Search Results (112)

Background/Objectives: Adrenomedullin (AM) is a circulating peptide involved in tumor progression, angiogenesis, and fibrosis. However, its clinical utility as a biomarker in gastrointestinal cancers remains unclear. Methods: This single-center prospective observational study included patients with unresectable advanced gastrointestinal cancers (esophageal, gastric, colorectal, biliary tract, and pancreatic cancers) and healthy volunteers. Plasma AM levels were measured before the initiation of systemic chemotherapy in patients with cancer and at the time of enrollment in healthy volunteers. Results: In the unadjusted analyses, plasma mature and total AM levels were significantly higher in the cancer group than in healthy volunteers. Age was significantly associated with both mature and total AM levels, whereas sex did not show a significant association. After adjustment for age, between-group differences in mature and total AM levels were not statistically significant. Among patients with pancreatic cancer, plasma mature and total AM levels were significantly higher in stage IV than in stage III disease. Conclusions: Higher plasma AM levels were observed in the cancer group than in healthy controls in the unadjusted analyses; however, these differences were not statistically significant after adjustment for age. A stage-related difference was observed in pancreatic cancer. These findings should be considered hypothesis-generating and require validation in larger studies with appropriately matched control groups. Full article

High-altitude hypoxic environments constrain yaks’ survival capacity and metabolic adaptability. Subcutaneous adipose tissue helps yaks withstand cold and resist hypoxic stress, and ADM participates in cellular stress and metabolic regulation. To explore the regulatory role of ADM in the hypoxia adaptation of yak subcutaneous preadipocytes in high-altitude environments, we established three cell culture groups (normoxia, physiological hypoxia, and hypoxia). We further systematically examined cell proliferation, apoptosis, adenosine triphosphate (ATP) production, and lipid metabolic markers, and we performed transcriptome sequencing to reveal their regulatory effects. ADM exhibited a bidirectional regulatory effect: Low doses alleviated hypoxia-induced cell damage and restored energy and lipid synthesis, whereas high doses, in conjunction with hypoxia, activated multiple metabolic pathways and altered cellular energy-supply patterns. Under physiological hypoxia, cells emphasized metabolic regulation, while under hypoxia, they prioritized stress defense. This study demonstrates that under hypoxic stress, ADM regulates the survival and physiological function of yak subcutaneous preadipocytes in a dose-dependent manner, with cells relying on staged stress-defense and metabolic-remodeling responses to achieve adaptation to hypoxia, providing important experimental and theoretical insights into the mechanisms of high-altitude hypoxia adaptation in yaks. Full article

Psoriasis is a chronic inflammatory autoimmune skin disease for which no standardised and reliable molecular biomarkers of disease course or activity are currently available. Here, we aimed to identify serum biomarkers of psoriasis. Serum samples from 40 patients with psoriasis and 40 healthy volunteers were analysed using ELISA and Proximity Extension Assay proteomics. ELISA revealed significantly increased serum levels of AGO2 and APOA1 in psoriatic patients versus controls, with a strong association between APOA1 and psoriasis (OR = 20.72, 95% CI of 4.57–93.87, p = 0.000137). Targeted serum proteomics additionally identified 35 differentially expressed proteins, including well-known psoriasis drivers (e.g., top upregulated IL17A and SERPINB4). The most downregulated was adrenomedullin (ADM, FC = −10.12). For 14 altered proteins, no previous direct associations with psoriasis were reported. Among them, DEFB103A_DEFB103B and DSG3 showed the best discrimination between psoriasis and control samples, while SERPINB4 correlated with psoriasis severity. APOA1, DEFB103A_DEFB103B, and DSG3 emerge as novel candidate circulating psoriasis biomarkers, and SERPINB4 as a biomarker of psoriasis severity. The functional role of DSG3 and other newly identified proteins (ACRV1, HAO1, ADH4, GPD1, GFER, PTGES2, DSG3, AFAP1L1, GALNT3, RASGRP2, MAP2K6, LXN, NBEAL2, and VPS54) in psoriasis requires further studies. Full article

Background: Women face underdiagnosed cardiovascular disease (CVD)/stroke risks due to sex-specific pathophysiological mechanisms, including hormonal variations such as oestrogen decline, adverse pregnancy outcomes (APOs), endothelial dysfunction, autoimmune-mediated factors, and sexual dimorphism in cardiac remodelling. Conventional risk assessment tools, predominantly calibrated to male pathophysiology, lack sensitivity in detecting these female-specific determinants. We hypothesise that artificial intelligence (AI), machine learning (ML) and deep learning (DL) may offer a transformative approach by integrating multimodal data, including pathological biomarkers, clinical history, and vascular imaging, to enable precision CVD/stroke risk stratification, pending rigorous external validation in sex-stratified cohorts. Method: This narrative review adopts a PRISMA-informed study selection framework and oversees gender-specific biomarkers, including vasoactive peptides (adrenomedullin), adipocytokines (adiponectin), inflammatory mediators (hs-CRP, IL-6), and thrombogenic factors (homocysteine, D-dimer), alongside clinical variables (APOs, autoimmune disorders) and ultrasonographic markers, carotid intima-media thickness (cIMT), plaque burden and plaque area (PA). Advanced ML/DL algorithms were employed to synthesise these heterogeneous datasets, identifying nonlinear interactions for better outcomes. Findings: Key insights reveal that hormonal dynamics (e.g., hypoestrogenism post-menopause) modulate CVD risk, while APOs induce persistent endothelial dysfunction and subclinical atherosclerosis. Biomarker sexual dimorphism is evident; hs-CRP exhibits higher baseline levels in women, whereas adiponectin declines with metabolic dysfunction. Radiomic features (cIMT progression, plaque morphology) are a well-established biomarker for CVD risk stratification. Conclusions: The integration of AI-driven multimodal systems holds the potential to enable a paradigm shift from population-based to personalised risk assessment, addressing critical gaps in female CVD health. However, this potential is currently at the early validation stage, and widespread clinical implementation requires prospective, externally validated, and ethnically diverse studies. Future applications should incorporate longitudinal biomarker profiling and advanced imaging, namely shear wave elastography and plaque radiomics, to optimise predictive models. Full article

Sepsis is a leading cause of morbidity and mortality worldwide, and its outcomes depend on early recognition and timely intervention. Conventional clinical scores and biomarkers provide prognostic value but often lack accuracy for individualized prediction. Machine learning (ML) offers the ability to integrate multidimensional data to improve risk stratification. We analyzed 477 patients admitted to our hospital, including 251 with sepsis, 100 with septic shock, and 126 controls. Demographic, clinical, and laboratory data were collected. Univariate correlation analyses explored associations with sepsis severity and mortality (in-hospital, 30-day, and 90-day). Several ML models were tested, with performance assessed by area under the receiver operating characteristic curve (AUC-ROC) and Matthews’s correlation coefficient (MCC). Model interpretability was evaluated using SHAP (SHapley Additive exPlanations). Sepsis severity and mortality correlated with biomarkers (procalcitonin, mid-regional pro-adrenomedullin, lactate) and clinical scores (SOFA, qSOFA). In-hospital mortality was associated with ADM, catecholamine use, and SOFA, while 90-day mortality involved smoking and Gram-negative or polymicrobial infections. Different machine learning models were evaluated, and the model achieving the highest performance on the validation set was selected. The selected model either outperformed or demonstrated comparable performance to logistic regression, depending on the specific prediction task (AUC 0.99 for sepsis, 0.96 for septic shock, 0.70 for ICU admission; 0.90, 0.72, and 0.87 for in-hospital, 30-day, and 90-day mortality). SHAP confirmed the clinical relevance of these predictors. ML models integrating clinical and biochemical data outperform conventional methods in predicting sepsis progression and mortality, while maintaining interpretability. These findings support the use of ML-based tools for early diagnosis and personalized risk stratification in sepsis, though external validation is required before clinical application. Full article

Background/Objectives: Mid-regional pro-adrenomedullin (MR-proADM) is a biomarker of endothelial dysfunction in sepsis. Its relationship with real-time microcirculatory alterations in critically ill patients remains insufficiently characterised. Methods: In a prospective cohort of 59 ICU patients with sepsis, serial sublingual microcirculation assessments were performed using sidestream dark field (SDF) imaging. Serum MR-proADM concentrations were measured with BRAHMS Kryptor assays. Automated software quantified microvascular structure and flow. Associations with disease severity and outcomes were evaluated using correlation, regression, and receiver operating characteristic (ROC) analyses (ClinicalTrials.gov Identifier: NCT05357339). Results: Higher MR-proADM concentrations at ICU admission were modestly associated with impaired microvascular perfusion (perfused number of crossings [PNOC]: ρ = −0.32; perfused De Backer density [PDBD]: ρ = −0.32; consensus proportion of perfused vessels [CPPV]: ρ = −0.26; all p < 0.05). Rising MR-proADM levels over time were strongly associated with worsening perfusion (ΔPDBD: ρ = 0.52; ΔPNOC: ρ = 0.54). MR-proADM correlated with SOFA and APACHE II scores and predicted the need for renal replacement therapy (AUC = 0.799, p = 0.041), but not ICU length of stay or hospital mortality. Conclusions: MR-proADM correlates with in vivo microcirculatory dysfunction in sepsis. Its dynamic association with microvascular impairment supports its potential role as a translational biomarker for monitoring endothelial and microcirculatory failure in critically ill patients. Full article

Background and Objectives: Procalcitonin (PCT), presepsin (PSEP), interferon-λ3 (IFN-λ3), and bioactive adrenomedullin (bio-ADM) are promising sepsis biomarkers. We explored the clinical utility of a multi-marker approach using these four biomarkers in patients with suspected sepsis. Materials and Methods: In a total of 248 patients, the biomarkers were evaluated with the sequential organ failure assessment (SOFA) score. Receiver operating characteristic curves with area under the curve (AUC) were analyzed to diagnose sepsis and predict in-hospital mortality. Survival and reclassification analyses were also used to predict in-hospital mortality. Results: The four biomarkers showed comparable diagnostic performance (AUC = 0.61–0.95, p < 0.001–0.003), and sepsis proportion increased significantly as the number of biomarkers used in the multi-marker approach increased (7.7–91.7%, p < 0.001). The proportion of biomarker quartiles (Q1–Q4) differed significantly according to SOFA score (p < 0.001). The four biomarkers predicted in-hospital mortality (AUC = 0.63–0.84, p < 0.001–0.004). The multi-marker approach performed better than the SOFA score (mortality rate, 58.3% vs. 31.3%; adjusted hazard ratio [HR], 14.7 vs. 4.6), and the addition of biomarkers to the SOFA score increased the performance. The multi-marker approach resulted in a higher HR in patients aged ≥75 years than in the overall population (9.2 vs. 4.2). Conclusions: Each biomarker showed clinical utility in patients with suspected sepsis. The multi-marker approach showed complementary clinical utility in addition to the SOFA score and better prognostic performance in patients aged ≥75 years. The use of biomarkers, alone or in combination, would be a valuable tool in combination with the SOFA score. Full article

Analysis of pulmonary vascular dysfunction in various lung pathologies remains challenging due to the lack of functional ex vivo models. Paracrine signaling in the lung plays a critical role in regulating endothelial maturation and vascular homeostasis. Previously, we employed single-cell RNA-sequencing (scRNAseq) to systematically map ligand–receptor (L/R) interactions within the lung vascular niche. However, the functional impact of these ligands on endothelial biology remained unknown. Here, we systematically evaluated selected ligands in vitro to assess their effects on endothelial barrier integrity, anti-inflammatory responses, and phenotypic maturation. Among the top soluble ligands, we found that adrenomedulin (ADM) exhibited superior barrier enhancing effect on human pulmonary endothelial cell monolayers, as evidenced by electrical cell impedance sensing (ECIS) and XperT assays. ADM also exhibited anti-inflammatory properties, decreasing ICAM1 and increasing IkBa expression in a dose-dependent manner. Perfusion is commonly used in bioengineered vascular model systems. Shear stress (15 dynes/cm²) alone increased endothelial characteristics, including homeostatic markers such as CDH5, NOS3, TEK, and S1PR1. ADM treatment maintained the enhanced level of these markers under shear stress and further improved anti-coagulation by increasing THBD and decreasing F3 expression and synergistically enhanced the expression of the native lung aerocyte capillary endothelial marker EDNRB. This effect was completely attenuated by a blockade of ADM receptor, RAMP2. Together, these findings identify ADM/RAMP2 signaling as a key paracrine pathway that enhances vascular barrier integrity, anti-inflammatory phenotype, and endothelial homeostasis, providing a framework for improving the physiological relevance of engineered vascular models. Full article

Background and Objectives: Sepsis is a life-threatening condition caused by a dysregulated host response to infection. Early recognition is crucial to improve outcomes, but conventional biomarkers such as C-reactive protein (CRP) and procalcitonin (PCT) show limited diagnostic accuracy. Materials and Methods: We performed a narrative review of the literature on sepsis biomarkers, with a focus on their biological role, diagnostic performance, clinical applicability, and limitations. Particular attention was given to presepsin (P-SEP) and monocyte distribution width (MDW), which have recently gained relevance. Results: Several novel biomarkers—including lipopolysaccharide-binding protein (LBP), soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), mid-regional pro-adrenomedullin (MR-proADM), neutrophil gelatinase-associated lipocalin (NGAL), Proenkephalin (PENK), and circulating microRNAs—have been studied, though most remain investigational. Among them, P-SEP shows rapid kinetics and correlation with disease severity, while MDW, derived from routine complete blood count, offers encouraging sensitivity and cost-effectiveness in emergency settings. Both biomarkers appear practical and potentially valuable for early sepsis detection. Conclusions: P-SEP and MDW emerge as the most promising biomarkers for timely sepsis recognition and risk stratification. Further validation and standardization are required to include them into routine clinical practice. Full article

Background: Adrenomedullin (ADM) is a multifunctional peptide with vasoregulatory, antimicrobial, and anti-inflammatory properties. Its stable fragment, mid-regional pro-adrenomedullin (MR-proADM), is a validated biomarker in sepsis and systemic infections, but its role in viral neuroinfections remains unexplored. Tick-borne encephalitis (TBE), caused by the tick-borne encephalitis virus (TBEV), is a major viral infection of the central nervous system (CNS) associated with long-term neurological sequelae. This study aimed to assess MR-proADM levels in cerebrospinal fluid (CSF) and serum of patients with TBE and to evaluate their diagnostic utility and pathophysiological significance. Methods: This retrospective observational study included 20 patients with confirmed TBE and 14 non-infectious neurological controls. MR-proADM concentrations were measured in paired CSF and serum samples using an ELISA assay. Statistical analyses included group comparisons (Mann–Whitney U test), correlation analyses (Spearman’s r), and receiver operating characteristic (ROC) curve evaluation. Results: Serum MR-proADM levels at baseline (SER1) were significantly lower in TBE patients compared with controls (p = 0.0197). The CSF/serum MR-proADM ratio differed significantly between groups (p = 0.0063) and showed the best diagnostic performance (AUC = 0.816, 95% CI 0.63–0.93; sensitivity 79%, specificity 80%). MR-proADM concentrations in CSF correlated with total CSF protein (r = 0.53), suggesting an association with blood–CSF barrier dysfunction. Strong reproducibility was observed for serum MR-proADM between sampling points (r = 0.83). Conclusions: MR-proADM levels in CSF and serum are altered in patients with TBE, indicating its potential as a biomarker of CNS infection and inflammation. The CSF/serum MR-proADM ratio may serve as a sensitive indicator of blood–CSF barrier involvement, while decreased serum levels may reflect impaired systemic neuroprotective response. These findings highlight a possible role of ADM in neuroimmune regulation during viral encephalitis and warrant validation in larger prospective studies. Full article

The current known data on the involvement of the peptidergic systems in breast cancer progression is overwhelmingly vast. Peptidergic systems are useful tools for imaging, diagnosis, prognosis and treatment of breast cancer. These systems play a crucial role in both basic and clinical breast cancer research by enabling the exploration of novel molecular mechanisms, signaling pathways, and the development of effective drug design strategies. Breast cancer cells overexpress peptide receptors; at the same time they are known to interact with peptides that (a) exert an oncogenic action (adrenomedullin 2, endothelin, gastrin-releasing peptide, neurokinin A, neuromedin, neuropeptide Y, neurotensin, substance P, vasoactive intestinal peptide), (b) exert an anticancer action (angiotensin (1–7), ghrelin, peptide YY) or (c) exert dual oncogenic and anticancer effects (adrenomedullin, angiotensin II, bradykinin, corticotropin-releasing factor, β-endorphin, glucagon-like peptide 1, gonadotropin-releasing hormone, kisspeptin, methionine-enkephalin, oxytocin). This indicates that peptides, as well as peptide receptor agonists and antagonists, may serve as antitumor agents due to their diverse actions against breast cancer development, including the inhibition of cell proliferation, migration and invasion, induction of apoptosis, and anti-angiogenesis. Multiple strategies have been developed to combat breast cancer, including peptide receptor silencing; antibodies conjugated to specific signaling proteins; antibodies targeting specific peptide receptors or oncogenic peptides; and the use of peptides or peptide receptor agonists/antagonists loaded with antitumor cargo. Future lines of research are suggested in breast cancer using promising anti-breast-cancer peptide receptor antagonists (HOE-140, exendin (9–39), bosentan, macitentan, PD168,368, CGP71,683A, SR48,692, aprepitant) or agonists (FR190,997, semaglutide, exendin 4, goserelin) mentioned in this review. Peptidergic systems have tremendous anti-breast-cancer clinical potential which must be exploited and developed. Taken together, the available data highlight the enormous promise of translational research into breast cancer and peptidergic systems for the development of effective treatments. A full understanding of the roles played by the peptidergic systems in breast cancer will serve to improve diagnosis and treatment. Full article

Adrenomedullin (AM) is a regulatory peptide that stimulates proliferation, migration, and invasion of melanoma cells, and promotes neovascularization within the tumor microenvironment, making it a compelling therapeutic target in melanoma and other cancers. As a continuation of our previous study on a metastatic tumor model, here we tested an mRNA vaccine encoding a fusion antigen comprising keyhole limpet hemocyanin (KLH) and mouse AM in a subcutaneous melanoma mouse model. In vitro synthesized mRNA was encapsulated in lipid nanoparticles (LNPs) and administered to C57BL/6J mice; empty LNPs served as negative controls. After a four-dose immunization schedule, B16-F10 melanoma cells were injected subcutaneously, followed by a fifth immunization. Mice were sacrificed once tumors reached humane endpoints. Immunization led to a significant increase in anti-AM IgG titers (p = 0.033) and CD8⁺ T cell (p = 0.049) numbers in treated mice. Tumor initiation was significantly delayed (p = 0.005) and subcutaneous tumor volume was reduced (p = 0.0004) compared to controls. A marked decrease in the area occupied by tumor blood vessels (p = 0.028) was also observed, with no signs of systemic toxicity or weight loss. In addition, there was no significant impairment of Ki67⁺ tumor cell proliferation nor changes in the tumor infiltration of CD4⁺, CD8⁺, FoxP3⁺ nor Arg1⁺ cells. The vaccine also proved highly stable at 4 °C, in the absence of cryoprotectants, for more than a month. In summary, we confirmed that a KLH-AM mRNA vaccine is very stable and can elicit humoral and cellular immune responses, inhibit angiogenesis, and delay tumor growth in subcutaneous melanoma, without inducing an immunosuppressive tumor microenvironment (TME), further supporting mRNA vaccines targeting AM as an attractive immunotherapeutic approach. Full article

Mid-regional pro-adrenomedullin (MR-proADM) has emerged as a promising biomarker reflecting endothelial dysfunction and systemic inflammation. Its prognostic role in cardiovascular complications, particularly in the context of COVID-19 infection, remains under investigation. This study aimed to evaluate MR-proADM concentrations in patients with and without cardiovascular disease and COVID-19 and to assess its association with cardiac complications and biomarkers of myocardial injury. A total of 157 patients (mean age: 72.3 years; 66 men) hospitalized in a tertiary referral center were enrolled. The study population consisted of three groups: patients with cardiovascular disease and COVID-19 (n = 64), patients with cardiovascular disease but no COVID-19 (n = 74), and a control group without cardiovascular disease or COVID-19 (n = 17). Plasma MR-proADM levels were measured, and their relationship with cardiovascular complications (chronic heart failure and myocardial infarction) and standard cardiac biomarkers (troponin T, troponin I, and proBNP) was analyzed. The mean MR-proADM concentration in the overall cohort was 91.48 ± 71.96 pmol/L (median: 77.95; range: 5.81–429.20). Distributions of MR-proADM, troponin T (M = 143.12 ± 733.93 ng/L), troponin I (M = 143.37 ± 749.85 ng/L), and proBNP (M = 2080.29 ± 3632.03 pg/mL) deviated significantly from normality (Shapiro–Wilk, all p < 0.001). No significant differences in MR-proADM concentrations were observed between patients with COVID-19 vs. without (93.78 ± 56.94 vs. 92.08 ± 82.82 pmol/L, p = 0.842) and between active infection vs. past COVID-19 (93.78 ± 56.94 vs. 85.98 ± 50.39 pmol/L, p = 0.869). A trend toward higher MR-proADM concentrations was observed in patients with cardiovascular disease compared to those without, with mean levels of 93.56 ± 74.90 vs. 74.33 ± 37.43 pmol/L, respectively. The frequency of chronic heart failure (55.0% vs. 54.5%, p = 1.000) and myocardial infarction (11.3% vs. 20.8%, p = 0.128) did not differ between patients with low vs. high MR-proADM (cut-off: median). Logistic regression confirmed that MR-proADM did not significantly predict either chronic heart failure (Nagelkerke R² = 0.002, p = 0.660) or myocardial infarction (Nagelkerke R² = 0.006, p = 0.465). Correlation analysis showed no significant associations between MR-proADM and proBNP (ρ = 0.09, p = 0.323), troponin T (ρ = 0.22, p = 0.065), or troponin I (ρ = 0.16, p = 0.088). MR-proADM levels did not differ significantly between patients stratified by COVID-19 infection or cardiovascular disease and were not predictive of heart failure or myocardial infarction. Moreover, no correlations were found with standard cardiac biomarkers. These results suggest that, in this cohort, MR-proADM did not provide additional prognostic information for cardiovascular complications. Full article

Cardiorenal syndrome (CRS) reflects the intricate and bidirectional interplay between cardiac and renal dysfunction, commonly resulting in diagnostic uncertainty, therapeutic dilemmas and poor outcomes. While traditional biomarkers like serum creatinine (Cr) and natriuretic peptides remain widely used, their limitations in specificity, timing and contextual interpretation often hinder optimal management. This narrative review synthesizes the current evidence on established and emerging biomarkers in CRS, with emphasis on their clinical relevance, integration into real-world practice, and potential to inform precision therapy. Markers of glomerular filtration rate beyond creatinine—such as cystatin C—offer more accurate assessment in frail or sarcopenic patients, while tubular injury markers such as NGAL, KIM-1, and urinary L-FABP (uL-FABP) provide early signals of structural renal damage. The FDA-approved NephroCheck^® test—based on TIMP-2 and IGFBP7— enables risk stratification for imminent AKI up to 24 h before functional decline. Congestion-related markers such as CA125 and bio-adrenomedullin outperform natriuretic peptides in certain CRS phenotypes, particularly in right-sided heart failure or renally impaired patients. Fibrosis and inflammation markers (galectin-3, sST2, GDF-15) add prognostic insights, especially when combined with NT-proBNP or troponin. Rather than presenting biomarkers in isolation, this review proposes a framework that links them to specific clinical contexts—such as suspected decongestion-related renal worsening or persistent congestion despite therapy—to support actionable interpretation. A tailored, scenario-based, multi-marker strategy may enhance diagnostic precision and treatment safety in CRS. Future research should prioritize prospective biomarker-guided trials and standardized pathways for clinical integration. Full article

Prognostic uncertainty and missed diagnoses of sepsis remain frequent after cardiopulmonary bypass (CPB) surgery, where systemic inflammatory response (SIRS) arises from surgical trauma, blood activation in the extracorporeal circuit, ischemia/reperfusion injury, and endotoxin release. Among innovative biomarkers, pro-adrenomedullin (pro-ADM), particularly its stable fragment mid-regional pro-adrenomedullin (MR-proADM), has shown promise for detecting endothelial dysfunction and predicting organ failure in sepsis. SeptiCyte^® RAPID (Seattle, WA, USA) also represents a novel diagnostic tool that assesses the host immune response by quantifying PLA2G7 and PLAC8 gene expression in whole blood, offering potential for early differentiation between sepsis and sterile inflammation. We analyzed traditional and innovative biomarkers within 24 h post-CPB in a pilot group of patients admitted to the cardiac Intensive Care Unit of the “Città della Salute e della Scienza” University Hospital (Turin, Italy) between June and November 2023. Data from the following 14 patients were collected: 7 undergoing surgery for infective endocarditis (IE, Group 1) and 7 having standard elective cardiac surgery (Group 2). Procalcitonin (PCT), lactate, and pro-ADM increased in Group 1 but not in Group 2. SeptiCyte^® RAPID showed a moderate, borderline increase in Group 1. The innovative biomarkers had a good performance in patients exhibiting signs of organ dysfunction and in subjects demonstrating at least cardiovascular and/or pulmonary damage and under vasopressor and inotropic support. Although limited by the small sample, our preliminary data suggest no biomarker alterations in patients with standard elective cardiac surgery, unlike in those with IE. Full article