Angiology最新文献

This study assessed the role of nucleotide-binding domain and leucine-rich repeat containing receptor, caspase recruitment domain containing 5 (NLRC5) in macrophages in atherosclerotic plaque formation in acute coronary syndromes (ACS) by modulating the nuclear factor-kappaB (NF-κB) cascade. Peripheral blood was obtained from ACS patients and matched controls, and NLRC5 expression and DNA methylation were analyzed. In vitro, peripheral blood mononuclear cells from donors were induced into macrophage-derived foam cells and transfected with small interfering RNA negative control (si-NC) or si-NLRC5 plasmids to assess foam cell formation and cytokine release. In vivo, ApoE^-/- mice fed a high-fat diet and subjected to NLRC5 silencing were used as an ACS model. Peritoneal macrophage phagocytosis, aortic lipid accumulation, plaque size, and collagen fiber content were evaluated, while lipid metabolism- and inflammation-related genes were measured in foam cells and aortas. NLRC5 was highly expressed and hypomethylated in ACS patients. NLRC5 knockdown suppressed foam cell formation and inflammation in vitro. In ACS mice, silencing NLRC5 reduced lipid levels and cytokines, inhibited lipid deposition, decreased plaque size, and enhanced collagen fiber content through NF-κB pathway inhibition. These findings suggest that NLRC5 silencing may protect against atherosclerosis in ACS by regulating macrophage function and inflammatory signaling.

Spontaneous coronary artery dissection (SCAD) is an under-recognized cause of acute coronary syndrome (ACS). We reviewed the characteristics, predictors, and outcomes of SCAD using the National Inpatient Sample (NIS) database. ACS and SCAD patients were identified from the 2016 to 2020 NIS database. Multivariable logistic regression was performed to identify risk factors associated with SCAD and in-hospital mortality. A risk score model was developed using the 2016 to 2019 cohort and validated with 2020 data. Among 7 219 004 ACS hospitalizations, 30 770 (0.43%) had SCAD (mean age 59.6 years; 58.5% female). Compared with non-SCAD ACS patients, SCAD patients had higher rates of all-cause mortality (8.0% vs 6.0%), and acute stroke (3.2% vs 1.7%). History of percutaneous coronary intervention (3.63 [3.33-3.96]), coronary artery aneurysm (8.87 [5.75-13.70]), and fibromuscular dysplasia (90.50 [69.86-117.25]), all with P < .001, are the strongest predictors of SCAD. Five mortality risk predictors in our risk model were cardiogenic shock, extracorporeal membrane oxygenation, balloon pump, cardiac arrest, and acute kidney injury. The area under the curve for the development and validation datasets was 0.867 and 0.860, respectively. SCAD is a rare but serious form of ACS with distinct risk factors and outcomes. Our risk model may help in early identification and management.

Carotid artery stenting (CAS) is an established alternative to endarterectomy, but stent fracture is an under-recognized complication with potential clinical consequences. We report a case of carotid stent fracture in a 69-year-old male with prior neck radiation, presenting with severe in-stent restenosis 10 months post-stenting. To place this case in context, a systematic review of PubMed, Embase, and Scopus (through June 2025) was conducted in line with PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses) guidelines. Ten retrospective studies (2365 patients) were included. Stent fracture was identified in 172 patients, with a pooled prevalence of 7.3%. Type I and II fractures were most common, while Type V was rare. Reported risk factors included prior neck irradiation, vessel tortuosity, long stent length, and closed-cell stent design. Fluoroscopy was the most reliable detection method. Restenosis rates varied widely (0%-36%), most patients remained asymptomatic and were managed conservatively. In conclusion, Carotid stent fracture occurs in approximately 7% of cases and is often clinically silent, though it may predispose to restenosis. Surveillance and management should be individualized, with intervention reserved for symptomatic patients or progressive disease.

May-Thurner syndrome (MTS) is an anatomical variant involving compression of the left iliac vein, predisposing to proximal deep vein thrombosis (DVT). Despite its clinical significance, population-level data remain limited. Using the RIETE (Registro Informatizado Enfermedad Trombo-Embólica) registry (2009-2024), we analyzed proximal DVT patients who underwent advanced imaging (CT-venography, contrast-venography, or MRI). Among 2872 patients with advanced imaging-confirmed proximal DVT, 124 (4.3%) had MTS. MTS patients were more likely to be female (78% vs 52%), younger (mean age 42 vs 62 years), and to present with left-sided DVT (92% vs 46%). They had fewer comorbidities, but greater exposure to estrogen or pregnancy. Endovascular therapy was more frequently used in MTS patients (44% vs 3.5%), who also received longer median anticoagulation (365 vs 164 days). Despite this, MTS patients had a significantly higher rate of recurrent DVT (rate ratio: 2.37; 95% CI 1.09-4.70). Multivariable analysis confirmed MTS as an independent predictor of recurrent DVT (adjusted hazard ratio: 2.26; 95% CI: 1.02-5.01). Major bleeding was non-significantly less frequent (rate ratio: 0.42; 95% CI: 0.13-1.04), though retroperitoneal bleeding was more common. MTS is underdiagnosed, has distinct clinical features and is associated with increased DVT recurrence despite aggressive therapy. Improved recognition and tailored management strategies are needed.

The systemic inflammation response index (SIRI) is a novel inflammatory biomarker that reflects the chronic inflammatory status. This study aimed to evaluate its clinical utility in determining coronary heart disease (CHD) severity. Participants in this study, sourced from the Cohort Study on the Treatment of Cardiovascular Diseases with Traditional Chinese Medicine (CSCD-TCM^plus), were divided into tertiles (T) based on their SIRI values. The number of diseased vessels (single- and multi-vessel CHD) was used as a measure of disease severity, assessed by coronary angiography. Logistic regression analysis was used to investigate the relationship between SIRI and the severity of CHD. Among the 7706 participants, 6215 (80.6%) had multi-vessel disease. Logistic regression analysis revealed a significant association between SIRI and CHD severity (odds ratio [OR]: 1.09; 95% confidence interval [CI]: 1.03-1.15). Compared with males, females had a higher risk of CHD severity at the SIRI T3 tertile (OR: 1.64; 95% CI: 1.28-2.10). Also, patients >55 years of age had a greater risk than those ≤55 years old (OR: 1.93; 95% CI: 1.67-2.01). The association between SIRI and CHD severity persisted even after adjusting for confounding factors.

The present study explored the association between serum uric acid/albumin ratio (UAR) and carotid artery plaque (CAP) in cases (n = 12 481) with coronary heart disease (CHD). Participants were stratified by UAR quartiles. Logistic regression analysis was used to analyze the association between the UAR and CAP. The relationship between the UAR and carotid plaques according to sex, age, blood pressure, and blood lipid groups was also assessed. Results showed that UAR was significantly associated with CAP (odds ratio [OR]: 1.03; 95% confidence interval [CI]: 1.02-1.05). The correlation between UAR and the presence of carotid plaque was strong in both females (OR: 1.03; 95% CI: 1.01-1.06) and males (OR: 1.03; 95% CI: 1.00-1.06). Patients aged ≥60 (OR: 1.60; 95% CI: 1.34-1.90) had a higher risk for carotid plaque at the Q4 UAR level than those <60. Hypertensive patients showed higher carotid plaque risk at Q4 UAR (OR: 1.46; 95% CI: 1.20-1.78) than normotensives. The correlation between UAR and the presence of carotid plaque was greater in dyslipidemic patients (OR: 1.06; 95% CI: 1.02-1.10) than in normolipidemic patients (OR: 1.03; 95% CI: 1.01-1.05). These results confirm a significant association between UAR and CAP, most pronounced in patients aged ≥60 or with hypertension/dyslipidemia.

The ratio of red cell distribution width (RDW) to albumin (RAR) has been shown to correlate with poor prognosis in patients with various diseases. However, the relationship between RAR and cardiovascular disease (CVD) remains inadequately elucidated. We conducted this study using data from 12 755 participants in the National Health and Nutrition Examination Survey (NHANES) 2007 to 2018. Multivariable regression analysis and subgroup analysis were conducted to analyze the potential relationship. In this study, RAR was significantly and positively associated with CVD mortality (hazard ratio [HR] = 1.99, 95% CI = 1.81-2.19, P < .001), total CVD (odds ratios [OR] = 1.42, 95% CI = 1.31-1.54, P < .001), congestive heart failure (CHF; OR = 1.70, 95% CI = 1.52-1.90, P < .001), coronary heart disease (CHD; OR = 1.18, 95% CI = 1.05-1.33 P = .006), and myocardial infarction (MI; OR = 1.32, 95% CI = 1.18-1.47, P < .001). Subgroup analyses confirmed the robustness of the findings. Our findings demonstrate significant and independent associations of RAR levels with CVD mortality and specific CVD. As a straightforward, cost-effective, and readily accessible metric, RAR has the potential to offer novel insights into CVD risk assessment.