Peripherally inserted central catheters (PICCs) are vital for long-term intravenous therapy but increase the risk of venous thromboembolism (VTE), a process commonly explained through the conceptual framework of Virchow's Triad: stasis, endothelial injury, and hypercoagulability. The catheter-to-vein ratio (CVR), a key modifiable thrombosis risk factor that primarily influences stasis, lacks a universal definition, causing variability in measurement, thresholds, and clinical use. This study compares the diameter-based approach commonly cited in the literature with the area-based approach later adapted for clinical CVR tools, emphasizing that both gain from standard geometric relationships rather than distinct mathematical formulations. Through mathematical conversion, the analysis reveals that a 45% diameter-based CVR corresponds to approximately a 20% area-based CVR, underscoring substantial discrepancies when assuming equivalence. The study endorses a 20% area-based (45% diameter-based) CVR threshold for oncology patients and a 33% area-based (57% diameter-based) threshold for noncancer patients. A harmonized CVR reference is proposed to bridge the gap between methods. To enhance consistency and patient safety, the study advocates for a standardized CVR definition, consistent vein measurement techniques, and stricter control of confounders in future research. It further recommends developing a next-generation CVR calculator integrating hemodynamic and clotting risk factors to refine VTE risk assessment.

Emerging from liposomes, nanomedicines have been rapidly developed into powerful tools for the diagnosis, therapy, and prevention of diseases. After bypassing from physiological barriers, most nanoparticles are interrupted on the way to subcellular organelles, causing less than 1% of nanoparticles to reach the desired organelles. As organelles actively participate and mediate the progression of cellular survival, proliferation, and apoptosis, targeting organelles is a promising strategy for nanomedicine to improve therapeutic specificity and minimize side effects. The direct delivery of therapeutic materials into organelles such as nuclei, mitochondria, or lysosomes presents major challenges; however, advances in the synthesis, surface modification, and structural optimization of nanomedicines raise promising prospects for overcoming these barriers. Building on our previous study on organelle-targeting nanomedicine, in this review, we summarize the key aspects of chemical modification and structural optimization. Moreover, current nanomedicines specialized for targeting the nucleus, mitochondria, lysosomes, Golgi apparatus, and endoplasmic reticulum are classified for a holistic view of organelle-specific nanomedicine. Although promoted by artificial intelligence (AI) and machine learning (ML), organelle-targeting nanomedicines struggle to reach clinical application, and the major challenges are critically discussed here.

Safe and accurate femoral venous access is fundamental to the success of radiofrequency catheter ablation (RFCA) for atrial fibrillation (AF), particularly under uninterrupted anticoagulation, where vascular injury may lead to amplified bleeding and thrombotic risk. Conventional landmark-based puncture is limited by anatomical variability, whereas ultrasound guidance has shown potential to enhance puncture safety. This multicenter retrospective cohort study included 300 AF patients undergoing RFCA across 3 tertiary hospitals from September 2024 to December 2025 under uninterrupted anticoagulation. Patients were assigned to a preprocedural ultrasound localization group (n = 150) or a conventional anatomical landmark group (n = 150). Baseline characteristics were compared, and puncture efficiency, intraoperative events, puncture-related complications, operative metrics, postoperative recovery, and additional intervention requirements were evaluated. Multivariable logistic regression was used to adjust for confounders. Preprocedural ultrasound markedly improved puncture performance, achieving a higher first-attempt success rate (87.3% vs 59.3%, P <.001), fewer attempts (1.3 ± 0.6 vs 2.4 ± 1.1, P <.001), and shorter puncture time (4.6 ± 1.2 vs 6.8 ± 1.5 minutes, P <.001). Ultrasound-detected anatomical variations in 44% of patients, including venous deviation, duplication, stenosis, and venous-arterial overlap. Safety outcomes favored the ultrasound group, showing reduced arterial mispuncture (2.7% vs 14.0%), blood vessel spasm (3.3% vs 11.3%), and abnormal catheter path events (2.0% vs 11.3%) (all P <.01). Puncture-related complications were significantly decreased, including overall hematoma (10.0% vs 31.3%), persistent oozing (6.7% vs 17.3%), infection (0.7% vs 4.7%), deep vein thrombosis (2.0% vs 7.3%), pseudoaneurysm (0% vs 4.0%), and arteriovenous fistula (0.7% vs 4.7%) (all P <.05). Ultrasound localization also reduced operative difficulty scores (1.9 ± 0.8 vs 3.2 ± 1.1, P <.001) and shortened total procedural duration (118.7 ± 25.4 vs 133.3 ± 30.4 minutes, P <.001). Postoperative pain at 2 and 24 hours was significantly lower, and bed rest time was shorter, though length of stay was similar between groups. Additional interventions - extended compression, hematoma drainage, and anticoagulation adjustment - were markedly less frequent in the ultrasound group (overall 4.7% vs 21.3%, P <.001). Preprocedural femoral venous ultrasound localization significantly enhances puncture accuracy, reduces vascular complications, improves procedural efficiency, and accelerates postoperative recovery in AF patients undergoing RFCA under uninterrupted anticoagulation. These findings support incorporating ultrasound-based localization into routine preprocedural assessment to optimize the safety and quality of electrophysiological interventions.

Acute ischemic stroke (AIS) is a major cause of functional disability and mortality in the geriatric population. This study aimed to evaluate the predictive performance of the prognostic nutritional index (PNI), geriatric nutritional risk index (GNRI), and the controlling nutritional status (CONUT) score for in-hospital mortality among critically ill geriatric patients. Critically ill AIS patients admitted to a tertiary hospital intensive care unit from January 2021 to January 2023 were retrospectively analyzed. Patients were classified into survivor and mortality groups. Nutritional scores were calculated: PNI = (10 × serum albumin [g/dL]) + (0.005 × total lymphocyte count); GNRI = (1.489 × albumin [g/dL]) + (41.7 × [body weight/ideal body weight]); CONUT (scored 0-12 based on serum lymphocyte count, cholesterol, and albumin). The predictive performances of the scores for in-hospital mortality were compared. A total of 142 patients were included, with 25 in the mortality group and 117 in the survivor group. The median age was 77 (range: 68-84) years, and 55.6% (n = 79) were female. Demographic characteristics (age, sex, body mass index) were similar between groups. Median PNI (36.3 vs 39.5, P = .017), GNRI (53.4 vs 56.6, P = .007), and CONUT (2 vs 2, P = .012) scores were significantly lower in the mortality group. Multivariate regression analysis showed that GNRI was an independent predictor of mortality (odds ratio = 0.935, 95% confidence interval = 0.877-0.998, P = .042). Receiver operating characteristic analyses showed a PNI cutoff value of ≤34.2 (area under curve [AUC] 0.653, 0.535-0.770), GNRI ≤56.2 (AUC 0.672, 0.577-0.767), and CONUT ≥1.5 (AUC 0.659, 0.545-0.773). Nutritional scores such as PNI, GNRI, and CONUT can predict mortality in critically ill geriatric AIS patients in the intensive care unit. Their prognostic performances were found to be similar.

Older adults face high risks of all-cause and cardiovascular disease (CVD) mortality; however, simple, inexpensive biomarkers for early risk identification are limited. The red cell distribution width-to-albumin ratio (RAR) is a low-cost, routinely measured marker, but its prognostic value in older adults is unclear. We examined whether RAR is independently associated with all-cause and CVD mortality in older adults. We conducted a retrospective cohort study using data from the United States National Health and Nutrition Examination Survey (1999-2018). The study included 16,558 adults aged ≥60 years, with median follow-up of 9.4 years. Multivariable Cox proportional hazards models estimated associations between RAR and mortality. Nonlinearity was evaluated using generalized additive models with penalized splines and two-piecewise Cox models combined with a recursive algorithm. Among 16,558 participants (mean age 70.7 ± 7.3 years; 49.8% men), RAR quartiles were Q1 (2.32-2.95), Q2 (2.95-3.16), Q3 (3.16-3.45), and Q4 (>3.45). Over a median 9.4-year follow-up, 6119 deaths occurred, including 2048 CVD deaths. In fully adjusted models, RAR was associated with greater risks of all-cause mortality (hazard ratio = 2.15, 95% confidence interval = 1.89-2.45) and CVD mortality (hazard ratio = 2.05, 95% confidence interval = 1.74-2.41). Associations were nonlinear, with a threshold at RAR = 4.05; below this level, higher RAR was linked to increased all-cause and CVD mortality, whereas above it, the association weakened and CVD mortality risk plateaued. RAR was independently and nonlinearly associated with all-cause and CVD mortality in older adults. These findings support RAR as a simple biomarker for mortality risk identification in older adults.

Coronary artery disease is a major cause of mortality worldwide, particularly in developing countries. Treatments such as coronary artery bypass grafting (CABG) and percutaneous transluminal coronary angioplasty (PTCA) are common; however, their long-term effects on patient quality of life (QoL), particularly in developing nations, are not well understood. This study assessed and compared the QoL of cardiac patients 6 months after post-angioplasty and bypass surgery. A prospective cohort study was conducted over 5 months in 100 patients with Coronary artery disease who underwent PTCA or CABG at the Cardiology Follow-up Clinic of the same hospital. The data were collected using structured questionnaires. The result of this study shows baseline characteristics were similar between PTCA and CABG groups, except for a higher SYNTAX score in the CABG group (29.1 ± 8.6 vs 22.5 ± 7.4; P = .002). At 6 months, symptom relief was reported by 98% (PTCA) and 94% (CABG), with return-to-work rates of 94% and 88%, respectively. The rates of dyspnea, angina, and hospitalization were low and did not differ significantly between the groups. Both groups showed significant improvements in SF-36 and WHO-QoL Physical domain scores (P < .05). No deaths were recorded during follow-up period. Both PTCA and CABG significantly improved patients' QoL at 6 months, particularly in the physical health domain. While CABG showed slightly more consistent improvements in angina and dyspnea, this was not statistically significant during the short-term follow-up.

Out-of-hospital cardiac arrest (OHCA) survival depends critically on early defibrillation. Coordinated automated external defibrillator (AED) systems, including registries, mapping initiatives, and integration with emergency medical services (EMS), enable real-time device location, strategic placement, and system-level quality improvement. However, implementation varies widely between countries.

To synthesize evidence on the impact of coordinated AED systems, including registries and public-access defibrillation programs, on OHCA outcomes and to identify lessons from Japan applicable to Poland.

A systematic review was conducted according to PRISMA guidelines. PubMed/MEDLINE, EMBASE, Cochrane Library, and Scopus were searched (January 2015-June 2025) for studies evaluating AED registries, mapping systems, and public-access defibrillation programs. Eligible designs included randomized trials, observational registry studies, economic evaluations, and policy analyses. Inclusion criteria comprised studies evaluating AED registries, mapping systems, or public-access defibrillation in OHCA settings with reported clinical, operational, or economic outcomes. Exclusion criteria included studies without primary data, conference abstracts without full text, animal studies, and studies focused solely on in-hospital cardiac arrest. Study quality was assessed using the Newcastle-Ottawa Scale, AMSTAR 2, and CHEERS 2022.

Seventeen studies met inclusion criteria. Japan's coordinated system, combining nationwide OHCA surveillance, public-access defibrillation programs, AED mapping initiatives, and EMS integration, has been associated in observational studies with increased bystander AED use among patients with bystander-witnessed OHCA with shockable rhythm (from 1.1 to 16.5%), reduced time to defibrillation, and improved neurological outcomes. In contrast, Poland currently lacks a fully coordinated national system, resulting in fragmented AED data and limited integration with emergency response. Modeling studies suggest that implementing a national system incorporating an AED registry, dispatcher integration, and community responder networks would be cost-effective.

Coordinated AED systems, rather than standalone registries, represent an effective system-level approach to improving OHCA outcomes. Japan's experience highlights the importance of integrating AED mapping, OHCA surveillance, EMS systems, and public training. Implementing such a coordinated approach in Poland could substantially improve survival and neurological outcomes after cardiac arrest. However, the observed benefits are likely multifactorial and reflect the combined effect of system-level interventions rather than a single component.

Primary aldosteronism (PA) is associated with a substantially higher cardiovascular risk than essential hypertension, a disparity that cannot be fully explained by blood pressure elevation alone. Clinical studies consistently demonstrate that cardiovascular morbidity and mortality often persist in patients with PA despite adequate blood pressure control and standard therapy, underscoring the existence of residual cardiovascular risk. Accumulating experimental and clinical evidence identifies inflammation as a central mediator of aldosterone-induced cardiovascular injury. Excess aldosterone drives immune-inflammatory remodeling through coordinated activation of innate and adaptive immune responses, including macrophage- and T cell-dependent pathways, as well as downstream signaling cascades such as inflammasome activation and interleukin-6-related trans-signaling. These processes promote myocardial fibrosis, vascular dysfunction, and adverse cardiac remodeling, providing a mechanistic basis for the heightened cardiovascular risk observed in PA. Although mineralocorticoid receptor (MR) antagonists remain the cornerstone of medical therapy for PA, MR blockade alone may be insufficient to fully suppress aldosterone-driven inflammatory and non-hemodynamic effects. Persistent activation of these pathways offers a plausible explanation for the residual cardiovascular risk observed in treated patients. Emerging therapeutic strategies aim to overcome these limitations through combination approaches. Aldosterone synthase inhibitors (ASIs), by targeting aldosterone production upstream, may complement MR antagonism, while interventions directed at inflammatory pathways and non-genomic aldosterone signaling could further enhance cardiovascular protection. This review integrates current mechanistic and clinical evidence on inflammatory drivers and residual risk in PA and discusses emerging combination strategies to optimize cardiovascular risk reduction in this high-risk population.

Metabolic syndrome (MS) is an atherogenic risk factor influenced by both modifiable and non-modifiable risk factors, including race, hypertension, obesity, and age. This study evaluated the association between MS and arterial stiffness (AS) in individuals of African ancestry.

Using WHO criteria, MS was assessed in 668 participants aged 18-70 years. Obesity was evaluated through body mass index (BMI), waist circumference (WC), and waist-to-hip ratio (WHR). Blood pressure (BP) measurements included office BP, 24-hour ambulatory BP monitoring (ABPM), and daytime/nighttime BP. Arterial stiffness was assessed via pulse wave velocity (PWV). Blood samples were analyzed for triglycerides (TG), high-density lipoprotein (HDL), and fasting blood glucose. Statistical analysis was performed using SPSS and STATA.

The prevalence of metabolic syndrome increased with age and was significantly higher in females. Participants with MS had a higher prevalence of hypertension and obesity. PWV was significantly associated with BP parameters and obesity indices (BMI, WC, WHR). Moreover, PWV was higher in individuals with MS compared to those without.

Obesity and hypertension, key diagnostic components of MS, are independently associated with arterial stiffness. This underscores their role in driving target organ damage among individuals with MS in this African ancestry cohort.

Peripheral artery disease (PAD) is a prevalent, disabling manifestation of systemic atherosclerosis that carries high risks of major adverse cardiovascular and limb events, yet remains incompletely explained by conventional risk factors and haemodynamic indices. Although genome-wide association studies have nominated reproducible susceptibility loci and high-throughput profiling has expanded the landscape of circulating, imaging, vascular and skeletal muscle biomarkers, most signals are noncoding, mechanistic attribution is often uncertain and few biomarkers have demonstrated durable incremental utility for risk stratification or therapeutic guidance in routine care. In this review, we summarise PAD-relevant genetic architectures and multiomics modalities-fine-mapped GWAS with tissue- and cell-resolved functional genomics, proteogenomic and metabolomic profiling and network-based integration across vascular, muscle and circulating compartments-and we appraise translational opportunities that span variant-anchored protein and metabolite prioritisation, composite biomarker panels for limb-specific ischaemic burden and residual atherothrombotic risk and biomarker-informed selection of antithrombotic, lipid-lowering, anti-inflammatory and revascularisation strategies. We also discuss enduring challenges-including ancestry-sensitive transferability of genetic instruments, limited access to disease-relevant tissues, cross-platform standardisation, confounding by disease stage and therapy and the need for prospective validation and trial-ready pharmacodynamic endpoints-that temper implementation. The purpose of this review is to delineate variant-to-biomarker pathways in PAD and specify integrative, clinically actionable solutions for discovery, validation and translation. We further distinguish diagnostic, prognostic, predictive/theragnostic and pharmacodynamic biomarker contexts of use, and emphasise that phenotype definition, sex, diabetes, exposure measurement and treatment effects all condition the interpretation and transferability of PAD multiomic signals.