Vascular Medicine最新文献

BackgroundIntraplaque neovascularization (IPN) is related to the progression of atherosclerotic plaque. The impact of lipid-lowering therapy (LLT) on IPN regression is unclear. We aimed to investigate the efficacy of LLT to regress IPN.MethodsBetween April 2022 and July 2024, 56 patients who had percutaneous coronary intervention (PCI) for angina or acute coronary syndrome and had not used LLT for at least 6 months were included. Contrast-enhanced ultrasound (CEUS) of the carotid artery was performed to evaluate IPN and intima-media thickness (IMT) within 7 days post-PCI. They received a combination of rosuvastatin 10 mg and ezetimibe 10 mg starting after PCI and continued for 1 year. Lipid profile changes and contrast enhancement were evaluated at baseline and 1 year later. The primary outcome was IPN regression, defined as the downgrade changes in the enhancement of contrast in atherosclerotic plaque at follow up.ResultsThe mean follow up was 12.6 ± 0.9 months. The IPN regression rate was 41%. Patients achieving IPN regression initially had a higher low-density lipoprotein-cholesterol (LDL-C) level and a greater percentage reduction in LDL-C. Whereas lipid profiles change significantly, no notable alterations were observed in IMT, plaque thickness, or plaque density. However, a 59% reduction in LDL-C was identified as the optimal cutoff level for IPN regression (OR 0.86, 95% CI 0.75-0.96).ConclusionLLT, such as rosuvastatin 10 mg with ezetimibe 10 mg, may effectively inhibit IPN by reducing LDL-C levels, providing a promising treatment option.

Marfan syndrome (MFS) is a genetic disorder caused by mutations in the FBN1 gene, which encodes fibrillin-1, a crucial protein involved in the structure of elastic fibers and the regulation of transforming growth factor-beta (TGF-β) bioavailability. Defective fibrillin-1 disrupts these fibers, leading to skeletal, ocular, and cardiovascular abnormalities. A key pathological mechanism in MFS is excessive TGF-β signaling, which has been targeted by angiotensin receptor blocker (ARB) therapies such as losartan, demonstrating potential in restoring normal phenotypes in experimental models. The aim of this narrative review was to highlight findings that demonstrate the potential of ARBs for MFS. Aortic root dilation is a defining feature of MFS. Studies have shown that losartan therapy significantly reduces the dimensions of the aortic root and sinotubular junction in children. However, its long-term efficacy remains uncertain. Beyond its primary effects on the aorta, chronic losartan treatment enhances endothelial function by promoting nitric oxide-mediated vasodilation, which may help prevent aortic root widening. The drug's effects are partly attributed to its metabolites, EXP3174 (an angiotensin II type 1 receptor [AT1] antagonist) and EXP3179 (an NADPH oxidase inhibitor). Overexpression of NADPH oxidase in MFS contributes to vascular dysfunction, and EXP3179 mitigates aortic vasoconstriction. Given these mechanisms, ongoing research explores the potential of AT1 receptor antagonists as therapeutic agents in MFS, aiming to improve vascular health and long-term patient outcomes.

Background: The association between ectopic fat and vascular stiffness is poorly studied and has never been systematically reviewed. We conducted a systematic review and meta-analysis aimed to systematize current literature and investigate the association of perivascular adipose tissue (PVAT) and the indices of vascular wall remodeling and arterial stiffness, such as pulse wave velocity (PWV), augmentation index (AI), cardio-ankle vascular index (CAVI), endothelium-dependent vasodilation (EDV), and intima-media thickness (IMT).

Methods: A systematic literature review was performed according to PRISMA guidelines via searching PubMed, Scopus, and Web of Science databases using specific keywords. Data were extracted from eight studies with 1244 participants that fit the criteria and analyzed using a random-effects model.

Results: Our pooled analysis revealed stronger correlations between carotid-femoral pulse wave velocity (cfPWV), AI, and the density of thoracic periaortic adipose tissue (r = 0.56, p < 0.05, n = 14); carotid extra-media thickness (EMT) and average daily PWV in the aorta (r = 0.56, p < 0.05, n = 84); and thoracic periaortic fat volume and CAVI (r = 0.49, p < 0.05, n = 318).

Conclusion: Our results demonstrate the association between PVAT and vascular wall remodeling, emphasizing the need for early detection of dysfunctional PVAT as the contributor to higher cardiovascular risk, not only in patients with risk factors and cardiovascular diseases, but also in healthy individuals. (PROSPERO Registration No.: CRD42023443139).

Introduction: The manifestations of the central lymphatic vessels in primary lower-extremity lymphedema (LEL) remain incompletely understood. Advanced magnetic resonance imaging (MRI) techniques offer the potential to noninvasively evaluate central lymphatic vessels and their relationship with disease severity. Our objective was to investigate the differences in imaging performance of central lymphatics and inguinal lymph nodes in primary LEL of different clinical stages, and to assess the ability of MRI to grade primary LEL. Methods: Patients were staged according to the International Society of Lymphology (ISL), with 92 cases in stage I, 134 in stage II, and 53 in stage III. All patients underwent lower-extremity MRI, pelvic MRI, and magnetic resonance thoracic ductography (MRTD). Chi-squared tests and Fisher's exact tests were used to compare the relationship between the central lymphatic vessels and inguinal lymph nodes with clinical staging. LEL was graded based on MRI images, and a partial correlation coefficient was employed to assess the correlation between MRI grading and clinical staging. Results: A significant correlation was observed between clinical staging and MRI grading (R = 0.728, p < 0.001). The incidence of abnormalities in the terminal thoracic duct and the lumbar and iliac lymphatic vessels differed significantly across clinical stages (p ⩽ 0.001). Additionally, the frequency of enlarged inguinal lymph nodes on both the affected and the unaffected sides showed statistically significant differences (p = 0.001). Conclusion: MRI grading demonstrates a high correlation with clinical staging. Changes in central lymphatic vessels and inguinal lymph nodes, as identified through MRTD, provide valuable insights for the clinical staging of primary LEL.

Rare vascular diseases are a diverse group of life-threatening conditions defined by their low prevalence but profound impact on patient morbidity and quality of life. Diagnosing these disorders remains a significant clinical challenge due to their genetic heterogeneity, overlapping phenotypes, and limited patient populations. As such, the development of robust and human-relevant disease models is critical for elucidating pathogenic mechanisms and guiding therapeutic discovery. The advent of human induced pluripotent stem cell (iPSC) technology has opened new avenues for modeling rare vascular diseases by enabling the generation of patient-specific vascular cell types, including endothelial cells, smooth muscle cells, and fibroblasts, and the creation of both two-dimensional cultures and three-dimensional vascular organoids. Together with genome editing and next-generation multiomics, these platforms represent new approach methodologies (NAMs) that allow for detailed investigation of disease biology, facilitate the correction of pathogenic mutations, and enable high-throughput drug screening in a personalized context. In this review, we highlight the advancements in iPSC-derived vascular modeling, discuss the integration of gene editing and multiomics technologies, and explore their transformative potential for uncovering mechanisms and developing precision therapies for rare vascular diseases.

Background: Peripheral vascular interventions (PVI) in chronic limb-threatening ischemia (CLTI) are used to prevent amputation. However, imaging practices following PVI and their correlation with amputation outcomes remain unclear. Methods: Using Medicare-linked Vascular Quality Initiative data (2017-2019), we identified imaging tests (ankle-brachial index [ABI], duplex ultrasound, magnetic resonance angiography, computed tomography angiography) ordered within 1 year post-PVI for CLTI. Site variability was assessed using median odds ratio (MOR) and intraclass correlation coefficient (ICC). The association between post-PVI imaging and 1-year major amputation was examined using competing risk analyses in a propensity-matched cohort. Results: We included 10,006 patients (mean age: 72.1 ± 11.0 years); 25.5% received no imaging. Over 50% of imaging tests were ABI and 83.1% were ordered within 3 months. Significant site variability was noted (none vs ⩾ 1: MOR 1.64, 95% CI 1.50-1.78; ICC 7.6%, 95% CI 5.2-9.9%; per one-unit increase in monthly volume: MOR 1.06, 95% CI 1.05-1.07; ICC 9.4%, 95% CI 7.0-11.8%). Having none versus ⩾ 1 imaging tests post-PVI occurred more in patients with lower 1-year major amputation rates (5.7%, 95% CI 5.0-6.6% vs 8.8%, 95% CI 7.9-9.9%, p < 0.001; subdistribution hazard ratio [SHR] 0.63, 95% CI 0.53-0.76, p < 0.001). More imaging ordered was correlated with a higher rate of major amputation (SHR 1.83, 95% CI 1.52-2.20, p < 0.001). Conclusions: Imaging practices post-PVI for CLTI are highly variable. Imaging tests are more often ordered in patients with higher amputation rates, but causality cannot be inferred. Additional information about symptom status and access to care are necessary. Standardized follow-up imaging protocols need to be developed and studied for improved clinical outcomes.