Evelin Claudia Ghitea

Background: Post-infarction heart failure (HF) remains a major contributor to morbidity and mortality despite advances in reperfusion and pharmacological management. However, the combined influence of clinical background, myocardial injury, neuro-hormonal activation, and angiographic disease on HF severity is not fully defined. Methods: We retrospectively analyzed 181 patients with confirmed myocardial infarction treated in a tertiary cardiology center. Demographics, cardiovascular risk factors, prior chronic HF, inflammatory markers (CRP, fibrinogen, ESR, leukocyte indices), and high-sensitivity troponin (hs-Tn) were measured at admission (pre-intervention), immediately after percutaneous coronary intervention (PCI), and at 48 h, angiographic lesion distributions were collected. HF severity was graded on a five-level scale and further dichotomized as no/mild HF (grade 0–1) versus moderate–severe HF (grade ≥ 2). Group comparisons and multivariable logistic regression were used to identify independent determinants of severe HF. Results: Moderate–severe HF occurred in 42.5% of patients (77/181). Compared to HF 0–1, the HF ≥ 2 group was older (64.0 vs. 60.5 years, p = 0.042) and exhibited substantially higher systemic inflammation (CRP 41.5 vs. 9.75 mg/L, p < 0.001; fibrinogen 435 vs. 346 mg/dL, p = 0.0002; ESR 28 vs. 18 mm/h, p = 0.0004). hs-Tn levels and NT-proBNP were significantly elevated in HF ≥ 2 (NT-proBNP 3449 vs. 1243 pg/mL, p = 0.0003), while left ventricular ejection fraction was reduced. Prior HF increased the likelihood of HF ≥ 2 (54.5% vs. 33.7%, p = 0.0078), and conservative therapy was associated with adverse outcomes (87.5% vs. 40.5%, p = 0.0235). In multivariable analysis, NT-proBNP remained the only independent predictor of moderate–severe HF, while CRP showed a positive but non-significant trend after adjustment. Conclusions: Post-MI HF severity reflects the combined influence of myocardial injury, neurohormonal stress, and systemic inflammatory activation. However, in multivariable analysis, NT-proBNP emerged as the dominant independent predictor of moderate–severe HF, while CRP reflected an associated but non-independent inflammatory signal.

Background: Multimorbidity frequently involves overlapping neuro-psychic, cardiometabolic, and renal disturbances, yet clinical assessment often relies on diagnosis-based comorbidity counts that may not fully capture cumulative physiological stress. We developed the Neuro–Cardio–Renal Stress Index (NCR-SI) as a pragmatic composite framework to describe multisystem burden using routinely available clinical data. Methods: This cross-sectional study analyzed electronic medical record data from adult patients with chronic conditions. NCR-SI integrates three domains: neuro-psychic burden (text-derived indicators and psychotropic medication use), cardiometabolic stress (triglyceride–glucose index and cardiometabolic diagnoses), and renal function (MDRD-estimated eGFR staging). Importantly, this study is not intended to demonstrate incremental predictive value over individual components or established comorbidity indices. Rather, it presents NCR-SI as a transparent, domain-based descriptive framework and reports its internal coherence and distribution across clinically recognizable multimorbidity contexts. Results: A total of 148 patient records were screened; 143 patients met complete-case criteria and were included in the main NCR-SI analyses. NCR-SI ranged from 0 to 10 (median 5). Higher scores were observed in renometabolic profiles. NCR-SI showed expected structural associations with declining renal function (eGFR; ρ ≈ −0.71), moderately with the TyG index (ρ ≈ 0.42), and weakly with medication burden. Correlation with age-adjusted CCI was minimal (ρ ≈ 0.09), indicating limited overlap with diagnosis-based comorbidity counts. Domain-specific correlations were consistent with predefined score construction rules, particularly between the renal domain and eGFR, and between the cardiometabolic domain and TyG. Conclusions: NCR-SI provides a pragmatic, integrative descriptor of neuro-cardio-renal stress using routinely collected clinical data. Rather than replacing established comorbidity indices, NCR-SI may complement them by summarizing multidimensional physiological burden patterns. NCR-SI is proposed as a research-oriented, hypothesis-generating descriptive framework. External validation in independent cohorts and longitudinal evaluation against clinically meaningful outcomes (e.g., hospitalization, mortality, functional status, healthcare utilization) are required before any claims of clinical performance can be made.

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 (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.

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: Renal and metabolic disorders frequently coexist with psychiatric and psychosomatic conditions, forming complex multimorbidity clusters that challenge traditional models of care. Anxiety, depression, and stress-related disorders may amplify the clinical trajectory of chronic kidney disease (CKD) and metabolic dysfunction. This study aimed to characterize the renal–psychiatric/psychosomatic burden profile of a real-world clinical cohort and to introduce a novel integrative multimorbidity score (RePsy-Risk) quantifying the combined renal, metabolic, and psychiatric burden. Materials and Methods: We conducted a cross-sectional analysis of 148 adult patients stratified into a reno-metabolic group (group 1) and a comparison group with other comorbidities (group 2). Clinical, biochemical, and psychiatric data were extracted from routine medical records. RePsy-Risk was constructed from three domains: renal impairment (eGFR, UACR), metabolic load (TyG index, diabetes/metabolic diagnosis), and psychiatric/psychosomatic involvement (diagnostic text-mining, psychotropic treatment). Group differences were assessed using Mann–Whitney U and t-tests, and associations were explored via Spearman correlation and heatmap visualization. Results: The reno-metabolic group exhibited significantly higher serum creatinine (1.07 vs. 0.86 mg/dL, p = 0.0027), a greater medication burden (7.07 vs. 5.70 drugs, p = 0.0007), and a higher RePsy-Risk score (mean 4.11 vs. 3.20, p = 0.00028). Overall, 52.0% of patients were classified as low risk, 45.3% as moderate risk, and 2.7% as high risk. RePsy-Risk correlated strongly with renal dysfunction (eGFR: ρ = –0.62; UACR: ρ = 0.38) and with metabolic load (TyG: ρ = 0.53), while psychiatric factors contributed independently (RePsy_C: ρ = 0.48). Heatmap analysis confirmed clustering of renal and metabolic domains, with psychosomatic features forming a distinct but additive dimension. Conclusions: Reno-metabolic disease is associated with a significantly elevated renal–psychiatric/psychosomatic burden, shaped by the interplay between impaired renal function, metabolic stress, and psychiatric comorbidity. The RePsy-Risk score offers a practical tool for capturing this multidimensional vulnerability, highlighting the need for integrated clinical strategies that simultaneously address renal, metabolic, and mental health pathways. Further validation in larger cohorts is 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 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 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/Objective: Adequate serum vitamin D levels are essential for overall health, particularly in preventing oropharyngeal infections. This study aims to explore the relationship between serum vitamin D (25(OH)D3) levels and the prevalence of oropharyngeal diseases—specifically rhinosinusitis, otitis media, and nasopharyngitis—in patients at a private specialist medical clinic. Materials and Methods: The study involved 311 patients with an average age of 15.96 ± 15.06 years. Statistical analyses, including Student’s t-test and chi-square test, were conducted to evaluate the significance of the findings. Results: Nasopharyngitis was highly prevalent, affecting 83.27% of participants, with higher recurrence rates in those with lower vitamin D levels (p = 0.001). Otitis media was present in 53.37% of cases, while rhinosinusitis was less common and more frequently associated with higher vitamin D levels. Patients with behavioral disorders had significantly higher mean vitamin D levels (34.82 ng/mL ± 11.85) compared to those without (28.49 ng/mL ± 14.37) (p = 0.001). Conclusions: A subgroup of children with neutropenia (ANC < 1500/μL) exhibited significantly lower vitamin D levels and higher infection recurrence rates, underscoring their heightened vulnerability. This study highlights the importance of maintaining optimal vitamin D levels for pediatric health and suggests that higher vitamin D levels may reduce the risk of oropharyngeal infections.