Angiology

Complications related to vascular closure devices (VCDs) remain relatively common after transcatheter aortic valve implantation (TAVI), while the optimal suture-based strategy remains a subject of debate. This systematic review and meta-analysis aim to evaluate the efficacy and safety of single versus double Perclose VCD in patients undergoing transfemoral TAVI. A literature search was conducted across PubMed, Scopus, and Cochrane databases to identify appropriate studies. The primary outcome was technical success; secondary outcomes included vascular and bleeding complications, bailout interventions, and all-cause mortality. Seven studies (3940 patients) fulfilled the inclusion criteria. Technical success was comparable between the two strategies (relative risk [RR]: .89; 95% confidence interval [CI]: .64-1.22), while the single Perclose strategy was associated with a lower risk of major vascular complications (RR: .61; 95% CI: .40-.92), major bleeding (RR: .28; 95% CI: .11-.73) and bailout surgical interventions (RR: .45; 95% CI: .24-.84). There were no differences in minor vascular complications and all-cause mortality. Stepwise closure with the upfront single Perclose strategy demonstrated comparable technical success and a more favorable safety profile regarding major vascular complications and bleeding compared with the double Perclose strategy. Additional randomized controlled trials are essential to validate these findings.

MicroRNAs (miRNAs) has emerged as a key regulatory factor in cardiovascular diseases, including acute myocardial infarction (AMI). We aim to explore the effects of miR-1306-5p on AMI. We enrolled 130 AMI patients and 85 healthy individuals. The levels of genes were measured by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, myocardial injury markers and inflammatory factor levels were assessed via cell counting kit-8 (CCK-8) and Enzyme-Linked Immunosorbent Assay (ELISA) assays. Target relationships were confirmed via dual-luciferase reporter assays and RNA immunoprecipitation (RIP) experiments. miR-1306-5p was remarkably diminished in AMI patients. It was an independent predictor of AMI, showing a positive correlation with the cardiac troponin I (cTnI) and a negative correlation with high-density lipoprotein cholesterol (HDL-C) and ejection fraction. Mechanistically, upregulated miR-1306-5p diminished the levels of cTnI, creatine kinase-MB (CK-MB), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) while promoting proliferation in hypoxia-reoxygenation (H/R)-treated AC16 cells. These effects could be reversed by overexpressing ten-eleven translocation 3 (TET3). Moreover, lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) was found to function as a microRNA sponge for miR-1306-5p. In conclusion, miR-1306-5p could bind to NEAT1 and subsequently mitigate cardiomyocyte damage by negatively regulating TET3.

The American Heart Association’s Predicting Risk of cardiovascular disease EVENTs (PREVENT) equations established estimated glomerular filtration rate (eGFR) as a component of cardiovascular risk assessment. However, the anatomical substrate underlying this risk—coronary atherosclerotic burden—remains inadequately characterized across renal function spectrum. This retrospective study included 1181 patients (mean age: 60.2 ± 8.9 years, 65.7% male) undergoing elective coronary angiography. Patients divided groups using eGFR; eGFR ≥90 (n = 596), 60 to 89 (n = 497), and 30 to 59 mL/min/1.73 m² (n = 88) were evaluated by stratification. Coronary atherosclerotic burden was determined using Gensini score. eGFR demonstrated a strong correlation with Gensini score (ρ = −0.352, P < .001). Each 10 mL/min/1.73 m² eGFR decline conferred 40% increased odds of severe coronary atherosclerosis (odds ratio [OR] = 0.960, 95% CI: 0.951-0.970, P < .001). Patients with eGFR 30 to 59 mL/min/1.73 m² exhibited 6-fold higher odds compared with preserved renal function (OR 6.073, 95% CI: 3.352-11.005, P < .001), independent of traditional risk factors. This study provides an anatomical validation for incorporating eGFR into cardiovascular risk assessment. Our angiographic evidence demonstrates that even mild renal dysfunction is accompanied by increased atherosclerotic burden. These findings bridge the gap between epidemiological risk prediction and pathophysiological reality, reinforcing the cardiovascular-kidney-metabolic health continuum and supporting aggressive risk modification strategies in patients with declining renal function, particularly among diabetic women.

This study examined the association between a blunted nocturnal heart rate decline and ventricular arrhythmias, echocardiographic findings, and clinical characteristics in patients with isolated hypertension (defined as hypertension in the absence of other systemic comorbidities). A total of 229 adults who underwent transthoracic echocardiography and 24-hour Holter monitoring were retrospectively evaluated. Patients were classified as dippers (≥10% nocturnal heart rate reduction; n = 170) or non-dippers (<10% reduction; n = 59), and were also compared according to Lown classes 0 versus 1-4. Baseline demographics, laboratory parameters, and antihypertensive treatments were similar between groups. Non-dippers demonstrated greater interventricular septal and posterior wall thickness, higher left ventricular mass and mass index, and a higher prevalence of left ventricular hypertrophy and concentric hypertrophy (P < .05 for all). They also exhibited more frequent ventricular and atrial ectopy. Patients in Lown classes 1-4 had higher systolic blood pressure, more pronounced left ventricular remodeling, and a greater arrhythmic burden. In multivariable analysis, concentric hypertrophy (Odds Ratio [OR]: 2.682; P = .034) and non-dipping nocturnal heart rate (OR: 9.254; P = .001) were independent predictors of arrhythmias. These findings suggest that non-dipping nocturnal heart rate (reflecting impaired parasympathetic activity and relative sympathetic predominance) is associated with adverse cardiac remodeling and increased arrhythmia risk in isolated hypertension.

Outcomes after intervention for chronic venous insufficiency (CVI) is difficult to predict. This study aimed to develop machine learning (ML) models to predict 90-day clinical improvement after varicose vein surgery and identify key factors. This retrospective multicenter study included patients with CVI undergoing first-time varicose vein surgery between 2014 and 2024. CVI was classified according to the Clinical-Etiologic-Anatomic-Pathophysiologic (CEAP) classification and Venous Clinical Severity Score (VCSS). Clinical improvement at 90 days was defined as any decrease in CEAP stage. Three ML classifiers (Logistic Regression, Random Forest, and XGBoost) were trained to predict improvement, with nested stratified cross-validation and undersampling to address class imbalance. In total, 4015 patients were included and 87.6% showed clinical improvement at 90 days. Non-improved patients were older, had higher body mass index (BMI), and higher baseline VCSS and CEAP scores. Random Forest achieved the best overall performance, with an accuracy of 80%, recall of 75%, and F1-score of 0.49 to predict the lack of improvement, indicating effective identification of at-risk individuals. Key predictors included baseline CEAP and VCSS scores, BMI, age, and surgical variables. The overall predictive performance of ML was modest, but the models highlighted patients at risk of poor outcomes.

This is a narrative review of the plasma kallikrein-kinin system (KKS) which has an important role in human physiology including the cardiovascular (CV) system. Kallikreins are serine proteases, enzymes that cleave proteins, participating in processes like blood pressure (BP) control, inflammation, and coagulation. Kallistatin is an endogenous kallikrein inhibitor with anti-inflammatory, anti-oxidative, and anti-atherosclerotic properties. Kallikrein controls the activity of several proteolytic cascades in the CV system comprising the intrinsic pathway of coagulation, the KKS, the fibrinolytic system, the renin-angiotensin system (RAS), and the complement pathways. Thus, kallikrein plays a crucial role in the pathogenesis of thrombosis, inflammation, and BP regulation. Plasma kallikrein exerts a cardioprotective role, however, when in high concentration or hyperactive, it perpetuates CV disease. Angiotensin-converting enzyme inhibitors and angiotensin AT1 receptor blockers act on both the RAS and the KKS. Moreover, angiotensin II enhances B1 and B2 bradykinin receptor expression via transcriptional mechanisms. These cross-talks explain why both the RAS and KKS are up-regulated in certain circumstances, whereas in others, both systems go the opposite direction (activated RAS/depressed KKS). As the cross-talks between RAS and KKS play an important role in response to different stimuli, considering these cross-talks may help develop drugs targeting the 2 systems.

Venous thromboembolism (VTE), comprising deep venous thrombosis (DVT) and pulmonary embolism (PE), are frequently observed during pregnancy and may cause maternal death. During pregnancy, several physiological and anatomical changes occur that enhance thrombotic risk. In addition, this risk might be significantly increased by several patient-specific risk factors. Therefore, VTE risk assessment in all pregnant women is essential for early identification of those at increased risk so as to obtain a timely diagnosis and plan a correct therapeutic approach. Unfortunately, clinical examinations may be complicated by the overlap between common physiological symptoms of pregnancy and those indicative of VTE. Thus, validated clinical decision tools such as the LEFt (Left lower extremity (L), Edema (E) and, symptom onset during the First Trimester of pregnancy) rule for suspected DVT and the YEARS algorithm for suspected PE have been developed to aid diagnostic assessment. Definitive diagnosis of DVT or PE requires confirmation with appropriate imaging modalities. An early diagnosis is important to facilitate prompt initiation of therapy that has Low Molecular Weight Heparin as the cornerstone of prevention and treatment during pregnancy and the postpartum period. In this narrative review, we consider the major risk factors for VTE during pregnancy, key diagnostic algorithms and updated therapeutic approaches.

This single-center prospective observational follow-up study aimed to evaluate 2-year changes in carotid plaque volume and echogenicity and to explore whether clinical and biochemical baseline factors are associated with plaque progression. It was an exploratory observational follow-up of patients with echolucent plaques previously enrolled in a 12-month randomized controlled trial. Plaque volume and grayscale median were measured at baseline and at 3, 6, 12, and 24 months using three-dimensional ultrasound (3D-US). Associations between baseline characteristics and plaque progression were evaluated using mixed-effects models with time-predictor interactions, adjusted for baseline plaque volume. Medication adherence from 12 to 24 months was examined. Plaque echogenicity remained stable over 24 months, whereas mean plaque volume increased with heterogeneous patterns. Approximately 20% of plaques were classified as progressors, 70% as stable, and 10% as regressors. Higher mean arterial pressure, low density lipoprotein cholesterol (LDL-C), and larger baseline volume were significantly associated with plaque progression. Poor statin adherence showed a non-significant trend toward greater progression. In conclusion, echolucent carotid plaques demonstrated stable echogenicity but volumetric progression over 24 months. Blood pressure, LDL-C, and baseline plaque size were associated with progression, although limited by sample size, supporting a role for longitudinal 3D-US plaque volume assessment in individualized cardiovascular prevention.

This study aimed to investigate the association between depression and advanced stages of cardiovascular-kidney-metabolic (CKM) syndrome. This cross-sectional study utilized nationally representative data from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2018. Depression was assessed using the Patient Health Questionnaire-9 (PHQ-9). Advanced CKM syndrome was defined as CKM stages 3-4. Weighted logistic regression models were applied to evaluate the association between depression and advanced CKM syndrome. Among 6677 adults, depression was positively associated with advanced CKM syndrome. Each 1-point increase in PHQ-9 score was associated with higher odds of advanced CKM syndrome (odds ratio [OR] = 1.05, 95% CI: 1.02-1.08), and individuals with moderate-to-severe depression had significantly increased odds (OR = 1.89, 95% CI: 1.25-2.87). Restricted cubic spline analysis revealed an L-shaped nonlinear relationship. A least absolute shrinkage and selection operator (LASSO) logistic regression model identified 9 factors associated with advanced CKM syndrome among individuals with depression, demonstrating high discriminative performance. Subgroup analyses indicated heterogeneity by sex, with a more pronounced association observed among women, highlighting the importance of early mental health screening in CKM syndrome risk stratification.

This study investigated the association between carotid ultrasound-derived plaque characteristics and the severity of coronary artery disease (CAD), and evaluated their incremental predictive value for identifying high coronary anatomical complexity. A total of 301 patients who underwent carotid ultrasound and coronary assessment (coronary angiography or coronary computed tomography angiography) within the same clinical period were included. CAD severity was assessed using the Gensini and SYNTAX scores. Carotid ultrasound parameters included intima-media thickness (IMT), plaque burden, plaque echogenicity, surface morphology, and carotid stenosis. Patients with higher SYNTAX scores demonstrated significantly increased IMT, greater plaque burden, and more high-risk plaque features. Spearman analysis showed that mean IMT exhibited the strongest correlation with both the Gensini score (r = 0.65, P < .001) and the SYNTAX score (r = 0.53, P < .001). In multivariable analyses, IMT remained independently associated with CAD severity. The addition of carotid ultrasound parameters improved model discrimination for identifying high SYNTAX scores, with the area under the receiver operating characteristic curve (AUC) increasing from 0.728 to 0.826. Carotid ultrasound parameters, particularly IMT, are associated with CAD severity and provide incremental value for identifying patients with complex coronary artery disease.