940349
DOI: 10.1021/acsami.4c01540 -
Critical Reviews in Food Science and... Jun 2024Mounting evidence implicates the gut microbiota as a possible key susceptibility factor for atherosclerosis (AS). The employment of dietary phytochemicals that strive to... (Review)
Review
Mounting evidence implicates the gut microbiota as a possible key susceptibility factor for atherosclerosis (AS). The employment of dietary phytochemicals that strive to target the gut microbiota has gained scientific support for treating AS. This study conducted a general overview of the links between the gut microbiota and AS, and summarized available evidence that dietary phytochemicals improve AS manipulating gut microbiota. Then, the microbial metabolism of several dietary phytochemicals was summarized, along with a discussion on the metabolites formed and the biotransformation pathways involving key gut bacteria and enzymes. This study additionally focused on the anti-atherosclerotic potential of representative metabolites from dietary phytochemicals, and investigated their underlying molecular mechanisms. In summary, microbiota-dependent dietary phytochemical therapy is a promising strategy for AS management, and knowledge of "phytochemical-microbiota-biotransformation" may be a breakthrough in the search for novel anti-atherogenic agents.
PubMed: 38940319
DOI: 10.1080/10408398.2024.2369169 -
Frontiers in Bioscience (Landmark... May 2024Epigenetics refers to heritable changes in gene expression and function that impact nuclear processes associated with chromatin, all without altering DNA sequences.... (Review)
Review
Epigenetics refers to heritable changes in gene expression and function that impact nuclear processes associated with chromatin, all without altering DNA sequences. These epigenetic patterns, being heritable traits, are vital biological mechanisms that intricately regulate gene expression and heredity. The application of chemical labeling and single-cell resolution mapping strategies has significantly facilitated large-scale epigenetic modifications in nucleic acids over recent years. Notably, epigenetic modifications can induce heritable phenotypic changes, regulate cell differentiation, influence cell-specific gene expression, parentally imprint genes, activate the X chromosome, and stabilize genome structure. Given their reversibility and susceptibility to environmental factors, epigenetic modifications have gained prominence in disease diagnosis, significantly impacting clinical medicine research. Recent studies have uncovered strong links between epigenetic modifications and the pathogenesis of metabolic cardiovascular diseases, including congenital heart disease, heart failure, cardiomyopathy, hypertension, and atherosclerosis. In this review, we provide an overview of the progress in epigenetic research within the context of cardiovascular diseases, encompassing their pathogenesis, prevention, diagnosis, and treatment. Furthermore, we shed light on the potential prospects of nucleic acid epigenetic modifications as a promising avenue in clinical medicine and biomedical applications.
Topics: Humans; Epigenesis, Genetic; Cardiovascular Diseases; DNA Methylation; Animals
PubMed: 38940023
DOI: 10.31083/j.fbl2906205 -
Current Medicinal Chemistry Jun 2024Tripartite-motif protein family member 65 (TRIM65) belongs to the tripartite motif (TRIM) protein family. Its typical structure consists of the RING, B-Box motif, and...
Tripartite-motif protein family member 65 (TRIM65) belongs to the tripartite motif (TRIM) protein family. Its typical structure consists of the RING, B-Box motif, and coiled-coil domains, which are highly conserved at the N-terminus and the variable SPRY domain at the C-terminus. TRIM65 is an E3 ubiquitin ligase that participates in physiological and pathological processes through the ubiquitination pathway, including intracellular signal transduction, protein degradation, cell proliferation, apoptosis, carcinogenesis, autophagy, and phenotypic transformation. Evidence shows that TRIM65 plays a remarkable and obscure role in diseases, including multisystem tumours, neurodegenerative diseases, immune system diseases, and inflammatory diseases. This review is devoted to elaborating on the relationship between TRIM65 and diseases and its pathogenic mechanism, providing a theoretical basis for TRIM65 as a possible pathogenic target of diseases and exploring the possible future research direction of TRIM65 and the challenges it may face.
PubMed: 38939997
DOI: 10.2174/0109298673304966240614091547 -
Circulation. Genomic and Precision... Jun 2024Clonal hematopoiesis of indeterminate potential (CHIP) occurs due to acquired mutations in bone marrow progenitor cells. CHIP confers a 2-fold risk of atherosclerotic...
BACKGROUND
Clonal hematopoiesis of indeterminate potential (CHIP) occurs due to acquired mutations in bone marrow progenitor cells. CHIP confers a 2-fold risk of atherosclerotic cardiovascular disease. However, there are limited data regarding specific cardiovascular phenotypes. The purpose of this study was to define the coronary artery disease phenotype of the CHIP population-based on coronary angiography.
METHODS
We recruited 1142 patients from the Vanderbilt University Medical Center cardiac catheterization laboratory and performed DNA sequencing to determine CHIP status. Multivariable logistic regression models and proportional odds models were used to assess the association between CHIP status and angiography phenotypes.
RESULTS
We found that 18.4% of patients undergoing coronary angiography had a CHIP mutation. Those with CHIP had a higher risk of having obstructive left main (odds ratio, 2.44 [95% CI, 1.40-4.27]; =0.0018) and left anterior descending (odds ratio, 1.59 [1.12-2.24]; =0.0092) coronary artery disease compared with non-CHIP carriers. We additionally found that a specific CHIP mutation, ten eleven translocase 2 ), has a larger effect size on left main stenosis compared with other CHIP mutations.
CONCLUSIONS
This is the first invasive assessment of coronary artery disease in CHIP and offers a description of a specific atherosclerotic phenotype in CHIP wherein there is an increased risk of obstructive left main and left anterior descending artery stenosis, especially among mutation carriers. This serves as a basis for understanding enhanced morbidity and mortality in CHIP.
PubMed: 38939956
DOI: 10.1161/CIRCGEN.123.004415