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: Pseudoxanthoma elasticum (PXE) is a rare disease caused by pathogenic ABCC6 variants, leading to arterial calcifications and increased cardiovascular risk. Validated intermediate endpoints are needed to evaluate cardiovascular risk-reducing therapies in PXE. This prospective cohort study investigates the relationship between arterial stiffness and cardiovascular events in patients with PXE. Methods: This prospective cohort study obtained patients from the Dutch University Medical Center Utrecht Expertise Center for PXE. Arterial stiffness was measured with carotid-femoral pulse wave velocity (cfPWV) and the augmentation index (AIx). Cardiovascular endpoints were cardiovascular death, cerebrovascular and coronary events, and peripheral artery interventions. Cox proportional hazard models analyzed associations between arterial stiffness and cardiovascular events, adjusting for confounders. Results: Among 390 patients (mean age 51 ± 15 years, 60% women), 45 cardiovascular events occurred during a median follow up of 6.1 years (IQR 3.2; 9.2). A 1-m/s higher cfPWV was related to an increased risk of cardiovascular events (hazard ratio [HR]: 1.28; 95% CI 1.06-1.53). The effect of cfPWV depends on age (p-value = 0.03), with a lower cardiovascular risk HR at older age (HR age at 40 years: 1.51; 95% CI 1.11-1.97 to HR age at 60 years: 1.12; 95% CI 1.00-1.26). A 10% higher AIx at baseline was related to future cardiovascular events (HR 1.46; 95% CI 1.10-1.95). No significant interaction between the AIx and age was found. Conclusion: This prospective cohort study shows that arterial stiffness, measured by cfPWV and AIx, is independently associated with increased cardiovascular risk in PXE. Measures of arterial stiffness could be explored as intermediate endpoints in trials evaluating cardiovascular risk-reducing therapies in PXE.