Coronary artery ectasia (CAE) is increasingly recognized as an active inflammatory vascular disorder rather than a benign anatomical variant. The pan-immune-inflammation value (PIV) is a novel biomarker integrating neutrophil, monocyte, platelet, and lymphocyte counts, providing a comprehensive measure of systemic inflammation. This study aimed to evaluate the association between PIV and CAE and to compare their diagnostic performance with that of conventional inflammatory indices. In this retrospective case-control study, 17,538 patients who underwent elective coronary angiography between 2018 and 2024 were screened. A total of 228 patients with isolated CAE and 296 age-, sex-, and Body Mass Index (BMI)-matched controls with normal coronary arteries were included. Hematologic and biochemical parameters were analyzed, and inflammatory indices were calculated. Logistic regression and receiver operating characteristic (ROC) analyses were performed to identify independent predictors and assess diagnostic performance. Patients with CAE had significantly higher PIV levels compared to controls (801.6 [504.4-1301.8] vs. 491.8 [302.4-872.7], P < 0.001). In multivariable logistic regression, log-transformed PIV remained independently associated with CAE (odds ratio [OR]: 1.987, 95% confidence interval [CI]: 1.057-3.737, P = 0.033), along with hypertension, triglycerides, high-density lipoprotein (HDL) cholesterol, and serum creatinine. PIV demonstrated the highest discriminative ability among all inflammatory indices (area under the curve [AUC]: 0.674, 95% CI: 0.623-0.722), and correlated strongly with the Systemic Immune-Inflammation Index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and Systemic Inflammation Response Index (SIRI) (P = 0.75-0.94). Elevated PIV levels are independently associated with CAE, reflecting the pivotal role of systemic inflammation in its pathogenesis. Given its simplicity and availability, PIV may serve as a practical adjunctive marker for identifying patients at risk of CAE, warranting validation in larger prospective studies.

BackgroundCardiovascular disease is the leading cause of death in patients receiving hemodialysis, yet effective preventive therapies remain limited. Supplementation with n−3 polyunsaturated fatty acids, especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may have cardiovascular benefits in the general population, but efficacy among patients receiving hemodialysis is uncertain.MethodsIn a double-blind, randomized, placebo-controlled trial conducted at 26 sites in Canada and Australia, we assigned adult patients receiving maintenance hemodialysis to daily supplementation with fish oil (4 g of n−3 polyunsaturated fatty acids [1.6 g of EPA and 0.8 g of DHA]) or corn-oil placebo. The primary end point was a composite of all serious cardiovascular events including sudden and nonsudden cardiac death, fatal and nonfatal myocardial infarction, peripheral vascular disease leading to amputation, and fatal and nonfatal stroke. Secondary end points included extension of the primary end point to include noncardiac causes of death, the individual components of the primary end point, and a first cardiovascular event or death from any cause.ResultsBetween November 28, 2013, and July 22, 2019, a total of 1228 participants underwent randomization; 610 were assigned to the fish-oil group and 618 to the placebo group. During 3.5 years of follow-up, the rate of serious cardiovascular events was significantly lower in the fish-oil group than in the placebo group (0.31 vs. 0.61 per 1000 patient-days; hazard ratio, 0.57; 95% confidence interval [CI], 0.47 to 0.70; P<0.001). The rate of the extended primary end point that included noncardiac causes of death appeared to be lower in the fish-oil group than in the placebo group, with a hazard ratio of 0.77 (95% CI, 0.65 to 0.90). The hazard ratio for cardiac death was 0.55 (95% CI, 0.40 to 0.75); for fatal and nonfatal myocardial infarction, 0.56 (95% CI, 0.40 to 0.80); for peripheral vascular disease leading to amputation, 0.57 (95% CI, 0.38 to 0.86); for fatal and nonfatal stroke, 0.37 (95% CI, 0.18 to 0.76); and for a first cardiovascular event or death from any cause, 0.73 (95% CI, 0.61 to 0.87). Adherence to the trial regimen and the incidence of adverse events did not differ meaningfully between the groups.ConclusionsThe rate of serious cardiovascular events among participants receiving maintenance hemodialysis was lower with daily supplementation with n−3 fatty acids than with placebo. (Supported by the Heart and Stroke Foundation of Canada and others; PISCES ClinicalTrials.gov number, ISRCTN00691795.)

Determinants of Prosthetic Referral and Functional Mobility for Vascular Patients after Major Lower Extremity Amputation.

Heparin decreases serum sphingosine-1-phosphate levels in patients with vascular diseases.

Atherosclerosis remains the primary cause of cardiovascular morbidity and mortality, with intercellular communication critically influencing vascular homeostasis and disease progression. The connexome comprises connexins, pannexins, and associated proteins, and coordinates endothelial, smooth muscle, and immune cell interactions. Krüppel-like factors (KLFs) are key transcriptional regulators that modulate endothelial phenotype, inflammation, and oxidative stress. Advances in nanomedicine provide targeted platforms for modulating these molecular networks, offering novel diagnostic and therapeutic possibilities. This review is integrated by a comprehensive literature review conducted across Pubmed, Scopus, and Web of Science focusing on connexome regulation in vascular biology, and transcriptional control in the context of atherosclerosis. The discussion draws on recent experimental and translational studies linking connexin biology, KLF signaling, and nanomedicine in vascular health and disease. Emphasis is placed on translational evidence for nanoparticle-based delivery systems, including small molecules, nucleic acids, and imaging agents designed to target vascular lesions, with attention to strategies that improve specificity and bioavailability. The convergence of nanomedicine with connexome and KLF-targeted interventions could redefine atherosclerosis management by enabling precision drug delivery and real-time monitoring. Achieving clinical translation will require overcoming challenges related to nanoparticle biocompatibility, targeted biodistribution, immune compatibility, and long-term safety to fully realize their therapeutic potential.

Network pharmacology and molecular docking reveal the multi-target mechanisms of Paeoniae Radix Rubra in functional angiogenesis: Synergistic regulation of ADAM10-NOTCH and VEGFR2-PI3K/AKT signaling.

FGF8 induces bone and joint regeneration at digit amputation wounds in neonate mice.

Cerebrovascular hemodynamics and cardiac biomarkers in multiple sclerosis: A case-control study.

While the primary goal of lung cancer screening CT is to detect early-stage lung cancer in high-risk populations, it often reveals asymptomatic cardiovascular abnormalities that can be clinically significant. These findings include coronary artery calcifications (CACs), myocardial pathologies, cardiac chamber enlargement, valvular lesions, and vascular disease. CAC, a marker of subclinical atherosclerosis, is particularly emphasized due to its strong predictive value for cardiovascular events and mortality. Guidelines recommend qualitative or quantitative CAC scoring on all noncontrast chest CTs. Other actionable findings include aortic aneurysms, pericardial disease, and myocardial pathology, some of which may indicate past or impending cardiac events. This article explores the wide range of incidental cardiovascular findings detectable during low-dose CT (LDCT) scans for lung cancer screening, as well as noncontrast chest CT scans. Distinguishing which findings warrant further evaluation is essential to avoid overdiagnosis, unnecessary anxiety, and resource misuse. The article advocates for a structured approach to follow-up based on the clinical significance of each finding and the patient's overall risk profile. It also notes the rising role of artificial intelligence in automatically detecting and quantifying these abnormalities, potentiating early behavioral modification or medical and surgical interventions. Ultimately, this piece highlights the opportunity to reframe LDCT as a comprehensive cardiothoracic screening tool.

BackgroundThe role of endovascular therapy for patients presenting with AMI continues to be debated. This study was undertaken to compare open and endovascular treatment of AMI.MethodsAll patients who presented with AMI between 2010 and 2022 were identified. Patient demographics, baseline laboratory studies, length of stay (LOS), and outcomes were recorded. Student's t-test was used for quantitative data and Fisher's exact test for qualitative data.ResultsSixty-five patients were treated for AMI: 47 with an open procedure; 18 with endovascular techniques. Of the 18 patients in the endovascular group, 8 (45%) underwent laparotomy/laparoscopy; four (22%) requiring bowel resection. Patients treated with an endovascular approach were more likely to be male (87% vs 45%, P = .025), be caused by thrombosis (78% vs 55%, P = .005), have lower incidence of other vascular disease (56% vs 87%, P = .015) and have a lower initial WBC (11.9 ± 3.9 vs 18.5 ± 8.4, P = .0017). There was shorter ICU LOS in the endovascular group (5.5 ± 5.7 vs 13.5 ± 13.8, P = .025). A trend for decreased bowel resection was seen in the endovascular group compared the open group [4 (22%) vs 19 (40%), P = .25]. A trend for lower mortality was seen in the endovascular group compared to the open group (22% vs 40%, P = .25). In the 23 patients that died, the cause of death was directly related to bowel ischemia in 16 (70%), cardiac in 5 (22%) and stroke in 2 (9%).ConclusionEndovascular treatment of AMI has potentially lower mortality and lengths of stay. When choosing endovascular vs open treatment, the status of the bowel should be an important initial determinate. We recommend that the underlying etiology (thrombosis vs embolic) also be a consideration with a low threshold for conversion to an open procedure if endovascular treatment does not rapidly restore mesenteric flow in patients with embolic disease.

Polycystin-1 as a Novel Biomarker for Peripheral Artery Disease: Findings from a Pilot Prospective Study.

Pharmacological profile and therapeutic evaluation of ROC-101, a potent and selective ROCK inhibitor, in arterial hypertension and pulmonary fibrosis.

Obesity and inactivity cluster the strongest risk factor for the development of heart failure in a population-based study.

An Elastin-like Polymer Targeting Vascular Endothelial Growth Factor Receptor-1 Reduces Survival in Serum-Starved Endothelial Cells.

Progressive loss of vascular smooth muscle cells (VSMCs) is the pathophysiological basis for aortic aneurysm and dissection (AAD), a life-threatening disease, but the underlying mechanisms are largely unknown. Sirtuin 6 (SIRT6), a class III histone deacetylase, is critical for maintenance of VSMC homeostasis and prevention of vascular remodeling-related diseases. In this study, we investigated the role of VSMC SIRT6 in AAD and the molecular mechanism. We showed that the expression levels of SIRT6 were significantly reduced in VSMCs of the thoracic aorta in AAD patients. We constructed a VSMC-specific Sirt6 deficient mouse line and found that loss of Sirt6 in VSMCs dramatically accelerated angiotensin II (Ang II)-induced AAD formation and rupture, even without an Apoe-deficient background. In human aortic smooth muscle cells (HASMCs), knockdown of SIRT6 led to mitochondrial dysfunction and accelerated VSMC senescence. We revealed that SIRT6 bound to and deacetylated NRF2, a key transcription factor for mitochondrial biogenesis. However, Sirt6 deficiency inhibited NRF2 and reduced mRNAs encoding mitochondrial complex proteins. Notably, MDL-811, a newly developed small-molecule SIRT6 agonist, effectively reversed Ang II-induced mitochondrial dysfunction in HASMCs. In a BAPN-induced TAAD mouse model, administration of MDL-811 (20 mg/kg, i.p., every other day for 28 d) effectively mitigated AAD progression and reduced mortality. These results suggest that SIRT6 plays a protective role against AAD development, and targeting SIRT6 with small-molecule activators such as MDL-811 could represent a promising therapeutic strategy for AAD.

Radiation Therapy for Benign Diseases and Premalignant Conditions.

Circadian regulation of vascular function: Metabolism as a link from molecular mechanisms to clinical implications.

Spatial transcriptomic modeling of vascular remodeling in aortic aneurysm using integrated single-cell RNA sequencing analysis.

Studies in the past have demonstrated an association between sarcoidosis and pulmonary embolism (PE), but little is known about its impact, especially in young adults. We aim to determine the burden and impact of PE in young adults hospitalized with sarcoidosis. This study investigates the prevalence and consequences of PE in young adults aged 18-44 years hospitalized with sarcoidosis using data from the National Inpatient Sample (2016-2020) with relevant International Classification of Diseases (ICD)-10 codes. This study aims to address the primary outcomes of the burden and trends of PE and its associated impact on in-hospital mortality. Additionally, it explores secondary outcomes such as healthcare resource utilization and discharge patterns. Among 50,385 young adults (median age 37 years) hospitalized with sarcoidosis, 1120 had PE, showing a linear increase from 2% in 2016 to 2.9% (P < 0.001) in 2020. The sarcoidosis-PE+ group, predominantly in young blacks, exhibited a higher prevalence of comorbidities such as obesity, smoking, drug use, peripheral vascular disease, hypothyroidism and prior history of venous thrombus embolism. In contrast, the sarcoidosis-PE- group had a higher prevalence of diabetes (with/without chronic complication), hyperlipidemia and chronic pulmonary disease. Multivariable regression analysis adjusted for all potential sociodemographic and comorbid variables showed higher odds of all-cause mortality (odds ratio [OR]: 2.92, 95% confidence interval [CI]: 1.18-7.24, P < 0.02) in the sarcoidosis-PE+ group as compared to the sarcoidosis-PE- group. The sarcoidosis-PE+ group also had higher hospital costs and length of stay. The higher odds of in-hospital mortality with an increased length of stay and hospital cost observed in the sarcoidosis-PE+ group highlight the often underreported complications of sarcoidosis, particularly in a younger demographic. The relevance of this study stems from its potential to uncover trends that could lead to improved diagnostic and therapeutic strategies.

Baicalin attenuates pulmonary hypertension by targeting AMPK/CPT1A-mediated fatty acid metabolism.