Primary graft dysfunction (PGD) is the leading cause of early morbidity and mortality after heart transplantation (HTx). We retrospectively analyzed 830 consecutive HTx performed between 1984 and 2021. After excluding patients <18 years and those with missing data, 667 adult recipients remained. ISHLT PGD criteria were applied and perioperative variables and outcomes were reviewed. PGD occurred in 70 patients (10.5%), including 41 (6.1%) with left ventricular PGD and 29 (4.3%) with right ventricular PGD. Most LV-PGD cases were severe (88%). Patients with PGD were younger and more frequently had pretransplant dialysis, ventricular assist device support, or prior cardiac surgery. No donor-related factors were associated with PGD. Recipient-related factors and longer cardiopulmonary bypass time were associated with increased risk. PGD was associated with prolonged mechanical ventilation and ICU stay, and increased need for mechanical circulatory support, dialysis, reoperation, and treatment for sepsis. Mortality or re-transplantation was significantly higher in PGD patients at 30 days (45% vs. 3%) and 1 year (51% vs. 8%; HR 6.89, 95% CI 4.01-11.83, p < 0.0001).

Objective: To investigate the factors associated with recurrent in-stent restenosis (ISR) after drug-eluting stent (DES) implantation and to establish a screening model. Methods: This cross-sectional study enrolled patients who underwent DES implantation and subsequent coronary angiography at the Second Hospital of Dalian Medical University from January 2020 to July 2023, with confirmed ISR. Patients were divided into an ISR group (first episode) and a recurrent ISR (R-ISR) group (≥2 episodes at the same lesion). Clinical data, laboratory parameters, echocardiographic findings, and coronary angiography results were collected. Correlation analysis and multivariate logistic regression were performed to identify independent factors associated with R-ISR. A logistic regression model was constructed using stepwise regression, and its screening value was assessed by the area under the receiver operating characteristic curve (AUC). Results: A total of 292 patients with DES restenosis were included, aged (66.5±9.5) years, with 73.6% male. There were 202 in the ISR group and 90 in the R-ISR group. Correlation analysis showed that R-ISR was associated with lactate dehydrogenase (LDH) (r_pb=-0.159, P=0.007), number of stents (r_pb=0.256, P0.001), neutrophil-to-lymphocyte ratio (NLR) (r_pb=0.350, P0.001), and interleukin-1β (r_pb=0.324, P0.001). Multivariate logistic regression identified number of stents (OR=1.271, 95%CI 1.094-1.477, P=0.002), LDH (OR=0.989, 95%CI 0.982-0.996, P=0.002), NLR (OR=1.370, 95%CI 1.131-1.660, P=0.001), and interleukin-1β (OR=1.190, 95%CI 1.019-1.388, P=0.028) as independent factors for R-ISR. The combined model of these four indicators yielded an AUC of 0.742 (95%CI 0.641-0.843). Conclusions: LDH, number of stents, NLR, and IL-1β are independent related factors for R-ISR. The model based on these four variables demonstrates good predictive value for screening R-ISR, providing a reference for early identification and intervention in high-risk patients.

Objective: To explore the association between cumulative blood pressure load from childhood to midlife and the risk of arteriosclerosis in midlife. Methods: This study was based on the Hanzhong Children's Hypertension Cohort in Shaanxi Province. Using 36-year longitudinal follow-up data of 4 623 children and adolescents aged 6-18 years enrolled at baseline in 1987, the study period spanned from 1989 to 2023 with 7 follow-up assessments. A total of 1 845 participants were ultimately included in the analysis. Subjects were divided into the arteriosclerosis group and the non-arteriosclerosis group based on whether arteriosclerosis was detected at the final follow-up. Cumulative blood pressure load, including cumulative systolic blood pressure, diastolic blood pressure, and mean arterial pressure loads, was defined as the ratio of the area under the curve of blood pressure exceeding the standard threshold to the total area under the curve. Using the no-load group (cumulative blood pressure load=0) as the reference, participants were further divided into low-, medium-, and high-load groups based on tertiles. Multivariate logistic regression models were used to analyze the association between cumulative blood pressure load and arteriosclerosis. Restricted cubic spline models were applied to fit the dose-response relationship. Stratified analyses were performed by sex, age, smoking status, alcohol consumption, body mass index, and medication history. Results: The enrolled participants aged 49.00 (46.00, 51.00) years, with 1 016 males (55.1%). There were 506 cases (27.4%) in the arteriosclerosis group and 1 339 cases (72.6%) in the non-arteriosclerosis group. Compared with the non-arteriosclerosis group, the arteriosclerosis group had a higher proportion of males (328 (64.8%) vs. 688 (51.4%)), and higher levels of body mass index (25.72 (23.70, 27.78) kg/m²vs. 24.12 (22.26, 26.13) kg/m²), systolic blood pressure (138.17 (127.67, 150.00) mmHg vs. 121.33 (112.33, 132.00) mmHg, 1 mmHg=0.133 kPa), diastolic blood pressure (91.33 (83.67, 99.00) mmHg vs. 80.33 (73.67, 88.00) mmHg), and mean arterial pressure (107.34 (98.44, 115.89) mmHg vs. 94.00 (86.56, 102.11) mmHg) at the final follow-up (all P0.05). Multivariate logistic regression analysis, using the no-load group as the reference, showed that the risk of arteriosclerosis increased sequentially across the low-(OR=1.44, 95%CI: 0.99-2.11), medium-(OR=1.72, 95%CI: 1.15-2.57), and high-load groups of cumulative systolic blood pressure load. The association was stronger for cumulative diastolic blood pressure load (low-load: OR=2.98, 95%CI: 1.82-4.87; medium-load: OR=4.96, 95%CI: 3.05-8.06; high-load: OR=15.39, 95%CI: 9.34-25.37). Cumulative mean arterial pressure load showed a similar increasing trend (low-load: OR=2.31, 95%CI: 1.54-3.47; medium-load: OR=3.90, 95%CI: 2.63-5.80; high-load: OR=12.55, 95%CI: 8.28-19.02). Restricted cubic spline analysis revealed a non-linear positive correlation between all three cumulative blood pressure loads and the risk of midlife arteriosclerosis (all P0.05). Stratified analysis indicated that these associations were consistent across subgroups defined by sex, age, smoking status, alcohol consumption, body mass index, and medication use, with no interaction effects (all P_{for interaction}0.05). Conclusion: Cumulative blood pressure load from childhood to midlife is a risk factor for midlife arteriosclerosis, with a clear dose-response relationship. The association is most pronounced for cumulative diastolic blood pressure load.

Diet-disease-related knowledge (DDRK) is theorized to foster healthier lifestyles; however, the structural interconnectedness between nutritional knowledge and personal biomarker awareness is not well understood. This study aimed to identify independent predictors of DDRK and cardiovascular health (CVH) literacy among Lebanese adults using a psychometric framework.

A cross-sectional convenience-sampled online survey was conducted among 406 Lebanese adults. Standard validated questionnaires were used, including the GNKQ-Section 4, GPAQ, and MEDAS. CVH literacy was computed as the total awareness of five main CV biomarkers: total cholesterol, LDL, HDL, triglycerides, and HbA1c. Data were analyzed through multivariable logistic regression and EBICglasso network analyses.

Overall, the prevalence of cardiovascular (CV) biomarker unawareness was 65.5% across participants. Fully adjusted regression models showed that a continuous DDRK score was a significant factor independently associated with lower odds of CV biomarker unawareness (aOR = 0.878, 95% CI [0.824-0.936], p < 0.001), followed by a higher MEDAS score (aOR = 0.842, p = 0.003) and aging (aOR = 0.961, p < 0.001). The network model was dense (sparsity = 0.133) and showed DDRK-CVH literacy as the strongest conditional edge (r_partial = 0.202). The conditional associations of BMI (r = 0.000) and physical activity (r = 0.036) with CVH literacy collapsed after conditioning on DDRK and MEDAS. Centrality indicators showed that DDRK had the highest closeness and strength (both = 1.000).

DDRK shows strong conditional network associations with Mediterranean diet adherence and CVH literacy. These exploratory findings generate hypotheses for future longitudinal or interventional research.

Background: Several studies reveal an inverse relation between serum 25-hydroxyvitamin D [25(OH)D] concentration and the risk of acute ischemic stroke (AIS). The aim of this study was to determine relationships between 25(OH)D concentration and the course and outcomes of AIS treatment and the level of indices of inflammatory response to brain injury. Patients and Methods: Retrospective analysis of medical documentation of 1381 real-world AIS patients hospitalized in a single center between 1 January 2020 and 31 May 2025. Serum 25(OH)D level, several inflammatory indices, and clinical data were assessed. Results: Compared to patients in the lowest quartile of 25(OH)D concentration, those in the highest quartile had a shorter length of in-hospital stay, a lower risk of all-cause death, and a lower score for disability on a modified Rankin scale (mRS). Along with an increase in 25(OH)D quartiles, we found: a decrease in neutrophil count; a decrease in glucose, HbA1c, albumin, C-reactive protein (CRP), and CRP-to-albumin, -lymphocyte, -neutrophil, and -platelet ratios; lower neutrophil-to-lymphocyte and -albumin ratios, and lower systemic immune inflammation, and systemic inflammation response indices. In multifactorial logistic regression, the quartile of 25(OH)D (OR, 95% CI: 1.52, 1.09-2.12; p = 0.012) was the only variable to have a positive association with a mRS score ≤ 2 at discharge from hospital, and neutrophil-to-lymphocyte ratio, age, diabetes, and treatment with endovascular mechanical thrombectomy were biomarkers of poor functional status at discharge. Conclusions: Higher 25(OH)D concentration in AIS patients is related to better survival and a lower level of inflammatory response indices and disability at discharge.

Chronic inflammation and metabolic dysregulation of heart failure (HF) often result in sarcopenia. The combined effect of Mediterranean diet (MD) and omega-3 polyunsaturated fatty acids on the advanced lipidomic profile of HF patients remains poorly defined.

Our objective was to analyze the specific effects of a MD plus omega-3-enriched oral nutritional supplements (MD+ONS) versus MD alone on the metabolic lipid profile of patients with HF, stratified by sarcopenia status.

In this prospective, open-label, randomized controlled trial, 38 patients with HF were assigned to MD alone or MD+ONS (24 weeks). Advanced lipoprotein profiling (triglycerides, cholesterol, particle size, and concentration for VLDL, LDL, and HDL subclasses) was performed using 2D ¹H-NMR spectroscopy.

At baseline, NT-proBNP levels correlated positively with ω6/ω7ω9 fatty acids and IDL-TG (p < 0.05). Over 24 weeks, VLDL-C, VLDL-TG, and VLDL-P significantly decreased in the whole cohort (p < 0.001). However, stratified analysis revealed that in patients with sarcopenia, these reductions were primarily driven in the MD group (p < 0.01). Conversely, in patients without sarcopenia, the MD+ONS group showed significant reductions in VLDL-TG, VLDL-P, and VLDL-Z (p < 0.05). Regarding intermediate lipoproteins, IDL-C significantly increased in the MD group (p < 0.05) but not in the MD+ONS group. In the LDL fraction, total LDL-P and small LDL-P decreased in the MD group (p < 0.05), while medium LDL-P increased across both groups (p < 0.01). Total HDL-P decreased (p < 0.05), yet large HDL-P significantly increased in the whole cohort and the MD group (p < 0.05). No significant changes were observed in structural lipids or total fatty acid families.

MD+ONS induces lipidomic shifts that are significantly modulated by baseline sarcopenia. The intervention appears to stabilize VLDL and IDL levels in patients with sarcopenia compared to diet alone, while promoting a more favorable VLDL reduction in individuals without sarcopenia, suggesting that early nutritional support for improving body composition is a critical determinant of the metabolic response to specific interventions in patients with HF.

Background: We previously reported that consuming a Mediterranean-style healthy dietary pattern (MED-HDP) with lower vs. higher glycemic index foods differentially changed indices of postprandial glucose control and daily glycemic variability but did not influence improvements in cardiovascular health indices. Methods: Fifty-two adults (31 females, 21 males; aged 49 ± 11 y, BMI 31 ± 3.1 kg/m², mean ± SD) with two or more features of metabolic syndrome participated for 12 weeks in the randomized, controlled trial with all foods provided. At dinner only, participants could select from protocol-approved foods, including unprocessed chicken breast, unprocessed lean beef, and unprocessed salmon and shrimp (seafood). Objective: Herein, we retrospectively assessed whether the frequency of consuming different sources of meat (i.e., the exposures) was associated with MED-HDP-induced changes in cardiovascular health indices (i.e., the outcomes). Results: Among all participants, consuming the MED-HDP foods (88% adherence) reduced fasting systolic (SBP) and diastolic (DBP) blood pressures and serum total cholesterol (TC), triglycerides (TGs), and HDL. More frequent consumption of chicken at dinner, in place of beef and seafood, was associated with greater reductions in SBP (p = 0.034 and p = 0.047 for replacing beef and seafood, respectively) and DBP (p = 0.021 and p = 0.043, respectively). Frequency of chicken, beef, and seafood intakes at dinner did not associate with the reductions in serum TC, TG, HDL, or LDL. Conclusions: These results support that adoption of a MED-HDP improved multiple cardiovascular risk factors among middle-aged and older adults at elevated cardiovascular risk. The observed modest associations between more frequent consumption of unprocessed chicken at dinner and greater blood pressure reductions, which do not mean that eating more chicken at dinner causes lower blood pressure, warrant independent replication.

Per- and polyfluoroalkyl substances (PFAS) are persistent environmental contaminants increasingly associated with cardiovascular disease. Identifying early manifestations of vascular aging before the onset of overt disease is essential for improving cardiovascular risk stratification and prevention. Emerging evidence suggests that PFAS exposure contributes to early vascular and atherosclerotic alterations detectable by imaging techniques, including increased carotid intima-media thickness (CIMT), arterial stiffness, and endothelial dysfunction. In contrast, evidence for associations with coronary artery calcium progression and coronary stenosis remains scarce. Mechanistically, PFAS exposure promotes endothelial dysfunction, oxidative stress, chronic inflammation, lipid dysregulation, and genetic and epigenetic modifications, all of which contribute to premature vascular aging and metabolic disturbances. The integration of imaging and molecular biomarkers may provide complementary insights into the structural, functional, and biological processes underlying PFAS-related vascular damage; however, to date, this field remains largely unexplored. This narrative review summarizes current evidence on imaging and molecular biomarkers of PFAS-induced vascular aging and discusses their potential role in cardiovascular risk assessment. It also highlights key knowledge gaps and the need for robust epidemiological and multi-omics studies to validate these biomarkers, clarify causal mechanisms, and support their application in cardiovascular and environmental health surveillance.

In the present study, cardiovascular risk indices (Atherogenic Index of Plasma [AIP], Atherogenic Coefficient [AC], Castelli Risk Index-1 [CRI-1], and Castelli Risk Index-2 [CRI-2]) and bone mineral density (BMD SDS) were evaluated in patients with Familial Mediterranean Fever (FMF), and the association of these parameters with disease severity and MEFV gene mutations was investigated. A total of 126 participants (96 FMF patients and 30 healthy controls) were included in the study. FMF patients were classified as mild, moderate, or severe according to the PRAS severity score. Cardiovascular risk indices, biochemical parameters of bone metabolism, and BMD SDS values were compared among the groups. The relationship between BMD SDS and atherogenic indices was assessed by Spearman correlation analysis. The results were also analyzed according to MEFV gene mutations. No significant difference was detected among the groups in terms of sex or age (p > 0.05). FMF patients were found to have substantially higher cardiovascular risk indices than the control group, and these indices increased in parallel with disease severity (p < 0.05). The BMD SDS value of the severe FMF group was significantly lower than that of the other groups (p = 0.025). No difference was detected among the groups with respect to bone metabolism parameters (p > 0.05). No significant correlation was observed between BMD SDS and cardiovascular risk indices (p > 0.05). M694V was the most frequently detected mutation, and the BMD SDS value was lower in patients carrying mutations other than M694V (p = 0.011). The increased cardiovascular risk in FMF patients is associated with disease severity. Severe disease is accompanied by a reduction in bone mineral density. The lack of an association between cardiovascular risk and bone mineral density suggests that these systems may be affected through different mechanisms. It is important that FMF patients are monitored with respect to cardiovascular and bone health.

Stroke remains one of the leading causes of long-term disability and death worldwide. Growing evidence suggests that both stroke onset and severity exhibit strong circadian patterns. This blood-brain interface (BBI), which regulates bidirectional communication between the peripheral circulation and the central nervous system, plays a critical role in cerebrovascular injury. Aging further exacerbates these processes by dampening the molecular clock function and increasing inflammatory activation. In this review, we examine the circadian regulation of the BBI, aging, and its implications in stroke vulnerability. Understanding how circadian biology modulates neurovascular function may reveal novel therapeutic targets and time-of-day-dependent approaches for stroke prevention and treatment.