Cardiac sarcoidosis (CS) is an inflammatory granulomatous cardiomyopathy associated with atrioventricular block, ventricular arrhythmias, heart failure (HF), and sudden cardiac death (SCD). Diagnosis and management remain challenging because myocardial involvement is patchy and evidence from randomized trials is limited. This review summarizes current knowledge on CS, focusing on advances in diagnosis, immunosuppression, and prevention of arrhythmic events.

Cardiac involvement is clinically recognized in 5-10% of patients with sarcoidosis but is more frequent in imaging and autopsy studies. Cardiac magnetic resonance (CMR) and ^18F-fluorodeoxyglucose positron emission tomography (FDG-PET) provide complementary information on myocardial scar and active inflammation. Multimodality imaging, extracardiac tissue diagnosis, guided endomyocardial biopsy, and consensus criteria improve diagnostic confidence. Corticosteroids remain first-line therapy for active inflammation, while steroid-sparing agents are increasingly used to reduce corticosteroid exposure or treat persistent disease. Inflammasome/interleukin-1 inhibition is an emerging targeted strategy, but its clinical efficacy remains unproven. SCD risk stratification now extends beyond left ventricular ejection fraction to include ventricular arrhythmias, conduction disease, ventricular dysfunction, and myocardial scar burden. Implantable cardioverter-defibrillator therapy remains central in selected high-risk patients. CS requires early recognition of both inflammation and myocardial scar. CMR and FDG-PET are central to diagnosis, prognosis, and therapeutic decisions, while management combines immunosuppression, HF therapy, and arrhythmia prevention. Major uncertainties remain regarding optimal diagnostic criteria, immunosuppression strategies, serial imaging, and primary-prevention ICD selection. Prospective studies and randomized trials are needed to refine treatment and risk stratification.

The optimal management of asymptomatic carotid stenosis remains controversial despite advances in medical therapy. Although intraplaque hemorrhage (IPH) is an established marker of plaque vulnerability, the prospective natural history of magnetic resonance imaging (MRI)-defined IPH-positive asymptomatic carotid stenosis remains incompletely characterized. We investigated the clinical course of this population. The Stratification by Multidimensional Approach for Rational Treatment of Asymptomatic Carotid Stenosis (SMART-K) study is a prospective multicenter cohort of patients with asymptomatic carotid stenosis and MRI-confirmed IPH. Patients were followed for up to 36 months under medical management according to contemporary clinical practice. Baseline assessments included plaque-to-muscle (PM) ratio and soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1). The primary endpoint was ipsilateral ischemic events, including ischemic stroke, transient ischemic attack (TIA), and amaurosis fugax. Kaplan-Meier and exploratory Cox proportional hazards analyses were performed. Among 76 patients included in the final analysis, 11 (14.5%) developed primary endpoint events: ischemic stroke in 8, TIA in 2, and amaurosis fugax in 1. The 3-year cumulative incidence was 14.8%. Stenosis severity showed a trend toward association with ischemic events (hazard ratio per 10% increase, 1.46; 95% confidence interval, 0.92-2.31; P = 0.11), whereas PM ratio and sLOX-1 were not associated with events. Patients with MRI-defined IPH-positive asymptomatic carotid stenosis remained at clinically meaningful risk of ipsilateral ischemic events under contemporary clinical management. These findings provide prospective natural history data for this specifically defined population and support further evaluation of MRI-defined IPH in individualized risk-stratification strategies.

Type 2 diabetes (T2D) is associated with a substantial burden of cardiovascular and renal complications. Although current evidence supports early implementation of organ-protective strategies, therapeutic inertia and uncertainty regarding guideline implementation may delay treatment intensification. The goal of this review is to discuss the rationale for early cardiorenal protection in T2D and to explore real-world perspectives on the use of SGLT2 inhibitors and GLP-1 receptor agonists through insights from the PRECARE NO LiMITS initiative. This narrative review integrates current evidence with exploratory findings from the PRECARE NO LiMITS project, a multicentre educational initiative involving diabetologists from ten diabetes centres in Lombardy, Italy. The initiative included two descriptive clinician survey rounds, conducted at baseline (T0) and after six months (T1), together with moderated expert discussions. At T1, a higher proportion of respondents reported considering SGLT2 inhibitor initiation in a greater proportion of patients with early cardiorenal risk markers, including albuminuria and mildly reduced eGFR, even in the absence of established cardiovascular or renal disease. Survey responses also suggested greater consideration of risk-based treatment strategies extending beyond glycaemic control alone. Persistent perceived barriers included reliance on HbA1c as a primary driver of treatment intensification, uncertainty regarding the timing and implementation of organ-protective therapies, and concerns related to treatment complexity and access. Given the descriptive nature of the survey, differences between T0 and T1 should be interpreted as exploratory. Overall, these exploratory observations, considered alongside current evidence and guideline recommendations, highlight the potential value of a proactive approach to T2D management focused on early identification of cardiorenal risk and appropriate consideration of organ-protective therapies. Educational initiatives, multidisciplinary collaboration, and improved translation of guideline recommendations into routine clinical practice may help address therapeutic inertia and facilitate timely, individualised treatment decisions.

Adults aged 80 years or older with nonvalvular atrial fibrillation (NVAF) often have competing thromboembolic and bleeding risks, renal impairment, frailty, and dose-selection challenges. This single-center retrospective observational cohort included 202 adults aged 80 years or older who received warfarin (n = 56), edoxaban 60 mg once daily (n = 38), edoxaban 30 mg once daily (n = 41), rivaroxaban 15 mg once daily (n = 35), or rivaroxaban 10 mg once daily (n = 32). Six-month embolic events, International Society on Thrombosis and Hemostasis (ISTH) bleeding categories, other adverse reactions, official-label dose concordance, dynamic risk scores, and serial laboratory measurements were evaluated. Exploratory generalized overlap weighting addressed measured treatment-selection differences. Embolic events occurred in 8 patients and ISTH minor bleeding in 21; neither outcome differed significantly among groups (exact p = 0.846 and p = 0.199, respectively). No ISTH major or clinically relevant non-major bleeding occurred. Other adverse reactions differed overall (p = 0.014), but pairwise estimates were imprecise. Of 146 direct oral anticoagulant recipients, 72 (49.3%) received a baseline dose concordant with the prespecified official-label framework, 72 (49.3%) received a lower-than-label dose, and 2 (1.4%) received a higher-than-label dose. Low event counts and marked treatment-selection imbalance prevented conclusions of equivalence, superiority, or greater safety. The findings require confirmation in larger, prospectively defined cohorts with longer follow-up, predefined label-dose criteria, and stronger control of confounding.

Vascular tortuosity and aneurysms pose significant health risks across a variety of human tissues and blood vessel types. These alterations in vessel shape cause anomalies in blood flow dynamics, which significantly impact endothelial function. Animal models of these vascular disease states have been illustrative in some cases, but are both expensive to establish and limited to the animal species' physiology. In response to this, in vitro 3D organ-on-a-chip (OOC) models have become a powerful toolset for assessing vascular function and endothelial responses in human cells. While each of the OOC models has its strengths, an accessible system is needed for studying vessel permeability, a key indicator of vascular function in curved vessels and aneurysms under physiological shear rate and pressure. Here, the presented methodology enables the study of human endothelial cell responses to flow anomalies in an economical curved-vessel model system using an entry-level bioprinter that produces vessels that are compatible with physiological fluid flow rates, permeability studies, high-resolution light microscopy, and extracellular matrix support with physiological stiffness.

Coronary artery involvement (CAI) in Kawasaki disease (KD) is time-dependent, yet some published risk models combine pretreatment findings with variables that become known only after therapy. This retrospective single-center study examined admission-available factors associated with CAI present before intravenous immunoglobulin (IVIG) in an infant-enriched cohort and internally evaluated a timing-adjusted model. Children treated at Qingdao Women and Children's Hospital from January 2022 through December 2025 were eligible when pretreatment clinical data, laboratory measurements, and stored echocardiograms were available. Two pediatric cardiologists, blinded to clinical data and coronary classification, remeasured the left main coronary artery (LMCA), proximal left anterior descending artery (LAD), and proximal right coronary artery (RCA). Dallaire Z-scores were calculated, and CAI was defined as a maximum pretreatment Z-score of at least 2.0. The full model included age, illness day at echocardiography, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), platelet count, and extremity changes; complete/incomplete KD status and IVIG resistance were excluded from candidate predictors to reduce incorporation and temporal bias. Among 216 patients (median age, 5.7 months), 44 (20.4%) had pretreatment CAI. In the parsimonious model, CRP (adjusted odds ratio [aOR] per 10 mg/L, 1.151; 95% confidence interval [CI], 1.031-1.286), ESR (aOR per 10 mm/h, 1.158; 95% CI, 1.001-1.339), and illness day (aOR per day, 1.130; 95% CI, 1.020-1.252) were retained. The apparent area under the receiver operating characteristic curve was 0.745 and decreased to 0.710 after 1,000 bootstrap resamples; the bootstrap-corrected calibration slope was 0.82. At the data-derived threshold, the positive predictive value was 37.8%, and the negative predictive value was 92.1%. Extremity changes were not independently associated after adjustment for timing. The model showed moderate, cohort-specific performance and should not be used as a stand-alone test or substitute for echocardiography. Independent validation is required before clinical application.

Cardiovascular disease (CVD) remains one of the leading causes of death worldwide. Insulin resistance (IR) and central obesity are key contributors. The triglyceride-glucose (TyG) index is a simple surrogate for IR, while novel adiposity indices, such as the visceral adiposity index (VAI), lipid accumulation product (LAP), cardiometabolic index (CMI), body roundness index (BRI), and a body shape index (ABSI), better reflect body fat distribution. However, the predictive value of combining TyG with these indices for CVD risk remains unclear.

 This cross-sectional study used data from 19,822 adults aged ≥20 years in the U.S. NHANES (1999-2018). CVD was defined by self-reported physician diagnosis. The TyG index and its derivatives (TyG-BMI, TyG-WC, TyG-WHtR, TyG-CMI, TyG-VAI, TyG-LAP, TyG-BRI, TyG-ABSI) were calculated. Weighted logistic regression and restricted cubic spline (RCS) analyses assessed associations and potential nonlinear relationships. Receiver operating characteristic (ROC) curves compared predictive performance.

All TyG-derived indices were significantly associated with higher CVD risk (p<0.05). The strongest associations were observed for TyG-ABSI (OR=3.95, 95% CI: 1.99-7.85) and TyG-BRI (OR=2.10, 95% CI: 1.55-2.85). TyG-VAI and TyG-CMI showed nonlinear relationships with CVD. In ROC analysis, TyG-ABSI achieved the highest discriminative power (AUC=0.69), outperforming TyG and other indices. Subgroup analyses revealed stronger associations among younger, obese, hypertensive, and diabetic males.

Combining the TyG index with body-shape indices markedly improved CVD risk prediction. TyG-ABSI, TyG-BRI, and TyG-CMI showed superior diagnostic performance and may serve as cost-effective tools for early CVD risk assessment in clinical and public health settings.

Direct oral anticoagulants (DOACs) have become the mainstay of stroke prevention in patients with atrial fibrillation (AF). Decision to anticoagulate frail and post-stroke patients with AF may be challenging and complex. This study aimed to compare the outcomes of complex older patients with acute ischaemic stroke and AF who were treated with and without oral anticoagulants for secondary stroke prevention.

This is a retrospective observational study of all older persons (≥65 years) admitted to the geriatric medicine ward in our university hospital with acute ischaemic stroke and AF from January 2016 - December 2021. The inclusion criteria in our study were patients discharged alive from hospital post-ischaemic stroke with AF. Exclusion criteria were those who died as inpatient, those undergoing end-of-life care or with very severe frailty which are contraindication to anticoagulation. Comparison was done between patients who were anticoagulated and patients who were eligible for anticoagulation but were not anticoagulated for various reasons.

There were 539 patients with ischaemic stroke, of whom 110 (21%) had AF. Among them, 29 patients were excluded due to death during hospitalization (19), end-of-life (4), and very severe frailty (6). While 65 (80%, mean age 84.1 ± SD 6.3) were discharged on anticoagulation, 16 (20%, mean age 88.3 ± SD 4.3, p=0.388) were discharged without anticoagulation. The median clinical frailty score was six in both groups. Among the anticoagulated, 59 (91%) were commenced on DOACs and six (9%) were on warfarin. The main reasons recorded for not commencing anticoagulants in eligible patients were patient/family did not agree to start (8), high bleeding risk (7), and poor social support (1). Mortality was significantly higher in the non-anticoagulated group (n=10, 63%) compared to the anticoagulated group (n=22, 32%) (p=0.036).

Although frail older persons are perceived to have a poorer benefit/risk ratio when anticoagulated, our study demonstrated lower mortality in post-stroke anticoagulated complex older AF patients compared to those who were not anticoagulated. However, given the small numbers of participants in our study, further studies are required to determine characteristics of patients who may have better outcomes or lower risk of adverse events on anticoagulants. These findings also underscore the pressing need for a standardized, frailty-prescribing and monitoring protocol to maximise benefit and minimise risks of adverse outcomes.

This study aims to evaluate the cardiovascular disease risk and related factors among incarcerated individuals in a closed prison.

Cardiovascular diseases represent a leading cause of global mortality, among incarcerated individuals facing heightened risks attributable to environmental and lifestyle factors.

This cross-sectional study was conducted with foreign-nationed inmates aged 40-69 at Maltepe No. 3 L-Type Closed Prison in Istanbul, Türkiye, using World Health Organization (WHO) risk assessment tools. Data has been collected from January to March 2023 through in-person interviews, anthropometric assessments, and laboratory tests.

Of the 366 participants, all of them were male, mean age was 47.4 years (±6.2), as ethnic origin 74.6% were Asian. The median cardiovascular risk score was 6% (range: 1-52%), 74.6% classified as low-risk, 21.0% as moderate-risk, and 4.4% as high or very high-risk. Significant predictors of elevated cardiovascular risk included advanced age (p < 0.001), smoking (p < 0.001), systolic/diastolic hypertension (p < 0.001), and abdominal obesity (p = 0.005). Individuals exhibiting high-risk profiles showed increased levels of total cholesterol, LDL-C, HbA1c, and fasting blood glucose (p < 0.001). No correlation was found between incarceration duration and cardiovascular risk.

This study emphasises the importance of individual health evaluation including BMI and cardiovascular risk assessment and implementing preventive measures, such as smoking cessation, healthy diet and exercise programmes to protect low-and moderate-risk individuals and to lower the high risk as normal population. These preventive health services can be provided in primary care centres located in prison settlement.

Lipid metabolism, coagulation, inflammation, and vascular integrity are closely interconnected biological systems. Although statins are primarily prescribed to reduce low-density lipoprotein cholesterol (LDL-C) and prevent atherosclerotic cardiovascular disease, increasing evidence indicates that these agents exert multiple pharmacological effects beyond lipid lowering, including modulation of endothelial function, platelet activation, tissue factor expression, thrombin generation, fibrinolysis, and thrombo-inflammation. These pleiotropic properties have generated growing interest in the potential role of statins as adjunctive modulators of thrombotic risk in patients receiving anticoagulant therapy. Venous thromboembolism, which includes deep vein thrombosis and pulmonary embolism, is a major clinical setting in which anticoagulant treatment reduces recurrence and mortality but exposes patients to bleeding complications. Observational studies and registry-based analyses suggest that statin use may be associated with improved outcomes among anticoagulated patients with venous thromboembolism, particularly for all-cause mortality and early survival after pulmonary embolism. At the same time, emerging evidence suggests that very low LDL-C concentrations may be associated with increased bleeding risk during anticoagulation, raising important questions regarding the relationship between lipid availability, vascular stability, platelet function, and hemostatic balance. This review summarizes current pharmacological and clinical evidence linking lipid metabolism, statin therapy, anticoagulation, thrombosis, and bleeding. Particular attention is devoted to the mechanisms through which statins influence hemostatic pathways, the clinical evidence derived from venous thromboembolism cohorts, and the potential implications of LDL-C levels for personalized bleeding risk assessment. Future strategies that integrate lipid profiles, thrombotic and bleeding risk, and pharmacological modulation of coagulation may contribute to more individualized antithrombotic management.