Vascular Medicine最新文献

Background: The efficacy of venoactive drug (VAD) treatment for pelvic venous disorder (PeVD) has not been fully investigated. This study was aimed at evaluating the efficacy and safety of different diosmin-containing agents in women with PeVD. Methods: VENOTREAT was a single-center, randomized, open-label study included 150 women with symptomatic PeVD, who were allocated for the 2-month therapy a once-daily intake of: (1) micronized purified flavonoid fraction (MPFF) 1000 mg; (2) diosmin 600 mg, or (3) hesperidin and diosmin combination (HDC) 1000 mg. The effects on chronic pelvic pain (CPP), the time to pain relief, as well as adverse events (AEs) were investigated. Results: Patients receiving MPFF reported a CPP reduction, using visual analog scale (VAS) scores, from 5.7 ± 0.8 to 2.8 ± 0.4 (p = 0.001) by day 7 and its elimination by day 28 in all cases. In the diosmin and HDC groups, the CPP reduction became significant by day 14 (VAS scores from 5.3 ± 0.6 to 3.7 ± 0.3 and from 5.1 ± 0.3 to 3.5 ± 0.2, respectively, both p = 0.001), and pain was eliminated after 2 months in 37 and 35, and decreased in the remaining 13 and 15 patients to VAS scores 1.07 ± 0.2 and 1.1 ± 0.07, accordingly. AEs included headache, nausea, gastralgia, and diarrhea and were reported in 7.3% of cases in general and in 6%, 8%, and 8% of patients in the MPFF, diosmin, and HDC groups, respectively. No serious AEs were observed. Conclusion: VAD treatment is effective and safe for eliminating CPP in PeVD. MPFF provides a faster and greater effect on venous CPP of venous origin. ClinicalTrials.gov Identifier: NCT06584799.

Background: The carotid body (CB) detects blood oxygen changes and may play a role in metabolic diseases. Several studies have suggested a link between CB size and cardiovascular conditions. This study aimed to evaluate CB size using computed tomography angiography (CTA) and investigate its associations with cardiovascular and metabolic conditions.

Methods: A retrospective analysis of 279 patients undergoing CTA of the cervical vasculature was conducted. The CB was identified as an enhancing structure at the carotid bifurcation, and its area was measured on axial images. Clinical data, including comorbidities and vascular risk factors, were collected. Statistical analyses included univariate and stepwise multiple linear regression to identify significant predictors of CB size.

Results: The CB was identified in 163 patients (49.1% right, 50.9% left). The mean CB area was 3.183 mm² for the right side and 2.901 mm² for the left. Obstructive sleep apnea (OSA) and internal carotid artery (ICA) stenosis ⩾ 70% were significant predictors of increased CB size. In the final regression model, OSA was associated with a 1.049 mm² increase in CB area (p = 0.027), whereas ICA stenosis ⩾ 70% and renin-angiotensin system inhibitor treatment were associated with increases of 0.528 mm² (p = 0.036) and 0.494 mm² (p = 0.037), respectively. CB hypertrophy was also associated with hypertension, obesity, and smoking in univariate analyses.

Conclusions: This study highlights significant associations between CB hypertrophy and conditions such as OSA and ICA stenosis, suggesting that CB enlargement reflects the interplay between hypoxia, vascular pathology, and metabolic dysregulation. CTA may assess CB size as a cardiovascular biomarker.

Background: Impaired angiogenic response in peripheral artery disease (PAD) contributes to the progression of tissue ischemia, but methods to evaluate angiogenesis at the tissue level are limited. We describe a novel approach to measure angiogenesis and identify microRNA (miR)-gene pathways utilizing adipose tissue from patients with PAD. Methods: Patients with PAD undergoing infrainguinal bypass surgery or non-PAD control patients undergoing knee replacement surgery were recruited. Subcutaneous adipose tissue was obtained at the time of surgery. In patients with PAD, adipose tissue was taken from both the proximal and the distal ends of the surgical incision. Angiogenic capacity was measured and miR sequencing was performed. Differentially expressed miRs were defined by p < 0.01 and log₂ (fold change) > 1 or < -1. The miRs that correlated with angiogenic capacity and their gene targets were identified. Results: Participants with PAD (n = 10) and control participants (n = 5) were recruited. Capillary sprouting was impaired in distal (p = 0.0014) but not proximal (p = 0.12) PAD adipose tissue. In a subset of samples (controls: n = 4, PAD: n = 6), miR sequencing revealed 56 differentially expressed miRs in distal PAD. Six miRs with a correlation to impaired capillary sprouting and related to angiogenesis using Qiagen Ingenuity Pathway Analysis (IPA) software were identified (miRs 144-3p, 15b-5p, 18b-5p, 20b-5p, 454-3p, and 363-3p). These miRs are predicted to target regulators of angiogenesis including vascular endothelial growth factor A (VEGFA), phosphatase and tensin homologue (PTEN), and cyclin-dependent kinase inhibitor 1A (CDKN1A). Conclusion: Evaluation of ischemic adipose tissue represents a novel approach to gain insight into impaired angiogenesis in PAD. Integration with miR sequencing and target analysis has the potential to identify novel pathways of impaired angiogenesis in PAD.

IntroductionFew tests are validated for ischemia grading in chronic limb-threatening ischemia (CLTI). An additional, easily accessible and validated technique would be beneficial. This study aimed to determine whether transmetatarsal pressure (TMP) is valid in the evaluation of CLTI ischemia grade. We also aimed to assess if values for TMP were meaningful in patients with noncompressible ankle-brachial indices (ABI).MethodsA cohort of patients with peripheral artery disease (PAD) presenting to our vascular center from March 1 to May 1, 2022, underwent TMP measurement concurrent with ABI and toe pressure (TP) measurement. Linear and quadratic regression models were used to assess the relation between TMP and TP or ABI.ResultsA total of 108 patients who were being followed for PAD underwent testing. Half had a history of CLTI (55% of patients with diabetes and 43% of patients without diabetes). The relation between TP and TMP was best described by a quadratic formula with an R² value of 0.41. By combining the existing WIfI ischemia ranges defined by TP and the quadratic formula, new ischemia grades were calculated for TMP. Ischemia grades 0, 1, 2, and 3 corresponded to ranges of TMP pressure (mmHg) of ≥ 75, 45-74, 30-44, and < 30. There were 25 instances where a patient had an abnormally elevated ABI. None of these patients had a noncompressible TP or TMP.ConclusionWe demonstrated that TMP can be integrated into the WIfI classification. We believe that TMP evaluation may increase the reliability, accuracy, and accessibility of CLTI assessment and management.