Background and Objectives: Diastolic dysfunction (DD) is a frequent complication following percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS), potentially contributing to adverse outcomes. This study aimed to investigate the association between post-procedural inflammatory markers and the severity of DD and to propose a preliminary risk score for early prediction. Materials and Methods: We retrospectively analyzed 181 ACS patients undergoing PCI, assessing C-reactive protein (CRP), leukocyte, neutrophil counts, and N-terminal pro-B-type natriuretic peptide (NT-proBNP) measured 24–48 h post-PCI. Echocardiographic DD grading was performed according to ASE/EACVI guidelines. Spearman correlation, ordinal regression, and decision-curve analysis were used to evaluate predictive performance. Results: CRP correlated with DD severity (ρ = 0.232, p = 0.002) and showed a borderline independent association (OR 1.004, 95% CI 0.999–1.009, p = 0.081). NT-proBNP correlated positively with both CRP and DD severity, while leukocyte and neutrophil counts were not significant. A three-parameter risk score (CRP > 10 mg/L, NT-proBNP > 125 pg/mL, age ≥ 65 years) identified patients at higher risk of moderate-to-severe DD (score ≥ 2: sensitivity 62%, specificity 71%). Decision-curve analysis demonstrated clinical utility in guiding post-PCI monitoring. Conclusions: A simple 0–3 point score combining age, CRP, and NT-proBNP showed potential for early identification of patients at risk of moderate-to-severe diastolic dysfunction after PCI. While the model demonstrated acceptable discrimination and calibration, its single-center design, limited sample size, and timing of biomarker assessment warrant cautious interpretation. External validation in larger, multicenter cohorts is required before clinical application.

Background: Persistent gastrointestinal (GI) symptoms are common in adults and are often considered functional conditions. Emerging evidence suggests that gastrointestinal function may be intertwined with systemic metabolic regulation, yet the association between chronic GI symptoms and cardiometabolic risk assessed using routine clinical biomarkers remains insufficiently explored. Methods: In this cross-sectional observational study, 93 adults were consecutively enrolled during routine clinical evaluations. Anthropometric parameters, fasting plasma glucose, glycated hemoglobin (HbA1c), lipid profile, and blood pressure were assessed. Participants were classified as having persistent gastrointestinal symptoms (GI+) or being asymptomatic (GI−) based on symptom duration and clinical documentation. A composite metabolic stress score, derived from routinely available biomarkers, was used to summarize multidimensional cardiometabolic burden. Group comparisons and correlation analyses were performed using non-parametric methods. Results: Participants with persistent gastrointestinal symptoms exhibited higher triglyceride levels, lower HDL-cholesterol concentrations, and higher fasting plasma glucose compared with asymptomatic individuals (all p < 0.05). The composite metabolic stress score was significantly higher in the GI+ group, indicating greater overall cardiometabolic burden, while body mass index and HbA1c did not differ significantly between groups. Conclusions: Persistent gastrointestinal symptoms were associated with an unfavorable cardiometabolic profile characterized by atherogenic dyslipidemia and impaired fasting glycemia. An exploratory composite metabolic stress score based on routine clinical biomarkers effectively summarized this pattern. These findings support the biological plausibility of shared metabolic vulnerability between gastrointestinal symptom burden and cardiometabolic risk and highlight the need for longitudinal and mechanistic studies incorporating objective gastrointestinal and metabolic biomarkers.

Background and Objectives: Left ventricular diastolic dysfunction (LVDD) is a known precursor of heart failure with preserved ejection fraction (HFpEF), particularly in patients with metabolic comorbidities. Acute coronary syndrome (ACS) and percutaneous coronary interventions (PCI) may exacerbate LVDD via systemic inflammation. This study aimed to explore the association between post-procedural systemic inflammation and the severity of diastolic dysfunction in patients with ACS and metabolic comorbidities. Materials and Methods: A retrospective observational study was conducted in 181 patients with ACS who underwent PCI. Inflammatory markers (leukocytes, neutrophils, and C-reactive protein [CRP]) measured at 24–48 h post-intervention were analyzed in relation to diastolic dysfunction, assessed by echocardiography. Multivariable ordinal logistic regression and correlation analyses were performed. Results: CRP showed a non-significant trend toward association with more advanced diastolic dysfunction (p = 0.081). Hypertension had a positive but nonsignificant coefficient. Other metabolic comorbidities (diabetes, dyslipidemia, and obesity) were not significantly associated. The correlation between N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin was exploratory. NT-proBNP was the only marker significantly correlated with high-sensitivity troponin (TrHS) at 48 h, indicating a link between myocardial injury and wall stress. Conclusions: CRP may be weakly associated with the severity of diastolic dysfunction post-PCI. However, classical metabolic comorbidities were not independently predictive. Post-PCI inflammation showed only modest, non-significant trends toward diastolic impairment, warranting confirmation in larger prospective studies.

Background: Post-procedural infection worsens outcomes in acute coronary syndrome (ACS). High-sensitivity cardiac troponin (hs-cTn) reflects myocardial injury, but its utility for infection risk prediction after percutaneous coronary intervention (PCI) is uncertain. Objective: This study aimed to evaluate whether high-sensitivity troponin (hs-cTn) levels are associated with the risk of infection and systemic inflammation. Methods: We performed an exploratory pilot study of consecutive ACS patients undergoing PCI (n = 181) at a tertiary interventional cardiology unit in Romania. Herein, hs-cTn was measured at 24- and 48-h post-PCI. The primary outcome was in-hospital infection (clinical and/or microbiological documentation), with the acknowledgment that nearly half were clinically diagnosed without microbiological confirmation. We assessed discrimination for hs-cTn48h using ROC analysis and explored associations with systemic markers (CRP, ESR, and leukocytes) and NT-proBNP using Spearman correlations. Results: Infections occurred in 9/181 patients (5.0%; 95% CI, 2.6–9.2). Notably, hs-cTn48h showed AUC = 0.49 (approx. 95% CI, 0.30–0.68) for infection discrimination. Correlations between hs-cTn48h and inflammatory markers were weak and non-significant (CRP ρ = 0.126, p = 0.091; ESR ρ = 0.119, p = 0.111; fibrinogen ρ = 0.134, p = 0.073), whereas hs-cTn48h correlated modestly with NT-proBNP (ρ = 0.232, p = 0.002). Conclusions: In this cohort, hs-cTn48h did not predict in-hospital infection after PCI in ACS. These negative findings highlight that troponin should be interpreted primarily as a marker of myocardial necrosis, not infectious risk. Larger multicenter studies with microbiological adjudication and broader biomarker panels are warranted.

Background: Cardiometabolic disorders and psychiatric conditions frequently coexist and may interact bidirectionally through shared metabolic, inflammatory, and neuroendocrine pathways. However, real-world clinical datasets often reveal substantial heterogeneity in multimorbidity patterns, and the extent to which psychiatric comorbidity clusters with metabolic dysfunction remains insufficiently characterized. This study aimed to evaluate the relationships between psychiatric diagnoses, metabolic biomarkers, hepatic and renal indicators, and polypharmacy within a clinically diverse cohort. Methods: We conducted a cross-sectional analysis of 47 patients from a cohort in a real-world clinical database. Psychiatric comorbidity was identified using diagnostic text-mining. Cardiometabolic markers included TyG index, FIB-4 score, serum creatinine, UACR, and total medication count. Group comparisons used Shapiro–Wilk testing for normality and either unpaired t-tests or Mann–Whitney tests as appropriate. Spearman correlations and a heatmap visualization were used to explore interactions among biomarkers. Results: Psychiatric comorbidity was present in 48.9% of patients and was associated with higher medication burden (6.0 ± 2.5 vs. 3.3 ± 2.1) and elevated TyG index (9.15 ± 0.80 vs. 6.19 ± 4.80), although differences did not reach statistical significance. Hepatic (FIB-4) and renal (creatinine) biomarkers exhibited wide variability, particularly among individuals without psychiatric diagnoses. Correlation analyses revealed weak-to-moderate associations among biomarkers, underscoring the heterogeneous nature of organ involvement in this cohort. Conclusions: Psychiatric comorbidity clustered with increased metabolic stress and polypharmacy, suggesting an integrated cardiometabolic–psychiatric vulnerability. The marked heterogeneity of hepatic and renal markers indicates that multimorbidity follows non-linear patterns not captured by single biomarkers. Integrated, multidisciplinary management strategies and larger longitudinal studies are needed to clarify causal pathways and optimize care for patients with combined cardiometabolic and psychiatric risk.

Background: Plant-rich dietary patterns are widely associated with metabolic and gastrointestinal health benefits. However, individuals consuming predominantly plant-based foods may also experience chronic low-dose exposure to dietary pesticide residues. At the same time, physical activity is recognized as an important lifestyle factor influencing metabolic health and gut microbiome composition. How microbiome features and microbiome-related metabolic profiles vary according to physical activity level in adults consuming plant-rich diets and reporting gastrointestinal symptoms remains insufficiently characterized. Objective: To explore associations between physical activity level, gut microbiome characteristics, and urinary organic acid patterns in adults consuming predominantly plant-rich diets and experiencing gastrointestinal symptoms, within a cohort characterized by comparable estimated dietary pesticide exposure used as a contextual dietary background variable. Methods: This cross-sectional observational study included 93 adults consuming ≥50% plant-based foods for at least six months and reporting persistent gastrointestinal symptoms. Participants were stratified according to physical activity level using WHO-based thresholds (<150 vs. ≥150 min/week of moderate-intensity activity). Stool microbiota were assessed using a targeted quantitative PCR panel, and microbial diversity was summarized using a laboratory-derived Shannon index. A voluntary subgroup (n = 50) underwent targeted urinary organic acid analysis (LC–MS/MS). Dietary pesticide exposure was indirectly estimated using national surveillance data combined with individual dietary records and was applied uniformly across groups. Analyses were primarily descriptive and exploratory; results are presented as associations. Results: Estimated dietary pesticide exposure did not differ between physical activity groups. Participants with lower physical activity were older and exhibited lower microbial diversity and a higher prevalence of reduced abundance in selected commensal taxa. Differences were observed in selected intermediary organic acid markers, while no statistically significant difference was found for the bile acid-related indicator. Several cross-domain correlations were identified between microbial features and metabolite patterns. However, given the cross-sectional design, age imbalance between groups, and subgroup-based metabolomic analyses, the findings should be interpreted as hypothesis-generating rather than indicative of independent effects of physical activity. Conclusions: In adults consuming plant-rich diets and reporting gastrointestinal symptoms, physical activity level was associated with distinct microbiome and microbiome-related metabolic patterns under comparable estimated dietary pesticide exposure. These findings highlight the potential contribution of lifestyle factors to interindividual variability in gut microbial and metabolic profiles, while underscoring the need for age-adjusted, longitudinal, and biomarker-based studies to clarify directionality and mechanisms.