Search

INTRODUCTION: Rare myocarditis and pericarditis cases have occurred in coronavirus disease 2019 (COVID-19) messenger RNA (mRNA) vaccine recipients. Troponin levels, a potential marker of myocardial injury, were assessed in healthy participants before and after BNT162b2 vaccination. METHODS: Vaccine-experienced 12- to 30-year-olds in phase 3 crossover C4591031 Substudy B (NCT04955626) who had two or three prior BNT162b2 30-μg doses were randomized to receive BNT162b2 30 μg followed by placebo, or placebo followed by BNT162b2 30 µg, 1 month apart. A participant subset, previously unvaccinated against COVID-19, in the phase 3 C4591007 study (NCT04816643) received up to three vaccinations (BNT162b2 10 μg or placebo [5- to 11-year-olds]) or open-label BNT162b2 30 μg (12- to 15-year-olds). Blood samples collected pre-vaccination, 4 days post-vaccination, and 1-month post-vaccination (C4591031 Substudy B only) were analyzed. Frequencies of elevated troponin I levels (male, > 35 ng/l; female, > 17 ng/l) were assessed. RESULTS: Percentages of 12- to 30-year-olds (n = 1485) in C4591031 Substudy B with elevated troponin levels following BNT162b2 or placebo receipt were 0.5% and 0.8% before vaccination, 0.7% and 1.0% at day 4, and 0.7% and 0.5% at 1 month, respectively. In Study C4591007 (n = 1265), elevated troponin I levels were observed in 0.2, 0.4, and 0.2% of 5- to 11-year-old BNT162b2 recipients at baseline and 4 days post-dose 2 and 3, respectively; corresponding values in 12- to 15-year-olds were 0.4, 0.4, and 0.7%. No 5- to 11-year-old placebo recipients had elevated troponin levels. No myocarditis or pericarditis cases or deaths were reported. CONCLUSIONS: Among 5- to

Background Methods Results Conclusions Phase I clinical trial of an artificial oxygen carrier (liposome‐encapsulated hemoglobin vesicles [HbVs]) is safely completed, considering the other clinical application. Herein, we aimed to investigate the resuscitation effects of HbVs in cases of lethal hemorrhage, including the mechanisms involved.Optical mapping analysis (OMP) and electrophysiological studies (EPS), immunostaining pathological examination for hypoxia‐inducible factor‐1α (HIF1‐alpha) in the heart tissue, and blood troponin I (TnI) level measurements were performed in rats that underwent five rounds of spontaneous arterial bleeding with up to 65% hemorrhage.Ten rats in each group were resuscitated by a transvenous infusion of 5% albumin (ALB), washed erythrocytes (wRBC), HbVs (HbV), 50% HbV diluted by 5% albumin (50% HbV), and 66% HbV diluted by 5% albumin (66% HbV). The rats in the ALB and 50% HbV groups died, whereas those in the other groups survived. OMP showed impaired action potential duration dispersion (APDd) in the left ventricle in the ALB and 50% HbV groups, which was attenuated in the other groups. Lethal arrhythmias were provoked by EPS in the ALB and 50% HbV groups but not in the other groups. HIF1‐alpha was positively stained only in the ALB and 50% HbV groups. TnI levels were elevated in the ALB and 50% HbV groups.Acute lethal hemorrhage causes myocardial ischemia with hypoxia and arrhythmias, which may be induced by impaired APDd and myocardial damage, reflected in the increased levels of HIF1‐alpha and TnI. HbVs could be useful for resuscitation and may help save patients with injuries such as gunshot wounds. [ABSTRACT FROM AUTHOR]

Hyperglycaemia, hyperlipidaemia, hypertension and obesity are the main risk factors affecting the development and prognosis of ischaemic heart disease, which is still an important cause of death today. In our study, male Sprague–Dawley rats were fed either a standard diet (SD) or a high fat and high carbohydrate diet (HF‐HCD) for 8 weeks and streptozotocin (STZ) was injected at the seventh week of the feeding period. In one set of rats, a mixture of a prebiotic and probiotics (synbiotic, SYN) was administered by gavage starting from the beginning of the feeding period. Experimental myocardial ischaemia–reperfusion (30 min/60 min) was induced at the end of 8 weeks. Hyperglycaemia, hypertension and increased serum low‐density lipoprotein levels occurred in SD‐ and HF‐HCD‐fed and STZ‐treated rats followed for 8 weeks. Increased density of the Proteobacteria phylum was observed in rats with increased blood glucose levels, indicating intestinal dysbiosis. The severity of cardiac damage was highest in the dysbiotic HF‐HCD‐fed hyperglycaemic rats, which was evident with increased serum creatine kinase‐MB (CK‐MB), cardiac troponin I (cTnI), tumour necrosis factor‐α, and interleukin‐6 levels, along with a decrease in ST‐segment resolution index. SYN supplementation to either a normal or a high‐fat high‐carbohydrate diet improved gut dysbiosis, reduced anxiety, decreased CK‐MB and cTnI levels, and alleviated myocardial ischaemia–reperfusion injury in hyperglycaemic rats. [ABSTRACT FROM AUTHOR]

Objectives: This study was performed to identify predictive markers of worse outcomes in patients with severe COVID-19 in an intensive care unit. Methods: Sixty patients with severe COVID-19, hospitalized in the Intensive Care Unit (ICU) between March and July 2021, were stratified into two groups according to the outcome survivors and non-survivors. After admission to the ICU, blood samples were collected directly for biomarker analysis. Routine hematological and biochemical biomarkers, as well as serum levels of cytokines, chemokines, and immunoglobulins, were investigated. Results: Lymphopenia, neutrophilia, and thrombocytopenia were more pronounced in non-surviving patients, while the levels of CRP, AST, creatinine, ferritin, AST, troponin I, urea, magnesium, and potassium were higher in the non-surviving group than the survival group. In addition, serum levels of IL-10, CCL2, CXCL9, and CXCL10 were significantly increased in patients who did not survive. These changes in the biomarkers evaluated were associated with increased mortality in patients with severe COVID-19. Conclusion: The present study confirmed and expanded the validity of laboratory biomarkers as indicators of mortality in severe COVID-19. [ABSTRACT FROM AUTHOR]

AbstractBackgroundMethodsResultsConclusionIn Egypt, aluminum phosphide (ALP) is a known lethal poison due to its cardiotoxicity. This study aimed to evaluate the predictive ability of N-terminal pro-B-type natriuretic peptide (NT-proBNP) for mortality in ALP-poisoned patients.This prospective study was conducted on patients with ALP poisoning admitted to the Poison Control Center Ain Shams University Hospitals between July and December 2022. Upon admission, all patients were followed up and had their levels of NT-proBNP, troponin I (cTnI), and creatine kinase myocardial band (CK-MB) analyzed.Thirty patients were enrolled in the study and were divided into survivors and non-survivors. The initial NT-proBNP levels were significantly higher among non-survivors in contrast to the initial cTnI and CK-MB levels. The study identified that the best cutoff point of NT-proBNP for predicting mortality was ≥72 pg/ml, with AUC (0.869).It can be concluded that NT-proBNP can serve as an early predictor of mortality in ALP poisoning. [ABSTRACT FROM AUTHOR]

AbstractObjectiveMaterials and methodsResultsDiscussion and conclusionThis study aimed to investigate the mechanism of emulsified isoflurane in reducing myocardial ischemia-reperfusion injury (MIRI).Forty-eight healthy male Sprague-Dawley rats were randomly divided into four groups (n = 12). In the sham group (group S) and ischemia-reperfusion group (group I/R), saline (4 ml/kg/h) was administered intravenously for 30 min. In intralipid group (group L), intralipid (4 ml/kg/h) was administered intravenously. In the emulsified isoflurane group (group EI), emulsified isoflurane (4 ml/kg/h) was administered intravenously. The infusion was then discontinued for 15 min during the washout period. Apart from group S, ischemia was produced by occlusion of the left anterior descending artery (LADA) for 30 min. After 30 min of occlusion, all groups received reperfusion for two hours.Creatine kinase MB (CK-MB), cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were measured by enzyme-linked immunosorbent assay (ELISA). Myocardial infarct size was measured using triphenyl tetrazolium chloride staining. According to the result, pretreatment with emulsified isoflurane attenuated CK-MB and cTnI concentrations (p < 0.05). And serum TNF-α and IL-6 levels and infarct size in the emulsified isoflurane group obviously decreased. An obvious decrease in the expression of the toll-like receptor-4 (TLR-4) mRNA in group EI was observed compared with group I/R.Emulsified isoflurane precondition had a potent cardioprotective effect against myocardial ischemia-reperfusion injury. The mechanisms involved may be related to the decrease in the expression of TLR-4 and the reduced inflammatory response. [ABSTRACT FROM AUTHOR]

Aims Methods and results Conclusions The extent to which metabolic syndrome (MetS) severity influences subclinical myocardial remodelling, heart failure (HF) incidence and subtypes, remains unclear. We assessed the association of MetS with incident HF (including ejection fraction subtypes) among Black individuals.We included 4069 Jackson Heart Study participants (mean age 54.4 years, 63.8% women, 37.2% with MetS) without HF. We categorized participants based on MetS status and MetS severity scores (based on waist circumference [MetS‐Z‐WC] and body mass index [MetS‐Z‐BMI]). We assessed the associations of MetS indices with echocardiographic parameters, biomarkers of myocardial damage (high‐sensitivity cardiac troponin I [hs‐cTnI] and B‐type natriuretic peptide [BNP]) and incident HF hospitalizations including HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF). MetS severity was associated with subclinical cardiac remodelling (assessed by echocardiographic measures and biomarkers of myocardial damage). Over a median of 12 years, 319 participants developed HF (157 HFpEF, 149 HFrEF and 13 HF of unknown type). MetS was associated with a twofold greater risk of HF (hazard ratio [HR] 2.07, 95% confidence interval [CI] 1.64–2.61). Compared to the lowest quartile (Q1) of MetS‐Z‐WC, the highest quartile (Q4) conferred a higher risk of HF (HR 2.35, 95% CI 1.67–3.30), with a stronger association for HFpEF (Q4 vs. Q1: HR 4.94, 95% CI 2.67–9.14) vs. HFrEF (HR 1.69, 95% CI 1.06–2.70).Metabolic syndrome severity was associated with both HF subtypes among Black individuals, highlighting the importance of optimal metabolic health for preventing HF. [ABSTRACT FROM AUTHOR]

Background: There has been increasing evidence of association between cardiovascular and chronic kidney disease. Most of complications and mortality in these patients are due to development of cardiovascular disease (CVD) rather than due to chronic kidney disease (CKD) by itself. Though cardiac biomarkers are available but due to lack of clinical symptoms in early stages and delayed diagnosis mortality rate has increased. The present study was conducted to detect the cardiovascular dysfunction measured by various cardiac biomarkers like serum Cardiac high sensitivity Troponin I, Creatinine kinase and creatinine Kinase MB with eGFR in CKD patients to correlate the association of cardiovascular dysfunction in patients with CKD for early detection and initiation of aggressive treatment to reduce mortality. Methods: The present cross-sectional study was conducted on 110 patients of chronic kidney disease (CKD) at tertiary care hospital, Hyderabad. Cardiac HS Troponin I, Creatine Kinase (CPK) and Creatine Kinase- MB (CK-MB) were analysed and correlated with e-GFR, Urea and creatinine levels. Results: There was statistically significant association between Hs Troponin I, CK-MB and CPK with Chronic kidney disease. There was negative corelation of cardiac biomarkers with eGFR and positive correlation with Urea and creatinine. Multivariate regression analysis for predictors of cardiac dysfunction was done using ANOVA with renal parameters in patients with CKD which showed strong association between e-GFR and cardiac markers. Conclusion: High morbidity and mortality in patients with CKD is observed due to Cardiovascular disease. It is important to diagnose CVD with high index of suspicion and evaluate with commonly available biochemical cardiac markers. In our study there was significant elevation in Hs Trop I, CK MB and CPK in CKD patients which correlated negatively with eGFR. Routine use of these markers during follow-up of CKD patients helps in risk assessment, prevention of complications and timely interventions. [ABSTRACT FROM AUTHOR]

Aim: To analyze the blood levels of cardiac enzymes and urinary and serum levels of human heart-type fatty acid-binding protein (HH-FABP) in patients with ST-elevation myocardial infarction (STEMI); to analyze and assess the correlation of urinary protein HH-FABP with the blood levels of troponin I and creatine kinase (CK-MB) in patients with STEMI and to assess the correlation between serum and urine levels of HH-FABP in patients with STEMI Background: STEMI is one of several medical challenges. There is still lack of highly sensitive and specific cardiac markers for early detection of AMI and scope to develop. In this study the diagnostic yield of Human Heart type fatty acid binding protein (HH-FABP), an emerging biomarker was assessed in patients with STEMI in both serum and urine and correlated its diagnostic efficacy was correlated with other conventional markers (Troponin I and CKMB) Methods: Cross-sectional observational study. 41 patients with STEMI were studied. Serum and urine samples were collected within seven hours of onset of symptoms. HH-FABP was quantified using Enzyme Linked Immunosorbent Assay (ELISA) reader of Bio-Rad and the test result was correlated with data of Troponin I and CKMB collected from Laboratory information system (LIS). Results: Our investigation highlighted the link between plasma Troponin I and serum CKMB. However, there was no statistically significant correlation between serum and urine HH-FABP and with other markers. Conclusion: Plasma troponin I and CKMB were found to be consistently elevated in patient with STEMI. A significant correlation between serum and urine HH-FABP and other identified cardiac biomarkers was not found. [ABSTRACT FROM AUTHOR]

Background Although coronary artery bypass grafting (CABG) is performed via three different techniques, conventional, on-pump beating heart CABG (ONBHCAB), or off-pump CABG (OPCAB), data are limited to compare ONBHCAB with OPCAB. Methods We retrospectively investigated the postoperative cardiac biomarkers, creatine kinase-MB (CK-MB), and troponin I (cTnI), and early and late outcomes in 806 patients undergoing isolated ONBHCAB or OPCAB between February 2008 and September 2022. To eliminate the bias between different groups, propensity score matching was conducted to validate the findings. Results After matching, the number of each study group totaled 270 patients. In both complete and matched cohorts, early outcomes, including morbidities and mortalities, were similar. However, cTnI and CK-MB levels were significantly higher after ONBHCAB than after OPCAB with median peak cTnI of 9.85 versus 4.60 ng/mL and median peak CK-MB of 48.45 versus 17.10 ng/mL in the matched cohort, which were quite low, below the threshold for values defining perioperative myocardial infarction. At follow-up of 73 ± 45 months, the overall actuarial survival rates were similar between the ONBHCAB and OPCAB patients (86 vs. 87% at 5 years and 64 vs. 68% at 10 years, respectively, in the matched cohort). Conclusion ONBHCAB may be a comparable alternative to OPCAB with similar early and late outcomes, despite higher elevation of postoperative cardiac biomarkers. ONBHCAB provides more efficient hemodynamic support, providing a better surgical visual field, than OPCAB while reducing the risk of incomplete revascularization. [ABSTRACT FROM AUTHOR]

Limited data are available regarding myocardial injury and its risk factors in percutaneous coronary interventions (PCI) of severe calcified lesions using orbital atherectomy (OA). Patients who underwent OA at our institution were retrospectively enrolled into the present registry. High-sensitive Troponin I (hsTroponin I), EKG and echocardiography were used to assess myocardial injury after the procedure. A total of 27 patients between who underwent OA between January 2022 and June 2023 were included. Myocardial injury (elevation of hsTroponin I above the 99th percentile upper reference limit) occurred in all patients. Median hsTroponin I on the first day after the procedure was 1093 (557–4037) ng/l with a minimum of 86 ng/l and a maximum of 25,756 ng/l. Myocardial infarction occurred in two patients (7 %), who had severe coronary dissection after OA. Lesions were longer (47 [38–52] mm vs. 20 [14–47] mm; p = 0.009) in patients with hsTroponin I levels above the median compared to those with levels below. Furthermore, a moderate correlation between hsTroponin I and lesion length was detected (r = 0.54; p = 0.004). In the present study myocardial injury occurred in all patients after OA without loss of viable myocardium in the majority of patients. Lesions length was found to be a significant factor associated with markedly increased hsTroponin I after the OA procedure. • Myocardial injury defined as elevation of hsTroponin I above the upper reference limit occurred in all patients after OA. • However, the incidence of myocardial infarction in this complex coronary anatomy population was rather low (7%). • Lesion length was identified as risk factor for myocardial injury. [ABSTRACT FROM AUTHOR]

Background: Cardiac involvement following an acute stroke (Stroke Heart Syndrome—SHS) is an established complication and it is linked to the involvement of sympathetic activation, inflammation, and neuro-endocrine response. Troponin "rise and fall pattern" > 30% is one marker of SHS. The aim of this study was to evaluate the role of reperfusion treatments in the prevention/pathogenesis of SHS with different stroke sizes and locations (OCSP classification). Methods: We retrospectively analyzed data of 890 patients admitted to the Stroke Unit of Trieste (Italy) between 2018 and 2020. Out of them, 411 met the inclusion criteria (acute ischemic non-lacunar stroke). Clinical data were collected for each patient, imaging characteristics, and markers of cardiac injury [troponin I (TnI), NT-proBNP, "rise and fall pattern" > 30%]. We compared different stroke subtypes according to OCSP, while evaluating any differences in patients with and without SHS. Results: In treated total anterior circulation infarct (TACI) patients, the rate of SHS is lower than in non-treated TACI. Similar SHS rate was found in partial anterior (PACI) and posterior stroke (POCI), and between treated and non-treated patients. Focusing on TACI group, we compared SHS-TACI and non-SHS-TACI, we performed a univariate and multivariate analysis; treatment (OR 0.408 CI95% 0.185–0.900; p = 0.026) and diabetes (OR 2.618 CI95% 1.181–5.803; p = 0.018) were significantly associated to SHS. No clear insular effect was found in SHS development. Conclusions: In severe anterior stroke (TACI), reperfusion treatment may be effective in preventing SHS. Conversely, diabetes is an independent risk factor for SHS. PACI and POCI have similar troponin elevation rate. [ABSTRACT FROM AUTHOR]

Background: Pulmonary hypertension (PH) is a prevalent adverse cardiovascular event at high-altitude environments. Prolonged exposure to high altitudes may result in myocardial injury, which is associated with poor clinical outcomes. This study aims to investigate the clinical characteristics of myocardial injury in patients with PH at high altitude. Methods: Consecutive patients admitted to a general tertiary hospital at the altitude of 3,650 m were selected into this retrospective study. Clinical and biochemical data were collected, as well as based on cardiac troponin I (cTnI) and echocardiography, patients were divided into myocardial injury group and non-myocardial injury group. Results: A total of 231 patients were enrolled, among whom 29 (12.6%) had myocardial injury. We found that body mass index, left ventricular end-diastolic dimension, and serum level of creatine kinase-MB (CK-MB) in myocardial injury group were significantly higher than non-myocardial injury group. Spearman correlation analysis revealed that cTnI has a significant positive correlation with CK-MB and lactic dehydrogenase instead of aspartate aminotransferase. A receiver operating characteristic curve was drawn to demonstrate that CK-MB could significantly predict the occurrence of myocardial injury with an area under the curve of 0.749, and a level of 3.035 (sensitivity = 59.3%, specificity = 90.5%) was optimal cutoff value. Conclusion: The incidence of myocardial injury in highlanders with PH is significant. CK-MB, as a convenient and efficient marker, has been found to be closely associated with cTnI and plays a predictive role in the occurrence of myocardial injury with PH in individuals exposed to high altitude. [ABSTRACT FROM AUTHOR]

Aim: Post‐transcriptional modifications and their specific mechanisms are the focus of research on the regulation of myocardial damage. Stress granules (SGs) can inhibit the inflammatory response by inhibiting the cyclic GMP‐AMP synthase (cGAS)‐stimulator of interferon genes (STING) pathway. This study investigated whether alkylation repair homologue protein 5 (ALKBH5) could affect myocardial inflammation and apoptosis during diabetic myocardial ischaemia‐reperfusion injury (IRI) through the cGAS‐STING pathway via SGs. Methods: A diabetes ischaemia‐reperfusion rat model and a high glucose hypoxia/reoxygenation cell model were established. Adeno‐associated virus (AAV) and lentivirus (LV) were used to overexpress ALKBH5, while the SG agonist arsenite (Ars) and the SG inhibitor anisomycin were used as interventions. Then, the levels of apoptosis and related indicators in the cell and rat models were measured. Results: In the in vivo experiment, compared with the normal sham group, the degree of myocardial tissue damage, creatine kinase‐MB and cardiac troponin I in serum, and myocardial apoptosis, the infarcted area of myocardium, and the level of B‐cell lymphoma 2 associated X protein, cGAS‐STING pathway and inflammatory factors in the diabetes ischaemia‐reperfusion group were significantly increased. However, the expression of SGs and the levels of ALKBH5, rat sarcoma‐GTPase‐activating protein‐binding protein 1, T‐cell intracellular antigen‐1 and Bcl2 were significantly decreased. After AAV‐ALKBH5 intervention, the degree of myocardial tissue damage, degree of myocardial apoptosis, and extent of myocardial infarction in myocardial tissue were significantly decreased. In the in vitro experiment, compared with those in the normal control group, the levels of lactate dehydrogenase, inflammation and apoptosis were significantly greater, and cell viability and the levels of ALKBH5 and SGs were decreased in the high glucose and hypoxia/reoxygenation groups. In the high glucose hypoxia/reoxygenation cell model, the degree of cell damage, inflammation, and apoptosis was greater than those in the high glucose and hypoxia/reoxygenation models, and the levels of ALKBH5 and SGs were further decreased. LV‐ALKBH5 and Ars alleviated the degree of cell damage and inhibited inflammation and cell apoptosis. The inhibition of SGs could partly reverse the protective effect of LV‐ALKBH5. The cGAS agonist G140 antagonized the inhibitory effects of the SG agonist Ars on cardiomyocyte apoptosis, inflammation and the cGAS‐STING pathway. Conclusion: Both ALKBH5 and SGs inhibited myocardial inflammation and apoptosis during diabetic myocardial ischaemia‐reperfusion. Mechanistically, ALKBH5 might inhibit the apoptosis of cardiomyocytes by promoting the expression of SGs through the cGAS‐STING pathway. [ABSTRACT FROM AUTHOR]

Myocardial injury and cardiovascular dysfunction are the most common complications of sepsis, and effective therapeutic candidate is still lacking. This study aims to investigate the protective effect of oxycodone in myocardial injury of lipopolysaccharide‐induced sepsis and its related signalling pathways. Wild‐type and nuclear factor erythroid 2‐related factor 2 (Nrf2)‐knockout mice, as well as H9c2 cardiomyocytes cultures treated with lipopolysaccharide (LPS) were used as models of septic myocardial injury. H9c2 cardiomyocytes culture showed that oxycodone protected cells from pyroptosis induced by LPS. Mice model confirmed that oxycodone pretreatment significantly attenuated myocardial pathological damage and improved cardiac function demonstrated by increased ejection fraction (EF) and fractional shortening (FS), as well as decreased cardiac troponin I (cTnI) and creatine kinase isoenzymes MB (CK‐MB). Oxycodone also reduced the levels of inflammatory factors and oxidative stress damage induced by LPS, which involves pyroptosis‐related proteins including: Nod‐like receptor protein 3 (NLRP3), Caspase 1, Apoptosis‐associated speck‐like protein contain a CARD (ASC), and Gasdermin D (GSDMD). These changes were mediated by Nrf2 and heme oxygenase‐1 (HO‐1) because Nrf2‐knockout mice or Nrf2 knockdown in H9c2 cells significantly reversed the beneficial effect of oxycodone on oxidative stress, inflammatory responses and NLRP3‐mediated pyroptosis. Our findings yielded that oxycodone therapy reduces LPS‐induced myocardial injury by suppressing NLRP3‐mediated pyroptosis via the Nrf2/HO‐1 signalling pathway in vivo and in vitro. [ABSTRACT FROM AUTHOR]

[Display omitted] As an emerging fluorophore, aggregation-induced emission luminogens (AIEgens) have received widespread attention in recent years, but the inherent drawbacks of AIEgens, such as the poor water-solubility and insufficient fluorescence stability in complex environments, restrict their performance in practical applications. Herein, we report a universal strategy based on hydrophobic dendritic mesoporous silica (HMSN) that can integrate different AIE molecules to construct multi-color fluorescent AIE materials. Specifically, HMSN with central radial pores was used as a powerful carrier for direct loading AIE molecules and restricting their intramolecular motions. Due to the pore-domain restriction effect and hydrophobic interaction, the obtained silica-based AIE materials have bright fluorescence with a maximum quantum yield of 68.38%, high colloidal/fluorescence stability, and excellent biosafety. Further, these silica-based AIE materials can be conjugated with functional antibodies to obtain probes with different targetability. After integration with immunomagnetic beads, the prepared detection probes achieved the quantitative detection of cardiac troponin I with the limit of detection (LOD) of 0.508 ng/mL. Overall, the targeting probes stemming from silica-based AIE materials can not only achieve cell-specific imaging, but quantify the number of Jurkat cells (LOD = 270 cells/mL) to further determine the specific etiology of the disease. [ABSTRACT FROM AUTHOR]

Severely burned patients often develop cardiac dysfunction and heart failure. The purpose of this retrospective study is to evaluate the role of cardiac troponin I (cTI) and its association to patients with burns. Patients deidentified data were collected from a national database in May 2023. Adult patients with burns who had cTnI lab counted were enrolled in this study. Patients were grouped by the cTnI mean level within 72 h including patients with elevated cTnI levels at >0.3 ng/mL (n = 2188 patients) and patients with nonelevated cTnI level (<0.04 ng/mL) (n = 3200). The cohorts were further stratified by less than 20% TBSA mild burn population and >20% TBSA severe burn population to replicate the severity of burns. The 30-day incidences of acute myocardial infarction (MI), sepsis, and mortality were investigated after the cohorts were propensity-matching balanced. The odds ratios (ORs) with 95% CI for MI were (9.829/7.081-13.645), sepsis (1.527/1.269-1.959), and mortality (2.586/2.110-3.170), respectively (P <.05). The groups that were further stratified into mild burn and severe burn had the following results: The mild burn ORs and 95% CI for MI was (6.237/3.986-9.785), sepsis (1.603/1.132-2.270), and mortality was (2.298/1.629-3.242). The severe burn cohort had ORs and 95% CI for MI (3.145/1.469-6.732), sepsis (0.993/0.555-1.777), and mortality (2.934/1.924-4.475). In conclusion, the patients with earlier elevated cTnI levels had worse outcomes of MI and mortality in both severe and mild burns. [ABSTRACT FROM AUTHOR]

Copyright of Boletín Latinoamericano y del Caribe de Plantas Medicinales y Aromáticas is the property of Universidad de Santiago de Chile and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Sensitive detection and precise quantitation of trace-level crucial biomarkers in a complex sample matrix has become an important area of research. For example, the detection of high-sensitivity cardiac troponin I (hs-cTnI) is strongly recommended in clinical guidelines for early diagnosis of acute myocardial infarction. Based on the use of an electrode modified by single-walled carbon nanotubes (SWCNTs) and a Ru(bpy)32+-doped silica nanoparticle (Ru@SiO2)/tripropylamine (TPA) system, a novel type of electrochemiluminescent (ECL) magneto-immunosensor is developed for ultrasensitive detection of hs-cTnI. In this approach, a large amount of [Ru(bpy)3]2+ is loaded in SiO2 (silica nanoparticles) as luminophores with high luminescent efficiency and SWCNTs as electrode surface modification material with excellent electrooxidation ability for TPA. Subsequently, a hierarchical micropillar array of microstructures is fabricated with a magnet placed at each end to efficiently confine a single layer of immunomagnetic microbeads on the surface of the electrode and enable 7.5-fold signal enhancement. In particular, the use of transparent SWCNTs to modify a transparent ITO electrode provides a two-order-of-magnitude ECL signal amplification. A good linear calibration curve is developed for hs-cTnI concentrations over a wide range from 10 fg/ml to 10 ng/ml, with the limit of detection calculated as 8.720 fg/ml (S/N = 3). This ultrasensitive immunosensor exhibits superior detection performance with remarkable stability, reproducibility, and selectivity. Satisfactory recoveries are obtained in the detection of hs-cTnI in human serum, providing a potential analysis protocol for clinical applications. HIGHLIGHTS: • An integrated microfluidic chip is fabricated to confine immunomagnetic beads at the electrode surface, leading to improved electrochemiluminescent efficiency and increased sensitivity in electrochemiluminescent immunoassays. • The combination of single-walled carbon nanotubes with the excellent electrooxidation ability of TPA and SiO2 nanoparticles as carriers loading a large amount of [Ru(bpy)3]2+ enables a sensitivity improvement of at least two orders of magnitude. • The electrochemiluminescent magneto-immunosensor exhibits an ultralow detection limit of 8.72 fg/ml, excellent selectivity and reproducibility, and satisfactory recoveries in human serum. [ABSTRACT FROM AUTHOR]

The Siemens Point-of-Care Testing (POC) Atellica® VTLi high-sensitivity troponin I (hsTnI) device has been previously validated. Verification independently provides evidence that an analytical procedure fulfils concordance with laboratory assays, imprecision, and hemolysis interference requirements.Five whole blood samples spanning the measuring interval were analysed 20 times in succession. Hemolysis interference was assessed at three troponin concentrations by spiking five hemolysate concentrations to plasma to achieve free hemoglobin concentrations 35–1,000 mg/dL. Concordance between whole blood (VTLi) and plasma on laboratory analysers (Beckman, Roche, Siemens) was assessed by Pearson correlation and kappa statistics at the (LOQ) and upper reference limit (URL). This was repeated for frozen plasma samples.Coefficients of variation for whole blood were <10 % for whole blood troponin concentrations of 9.2 and 15.9 ng/L, thus below the URL. Hemolysis positively interfered; at 250 mg/dL affecting the low troponin sample (+3 ng/L; +60 %) and high troponin sample (+37 ng/L; +24 %). Correlation coefficients were 0.98, 0.90 and 0.97 between VTLi and Beckman, Roche and Siemens assays respectively. Corresponding kappa statistics were 0.80, 0.73 and 0.84 at the LOQ and 0.70, 0.44 and 0.67 at the URL.Concordances between VTLi and laboratory assays were at least non-inferior to those between laboratory assays. Imprecision met manufacturer claims and was consistent with a high sensitivity assay. There is potential for hemolysis interference, highlighting the need for quality samples. The results support performance characteristics previously reported in validation studies, and the device offers acceptable performance for use within intended medical settings. [ABSTRACT FROM AUTHOR]

Point-of-care (POC) high-sensitivity cardiac troponin assays may further accelerate the diagnosis of myocardial infarction (MI). This study sought to assess the clinical and analytical performance of the novel high-sensitivity cardiac troponin I (hs-cTnI)-SPINCHIP POC test. Adult patients presenting with acute chest discomfort to the emergency department were enrolled in an international, diagnostic, multicenter study. The final diagnosis was centrally adjudicated by 2 independent cardiologists using all clinical information. We compared the discriminatory performance of hs-cTnI-SPINCHIP with current established central laboratory assays and derived an assay-specific hs-cTnI-SPINCHIP 0/1-hour algorithm. Secondary analyses included sample type comparisons (whole blood, fresh/frozen plasma, and capillary finger prick) and precision analysis. MI was the adjudicated final diagnosis in 214 (19%) of 1,102 patients. Area under the receiver-operating characteristic curve was 0.94 (95% CI: 0.92-0.95) for hs-cTnI-SPINCHIP vs 0.94 (95% CI: 0.92-0.95) for hs-cTnI-Architect (P = 0.907) and 0.93 (95% CI: 0.91-0.95) for high-sensitivity cardiac troponin T Elecsys (P = 0.305). A cutoff <7 ng/L at presentation (if chest pain onset was >3 hours) or <7 ng/L together with a 0/1-hour delta of <4 ng/L ruled out 51% with a sensitivity and negative predictive value of 100% (95% CI: 97.7%-100%) and 100% (95% CI: 99.0%-100%), respectively. A hs-cTnI-SPINCHIP concentration ≥36 ng/L or a 0/1-hour delta ≥11 ng/L ruled in 27% with a specificity and positive predictive value of 90.9% (95% CI: 88.3%-92.9%) and 72.9% (95% CI: 66.4%-78.6%), respectively. Bootstrap internal validation confirmed excellent diagnostic performance. High agreement was observed between different sample types. The SPINCHIP hs-cTnI POC test has very high diagnostic accuracy. Its assay-specific 0/1-hour algorithm achieved very high sensitivity/negative predictive value and specificity/positive predictive value for rule-out/in MI. (Advantageous Predictors of Acute Coronary Syndromes Evaluation [APACE] Study [APACE]; NCT00470587) [ABSTRACT FROM AUTHOR]

Background: The protective effects of metformin (Met) against doxorubicin (Dox)-induced cardiotoxicity via potential hypotheses of mechanisms of action with unknown reliability and credibility. Objectives: This study aimed to investigate the protective effects of Met against Dox-induced cardiotoxicity and the underlying mechanisms of action, as well as examine their reliability and credibility. Methods: A comprehensive search was conducted within the PubMed, Embase, Web of Science, Science Direct, Scopus, and CNKI databases from inception to 31 December 2023. Animal experiments evaluating the efficacy of Met against Dox-induced cardiotoxicity were included in this study. The primary efficacy outcomes were markers of myocardial injury. Effect size was measured using the standardized mean difference for continuous variables. Data were pooled using a random-effects model in the Stata 18 statistical software package. Results: Twenty-one studies involving 203-208 animals treated with Dox and 271-276 animals treated with Dox and Met were included in this analysis. Quality assessment revealed high-quality scores. Pooled results favored Met treatment based on the serum lactate dehydrogenase (LDH), creatine kinase-myocardial band (CK-MB), cardiac troponin I (cTnI), and aspartate aminotransferase levels. Sensitivity analysis using the leave-one-out method demonstrated stable results. Funnel plots, Egger's test, and Begg's test confirmed potential publication bias. The oxidative stress hypothesis has been investigated extensively based on abundant evidence. Conclusion: Met is effective and safe for protecting against Dox-induced cardiotoxicity, thus making it an appropriate drug for clinical investigation. The oxidative stress hypothesis of mechanism of action is well established with highest reliability and credibility. [ABSTRACT FROM AUTHOR]

Context: IntelliSep by Cytovale has received United States (U.S.) Food and Drug Administration (FDA) approval as a sepsis biomarker test. However, the clinical utility of this new test is not assessed in emergency departments. Objective: We investigated the clinical utility of this test using 44 patients visiting the emergency department at The University of Kansas Medical Center by comparing it with the monocyte distribution width (MDW) and other biomarkers including the von Willebrand factor (vWF) and ADAMTS13. Design and Methods: IntelliSep assesses the cellular host response via deformability cytometry of biophysical leukocyte properties and produces a score (IntelliSep Index; ISI: from 0.1 (lowest risk) to 10 (highest risk). We measured the ISI in 44 patients (19 high probability and 25 low probability of sepsis groups) using EDTA-anticoagulated blood. Left over plasma was used for measuring the plasma von Willebrand factor (vWF) and ADAMTS13 antigen by ELISA assays. The MDW was obtained during routine CBC analysis using a Beckman hematology analyzer. The lactate and high-sensitivity troponin I levels were measured using a Beckman analyzer. Procalcitonin was measured using a Cobas e801 analyzer. Results: The median ISI was twofold higher in the high-probability group than in the low-probability group (p < 0.01) while the median MDW was 34.5% higher in the high-probability group than in the low-probability group (p < 0.01). However, the correlation between the ISI and MDW was only modest (r = 0.66). In addition, significantly higher levels of plasma vWF antigen but lower levels of plasma ADAMTS13 antigen in the high-probability group were found, resulting in significantly higher vWF/ADAMTS13 ratios in the high-probability group than in the low-probability group. Conclusions: The new IntelliSep test along with vWF/ADAMTS13 ratios may be useful for the early diagnosis of sepsis in patients visiting the emergency department, which appears to be superior to the traditional marker, MDW. [ABSTRACT FROM AUTHOR]

Background: Acute pulmonary embolism (PE) is a critical condition where the timely and accurate assessment of right ventricular (RV) dysfunction is important for patient management. Given the limited availability of echocardiography in emergency departments (EDs), an artificial intelligence (AI) application that can identify RV dysfunction from electrocardiograms (ECGs) could improve the treatment of acute PE. Methods: This retrospective study analyzed adult acute PE patients in an ED from January 2021 to December 2023. We evaluated a smartphone application which analyzes printed ECGs to generate digital biomarkers for various conditions, including RV dysfunction (QCG-RVDys). The biomarker's performance was compared with that of cardiologists and emergency physicians. Results: Among 116 included patients, 35 (30.2%) were diagnosed with RV dysfunction. The QCG-RVDys score demonstrated significant effectiveness in identifying RV dysfunction, with a receiver operating characteristic–area under the curve (AUC) of 0.895 (95% CI, 0.829–0.960), surpassing traditional biomarkers such as Troponin I (AUC: 0.692, 95% CI: 0.536–0.847) and ProBNP (AUC: 0.655, 95% CI: 0.532–0.778). Binarized based on the Youden Index, QCG-RVDys achieved an AUC of 0.845 (95% CI: 0.778–0.911), with a sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of 91.2% (95% CI: 82.4–100%), 77.8% (95% CI: 69.1–86.4%), 63.3% (95% CI: 54.4–73.9%), and 95.5% (95% CI: 90.8–100%), respectively, significantly outperforming all the expert clinicians, with their AUCs ranging from 0.628 to 0.683. Conclusions: The application demonstrates promise in rapidly assessing RV dysfunction in acute PE patients. Its high NPV could streamline patient management, potentially reducing the reliance on echocardiography in emergency settings. [ABSTRACT FROM AUTHOR]

Immunodetection of cardiac isoforms of troponin I (cTnI) and troponin T (cTnT) in blood samples is widely used for the diagnosis of acute myocardial infarction. The cardiac troponin complex (ITC-complex), comprising cTnI, cTnT, and troponin C (TnC), makes up a large portion of troponins released into the bloodstream after the necrosis of cardiomyocytes. However, the stability of the ITC-complex has not been fully investigated. This study aimed to investigate the stability of the ITC-complex in blood samples. A native ITC-complex was incubated in buffer solutions, serum, and citrate, heparin, or EDTA plasma at various temperatures. Western blotting and gel filtration were performed, and troponins were detected using specific monoclonal antibodies. The ITC-complex dissociated at 37 °C in buffers with or without anticoagulants, in citrate, heparin, and EDTA plasmas, and in serum, into a binary cTnI-TnC complex (IC-complex) and free cTnT. In plasma containing heparin and EDTA, the IC-complex further dissociated into free TnC and cTnI. No dissociation was found at 4 °C or at room temperature (RT) in all matrices within 24 h except for EDTA plasma. After incubation at 37 °C in EDTA plasma and serum, dissociation was accompanied by proteolytic degradation of both cTnI and cTnT. The presence of anti-troponin autoantibodies in the sample impeded dissociation of the ITC-complex. The ITC-complex dissociates in vitro to form the IC-complex and free cTnT at 37 °C but is mostly stable at 4 °C or RT. Further dissociation of the IC-complex occurs at 37 °C in plasmas containing heparin and EDTA. [ABSTRACT FROM AUTHOR]

This letter to the editor discusses the use of sigma metrics in laboratory medicine. The authors analyze data from an external quality assurance program to examine the correlation between sigma metric, analytical imprecision, and bias. They find that sigma metric is more strongly correlated with analytical imprecision than bias. The study highlights the importance of considering both imprecision and bias when assessing laboratory performance. The accompanying table provides data on various laboratory measurements and their correlation with different testing methods, offering valuable information for researchers and library patrons interested in laboratory testing methods and their correlation. However, it is important to interpret the results with caution due to potential differences in sample material and study limitations. [Extracted from the article]

Manganese dioxide (MnO2) nanosheets possess unique physical and chemical properties, making them widely applicable in various fields, such as chemistry and biomedicine. Although MnO2 nanosheets are produced using bottom-up wet chemistry synthesis methods, their scale is below the gram level and requires a long processing time, restricting their effective scale-up from laboratory to market. We report a facile, green and scalable synthesis of MnO2 nanosheets by mixing Shiranui mandarin orange juice and KMnO4 for 30 minutes. We produced more than one gram (1.095) of MnO2 nanosheets with a 0.65 nm mean thickness and a 50 nm mean lateral size. Furthermore, we established a visual colorimetric biosensing strategy based on MnO2 nanosheets for the assay of glutathione (GSH) and cardiac troponin I (cTnI), offering high sensitivity and feasibility in clinical samples. For GSH, the limit of detection was 0.08 nM, and for cTnI, it was 0.70 pg mL−1. Meanwhile, the strategy can be used for real-time analysis by applying a smartphone-enabled biosensing strategy, which can provide point-of-care testing in remote areas. [ABSTRACT FROM AUTHOR]

Reagentless molecular-imprinted polymer (MIP) electrochemical biosensors can offer the next generation of biosensing platforms for the detection of biomarkers owing to their simplicity, cost-efficacy, tunability, robustness, and accuracy. In this work, a novel combination of Prussian blue (PB), coated as an embedded redox probe on a gold working electrode (GWE), and a signal-off MIP assay has been proposed in an electrochemical format for the detection of troponin I (TnI) in biofluids. TnI is a variant exclusive to heart muscles, and its elevated level in the bloodstream is indicative of acute myocardial infarction (AMI). The proposed lab-manufactured PB/MIP electrochemical biosensor, consisting of a simple signal-off MIP assay and a PB redox probe embedded on the GWE surface, is the first of its kind that allows for reagentless, label-free, and single-step electrochemical biosensing of proteins. The preparation steps of the biosensor were fully characterized by cyclic voltammetry (CV), atomic force microscopy (AFM), and Raman spectroscopy. Finally, the performance of the optimized biosensor was investigated through the determination of various concentrations of TnI, ranging from 10 to 100 pg mL−1 within 5 min, in serum and plasma with limits of detection less than 3.6 pg mL−1, and evaluation of selectivity towards TnI using some relevant proteins that exist in biofluids with higher concentrations. [ABSTRACT FROM AUTHOR]

Tracer antibodies, which are labelled with fluorescent or other type of reporter molecules, are widely employed in diagnostic immunoassays. Time-resolved fluorescence immunoassay (TRFIA), recognized as one of the most sensitive immunoassay techniques, utilizes tracers labelled with lanthanide ion (Ln) chelates. The conventional approach for conjugating isothiocyanate (ITC) Ln-chelates to antibodies involves random chemical targeting of the primary amino group of Lys residues, requiring typically overnight exposure to an elevated pH of 9–9.3 and leading to heterogeneity. Moreover, efforts to enhance the sensitivity of the assays by introducing a higher number of Ln-chelates per tracer antibody are associated with an elevated risk of targeting critical amino acid residues in the binding site, compromising the binding properties of the antibody. Herein, we report a method to precisely label recombinant antibodies with a defined number of Ln-chelates in a well-controlled manner by employing the SpyTag/SpyCatcher protein ligation technology. We demonstrate the functionality of the method with a full-length recombinant antibody (IgG) as well as an antibody fragment by producing site-specifically labelled antibodies for TRFIA for cardiac troponin I (cTnI) detection with a significant improvement in assay sensitivity compared to that with conventionally labelled tracer antibodies. Overall, our data clearly illustrates the benefits of the site-specific labelling strategy for generating high-performing tracer antibodies for TRF immunoassays. [ABSTRACT FROM AUTHOR]

Background: Perinatal asphyxia remains a significant cause of morbidity and mortality among neonates, often leading to hypoxic-ischemic encephalopathy (HIE) and myocardial injury. Understanding the predictors and markers of these conditions is crucial for improving clinical management and outcomes. Methods: A prospective cohort study enrolled 50 asphyxiated neonates at Tirunelveli Medical College Hospital, assessing demographic factors, clinical parameters, and Troponin I levels. Data were analyzed using Chi-square test to determine associations and significance. Results: Demographic factors including gravida (χ²(2) = 0.499, p = 0.499), gestational age (χ² = 0.961, p = 0.961), mode of delivery (χ² = 0.507, p = 0.507), sex (χ² = 0.982, p = 0.982), and birth weight (χ² = 0.499, p = 0.499) showed no significant association with HIE severity. However, seizures (p = 0.001), ventilator requirement (p = 0.006), and shock (p = 0.001) were strongly associated with elevated Troponin I levels, indicative of myocardial injury. Conclusion: Clinical parameters such as seizures, ventilator requirement, and shock are critical indicators of myocardial injury in asphyxiated neonates. Early recognition and management of these factors may improve outcomes and guide therapeutic interventions in neonatal intensive care settings. [ABSTRACT FROM AUTHOR]

Background: Spontaneous intracerebral hemorrhage (ICH) is one of the leading causes of mortality in intensive care units. The role of systemic hyperintense inflammation (SHI) in the pathogenesis of critical complications of ICH remains a poorly understood problem. There is a specific variant of severe ICH associated with increased intracranial pressure and occlusion of intracranial vessels, defined as ineffective cerebral blood flow (IECBF). Methods: To evaluate the role of SHI in the pathogenesis of severe (comatose) ICH in a dynamic comparison of patients with IECBF (n-26) and without IECBF (n-52). The SHI integral score criterion (SI scale) was used, including certain values of plasma concentrations of IL-6, IL-8, IL-10; TNF-α, PCT, cortisol, myoglobin, troponin I, D-dimer, and, additionally, SOFA scale values. Blood levels of ACTH and neuron-specific enolase (NSE) were also assessed. Results: Twenty-eight-day mortality in severe ICH reached 84.6% (without IECBF) and 96.2% (with IECBF). Clear signs of SHI were detected in 61.5%/87.8% (without IECBF) and 0.0%/8.7% (with IECBF) within 1–3/5–8 days from the onset of ICH manifestation. The lower probability of developing SHI in the IECBF group was associated with low blood NSE concentrations. Conclusions: The development of SHI in ICH is pathogenetically related to the permeability of the blood–brain barrier for tissue breakdown products and other neuroinflammatory factors. [ABSTRACT FROM AUTHOR]

Blunt cardiac injury (BCI) can be challenging diagnostically, and if misdiagnosed, can lead to life-threatening complications. Our institution previously evaluated BCI screening with troponin and electrocardiogram (EKG) during a transition from troponin I to high sensitivity troponin (hsTnI), a more sensitive troponin I assay. The previous study found an hsTnI of 76 ng/L had the highest capability of accurately diagnosing a clinically significant BCI. The aim of this study was to determine the efficacy of the newly implemented protocol. Patients diagnosed with a sternal fracture from March 2022 to April 2023 at our urban level-1 trauma center were retrospectively reviewed for EKG findings, hsTnI trend, echocardiogram changes, and clinical outcomes. The BCI cohort and non-BCI cohort ordinal measures were compared using Wilcoxon's two-tailed rank sum test and categorical measures were compared with Fisher's exact test. Youden indices were used to evaluate hsTnI sensitivity and specificity. Sternal fractures were identified in 206 patients, of which 183 underwent BCI screening. Of those screened, 103 underwent echocardiogram, 28 were diagnosed with clinically significant BCIs, and 15 received intervention. The peak hsTnI threshold of 76 ng/L was found to have a Youden index of 0.31. Rather, the Youden index was highest at 0.50 at 40 ng/L (sensitivity 0.79 and specificity 0.71) for clinically significant BCI. Screening patients with sternal fractures for BCI using hsTnI and EKG remains effective. To optimize the hsTnI threshold, this study determined the hsTnI threshold should be lowered to 40 ng/L. Further improvements to the institutional protocol may be derived from multicenter analysis. [ABSTRACT FROM AUTHOR]

Aims Methods and results Conclusions The heterogeneous phenotype of hypertrophic cardiomyopathy (HCM) is still not fully understood. Clonal haematopoiesis (CH) is emerging as a cardiovascular risk factor potentially associated with adverse clinical events. The prevalence, phenotype and outcomes related to CH in HCM patients were evaluated.Patients with HCM and available biospecimens from the Peter Munk Cardiac Centre Cardiovascular Biobank were subjected to targeted sequencing for 35 myeloid genes associated with CH. CH prevalence, clinical characteristics, morphological phenotypes assessed by echocardiogram and cardiac magnetic resonance and outcomes were assessed. All patients were evaluated for a 71‐plex cytokines/chemokines, troponin I and B‐type natriuretic peptide analysis. Major adverse cardiovascular events (MACE) were defined as appropriate implantable cardioverter‐defibrillator shock, stroke, cardiac arrest, orthotopic heart transplant and death. Among the 799 patients, CH was found in 183 (22.9%) HCM patients with sarcomeric germline mutations. HCM patients with CH were more symptomatic and with a higher burden of fibrosis than those without CH. CH was associated with MACE in those HCM patients with sarcomeric germline mutations (adjusted hazard ratio [HR] 6.89, 95% confidence interval [CI] 1.78–26.6; p = 0.005), with the highest risk among those that had DNMT3A, TET2 and ASXL1 mutations (adjusted HR 5.76, 95% CI 1.51–21.94; p = 0.010). Several cytokines (IL‐1ra, IL‐6, IL‐17F, TGFα, CCL21, CCL1, CCL8, and CCL17), and troponin I were upregulated in gene‐positive HCM patients with CH.These results indicate that CH in patients with HCM is associated with worse clinical outcomes. In the absence of CH, gene‐positive patients with HCM have lower rates of MACE. [ABSTRACT FROM AUTHOR]

In this study, we investigated the mechanism underlying electrocardiogram (ECG) alterations in a rabbit model of acute pulmonary thromboembolism (PTE). Twelve healthy adult New Zealand white rabbits were used, with eight in the experimental group (PTE group) and four in the control group. After developing the rabbit model of acute PTE, ECG and coronary angiography were performed. HE staining was conducted on the right and left ventricular tissues, and polymerase chain reaction (PCR) was used to determine brain natriuretic peptide (BNP), tumor necrosis factor-alpha (TNF-α), and Troponin I (TNI) mRNA expression in the myocardium. There were considerable changes in the ST segment of the ECG in the PTE group. Coronary angiography revealed the absence of spasm, stenosis, and occlusion. In the plasma of the PTE group, the levels of D-dimer, BNP, TNF-α, and TNI were significantly elevated, and these changes were statistically significant (P<0.05). PCR analysis of ventricular myocardial tissue indicated significantly higher levels of BNP, TNF-α, and TNI mRNA in the PTE group than in the control group. These differences were statistically significant (P<0.05). The ST-T variations on the ECG of rabbits with acute PTE correlate strongly with the temporary changes in right heart volume caused by acute PTE. [ABSTRACT FROM AUTHOR]

Left ventricular dysfunction in dogs after the administration of doxorubicin (DOX) has been extensively examined. However, the effects of DOX on right ventricular (RV) function remain unknown. Therefore, the present study investigated whether the chemotherapy treatment with DOX decreases RV function. Twelve dogs (five with multicentric lymphoma, four with hemangiosarcoma, two with thyroid cancer, and one with lung adenocarcinoma) that received at least two doses of DOX were prospectively enrolled. Echocardiography and the measurement of troponin I were performed prior to each administration of DOX and approximately one month after the last administration. Right ventricular function was assessed by the RV fractional area change and RV Tei index. Two (n=4), three (n=3), four (n=3), and five (n=2) doses of DOX were administered. While no significant differences were observed in the RV fractional area change, the RV Tei index was significantly impaired after two doses of DOX. Troponin I level significantly increased after four doses. Cumulative doses of DOX correlated with the RV Tei index (r=0.77, P<0.001). The present results demonstrated that the chemotherapy treatment with DOX decreased RV function in a dose-dependent manner in dogs. [ABSTRACT FROM AUTHOR]

We aimed to identify the major determinants of cardiac troponin changes response to exercise among non-elite runners participating in the Beijing 2022 marathon, with a particular focus on the associations with the cardiac function assessed by tissue Doppler echocardiography and speckle tracking. A prospective study. A total of 33 non-elite participants in the 2022 Beijing Marathon were included in the study. Echocardiographic assessment and blood sample collection were conducted before, immediately after, and two weeks after the marathon. Blood samples were analyzed using the same Abbot high-sensitivity cTnI STAT assay. Echocardiography included tissue Doppler and speckle tracking echocardiography. Following the marathon, significant increases were observed in cardiac biomarkers, with hs-cTnI elevating from 3.1 [2.3–6.7] to 49.6 [32.5–76.9] ng/L (P < 0.0001). Over 72 % of participants had post-race hs-TnI levels surpassing the 99th percentile upper reference limit. There was a notable correlation between pre-marathon hs-cTnI levels (β coefficient, 0.56 [0.05, 1.07]; P = 0.042), weekly average training (β coefficient, − 1.15 [− 1.95, − 0.35]; P = 0.009), and hs-cTnI rise post-marathon. Echocardiography revealed significant post-race cardiac function changes, including decreased E/A ratio (P < 0.0001), GWI (P < 0.0001), and GCW (P < 0.0001), with LVEF (β coefficients, 0.112 [0.01, 0.21]; P = 0.042) and RV GLS (β coefficients, 0.124 [0.01, 0.23]; P = 0.035) changes significantly associated with hs-TnI alterations. All echocardiographic and laboratory indicators reverted to baseline levels within two weeks. Baseline hs-cTnI levels and weekly average training influence exercise-induced hs-cTnI elevation in non-elite runners. Echocardiography revealed post-race changes in cardiac function, with LVEF and RV GLS significantly associated with hs-TnI alterations. These findings contribute to understanding the cardiac response to exercise and could guide training and recovery strategies. [ABSTRACT FROM AUTHOR]

A 15‐month‐old female Ragdoll cat was evaluated for progressive lethargy, tachypnoea and increased respiratory effort for 1 week after routine ovariohysterectomy. Thoracic radiographs and an echocardiogram showed evidence of congestive heart failure and a hypertrophic cardiomyopathy phenotype, respectively. The maximum left ventricular wall thickness in end diastole was 6.2 mm. The serum cardiac troponin I concentration was 20.86 ng/mL. The cat was treated with furosemide and clopidogrel and discharged after 3 days. A repeat echocardiogram 2 weeks later showed complete resolution of the hypertrophic cardiomyopathy phenotype (maximum left ventricular wall thickness: 5.0 mm). A repeat cardiac troponin I concentration was 0.041 ng/mL. All cardiac medications were discontinued. A final recheck 4 weeks later revealed stable normal echocardiogram and further reduction in cardiac troponin I concentration to 0.004 ng/mL. This case report demonstrates that resolution of transient myocardial thickening can take 2 weeks after the echocardiographic diagnosis of left ventricular thickening. [ABSTRACT FROM AUTHOR]

Background Cardiotoxicity is a major toxic effect induced by several types of drugs. An electrocardiogram is done routinely in cardiovascular drug exposures. Cardiac troponin I (cTnI) is the usual biomarker for diagnosing myocardial injury. B-type natriuretic peptide (BNP) is a well-established predictor of disease state in suspected heart failure. Aim The study aimed to assess BNP's role as an early predictor of mortality compared with cTnI and ECG changes in acutely poisoned patients with cardiotoxicities. Methodology This study enrolled 70 patients with acute cardiotoxicity by drugs and toxins known to cause cardiac injury admitted to Tanta University Poison Control Center (TUPCC). Collected data included socio-demographic data, toxicological history, vital signs, ECG changes, Poison Severity Score (PSS), BNP, and cTnI serum levels. Result Patients were classified as survivors and non-survivors. Significantly more delay time was recorded in non-survivors. Moreover, vital signs were significantly abnormal in non-survivors. There was no statistical significance regarding the initial ECG abnormalities between survivors and non-survivors. BNP and cTnI levels were significantly higher among non-survivors. For mortality prediction, BNP had good predictive power (AUC = 0.841) with 100% sensitivity and 79.7% specificity while cTnI had an acceptable predictive power (AUC = 0.786), with 83.3% sensitivity and 78.1% specificity with insignificant difference between both biomarkers. Conclusion BNP and cTnI levels can predict mortality in acute cardiotoxicity compared to ECG which has no statistically significant prediction. BNP has a higher discriminatory power than cTnI for the prediction of mortality. [ABSTRACT FROM AUTHOR]

Exercise-induced muscle injury is one of the most common types of sports injuries. Skeletal muscle troponin I (skTnI) serves as an ideal biomarker in assessing such injuries, facilitating timely detection and evaluation. In this study, we develop a fluorescent sandwich lateral flow immunoassay (LFIA) combined with a desktop analyzer for rapid detection of skTnI. Through optimizing the reaction system, the assay achieves a satisfying detection performance, reaching a limit of detection (LOD) of 0.5 ng/mL with a turnaround time of 15 min. The proposed detection platform offers portability, ease of use, and high sensitivity, which facilitates the monitoring of exercise-induced muscle injuries at the point of care. This feature is particularly advantageous for end users, enabling timely detection of sports-related injuries and ultimately enhancing prognosis and sports life. [ABSTRACT FROM AUTHOR]

Due to the clinical similarities between pulmonary embolism (PE) and myocardial infarction (MI), physicians often encounter challenges in promptly distinguishing between them, potentially missing the critical window for the correct emergency response. This paper presents a biosensor, termed the PEMI biosensor, which is designed for the identification and quantitative detection of pulmonary embolism or myocardial infarction. The surface of the working electrode of the PEMI biosensor was modified with graphene oxide and silk fibroin to immobilize the mixture of antibodies. Linear sweep voltammetry was employed to measure the current-to-potential mapping of analytes, with the calculated curvature serving as a judgment index. Experimental results showed that the curvature exhibited a linear correlation with the concentration of antigen FVIII, and a linear inverse correlation with the concentration of antigen cTnI. Given that FVIII and cTnI coexist in humans, the upper and lower limits were determined from the curvatures of a set of normal concentrations of FVIII and cTnI. An analyte with a curvature exceeding the upper limit can be identified as pulmonary embolism, while a curvature falling below the lower limit indicates myocardial infarction. Additionally, the further the curvature deviates from the upper or lower limits, the more severe the condition. The PEMI biosensor can serve as an effective detection platform for physicians. [ABSTRACT FROM AUTHOR]

The present study evaluated the cardioprotective effect of astaxanthin (ASX) against isoproterenol (ISO) induced myocardial infarction in rats via the pathway of mitochondrial biogenesis as the possible molecular target of astaxanthin. The control group was injected with normal physiological saline subcutaneously for 2 days. The second group was injected with ISO at a dose of 85 mg/kg bwt subcutaneously for 2 days. The third, fourth and fifth groups were supplemented with ASX at doses of 10, 20, 30 mg/kg bwt, respectively daily by oral gavage for 21 days then injected with ISO dose of 85 mg/kg bwt subcutaneously for 2 successive days. Isoproterenol administration in rats elevated the activities of Creatine kinase‐MB (CK‐MB), aspartate transaminase (AST), lactate dehydrogenase (LDH), and other serum cardiac biomarkers Troponin‐I activities, oxidative stress biomarkers, malondialdehyde(MDA), Nuclear factor‐kappa B (NF‐KB), while it decreased Peroxisome proliferator‐activated receptor‐gamma coactivator (PGC‐1α), Nuclear factor erythroid‐2‐related factor 2 (Nfe212), mitochondrial transcriptional factor A (mt TFA), mitochondrial DNA copy number and glutathione system parameters. However, Astaxanthin decreased the activities of serum AST, LDH, CK‐MB, and Troponin I that elevated by ISO. In addition, it increased glutathione peroxidase and reductase activities, total glutathione and reduced GSH content, and GSH/GSSG ratio, mtDNA copy number, PGC‐1α expression and Tfam expression that improved mitochondrial biogenesis while it decreased GSSG and MDA contents and NF‐KB level in the cardiac tissues. This study indicated that astaxanthin relieved isoproterenol induced myocardial infarction via scavenging free radicals and reducing oxidative damage and apoptosis in cardiac tissue. [ABSTRACT FROM AUTHOR]

It remains unclear whether procedural myocardial infarction (pMI) and spontaneous myocardial infarction (spMI) have a similar impact on prognosis. The aim of this study was to assess mortality after pMI and spMI. Patients with chronic coronary syndrome (CCS) and baseline troponin ≤1× the upper reference level (URL) or with acute spMI who underwent percutaneous coronary intervention (PCI) were included. PMI was defined as post-PCI troponin increase >1× URL in patients with CCS. SpMI comprised any acute coronary syndrome with elevated troponin. The 1-year risk of all-cause death was assessed after pMI and spMI across 3 strata of troponin elevation (>1-5×, >5-35×, and >35× URL), with CCS patients having post-PCI troponin ≤1× URL as a reference group. Conventional troponin I was measured using the Architect methodology (Abbott). Among 10,707 patients undergoing PCI from 2012 to 2020, 8,515 patients presented with CCS and 2,192 with spMI. Among CCS patients, 913 (10.7%) had pMI. Troponin peaks >1-5×, >5-35×, and >35× URL were observed in 53%, 41%, and 6% of patients with pMI, and in 24%, 38%, and 37% of patients with spMI, respectively. Mortality at 1 year was higher after pMI (7.7%; adjusted HR: 4.40; 95% CI: 1.59-12.2), and spMI (8.5%; adjusted HR: 7.57; 95% CI: 5.44-10.5) with troponin peak >35× URL compared with no-MI (1.4%). Mortality was also increased after spMI with troponin peak >1-5× or >5-35× URL. Mortality at 1 year was significantly increased after pMI and spMI with troponin peak >35× URL, whereas for troponin levels ≤35× only spMI had a relevant impact on mortality. [ABSTRACT FROM AUTHOR]

Background: In the livestock industry, Foreign Body Syndrome is a devastating disease condition. Feeding management, lacking of food discrimination, and eating chopped food increase the risk of swallowing sharp foreign bodies in bovine species. In addition to the honeycomb cells shape of the reticulum, the contractions of the reticular wall, gravid uterine pressure, and parturition efforts, foreign bodies can penetrate the reticular wall, causing cascade of problems including traumatic reticulitis, traumatic reticuloperitonitis, and traumatic pericarditis. The present study was carried out to evaluate the diagnostic significance of cardiac troponin I rapid test cassette and other cardiac biomarkers including serum cardiac troponin I (cTn I), creatine kinase-myocardial band (CK-MB), lactate dehydrogenase (LDH), and aspartate aminotransferase enzyme (AST), in confirmed cases of traumatic pericarditis (TP) and/or traumatic reticuleoperitonitis (TRP) in cattle and buffaloes. Methods: A total number of 30 animals (22 cattle and 8 buffaloes) with different signs such as anorexia, jugular distension, brisket edema, and signs of pain (reluctance to move, arching back, and abduction of the forelimbs) were included in the present study. Based on case history, clinical signs, ferroscopic, pericardiocentesis, radiographic and ultrasonographic examinations, TP were confirmed in cattle (n = 10) and buffaloes (n = 8) while TRP were confirmed only in cattle (n = 12). Additionally, 20 clinically healthy animals (n = 10 cattle and 10 buffaloes) were used as a control group. Blood samples were collected for determination of blood level of Tn-I, and activity of CK-MB, LDH, and AST. Results: The obtained results revealed a highly significant increase in serum cTn I in diseased cattle with TP and TRP (P = 0.00), while buffaloes with TP showed no significant changes in serum cTn I (P = 0.111). Both diseased cattle and buffaloes showed increased serum activities of CK-MB, AST, and LDH enzyme. On the other hand, cardiac troponin I rapid test cassette failed to detect cTn I in diseased animals. Conclusion: The study concluded that the cardiac troponin I rapid test cassette did not have a diagnostic significance and could not be used as a point-of-care under field condition for diagnosis of TP and TRP in large ruminants. However, the serum troponin I level is helpful in diagnosis of TP and TRP in cattle. Although cardiac biomarkers have some diagnostic values in TP and TRP, the traditional diagnostic methods (clinical, radiography and ultrasonography examinations) are crucial for thorough evaluation of TP/TRP cases in bovine. [ABSTRACT FROM AUTHOR]

Rationale & objective: Glomerulonephritis (GN) is a leading cause of chronic kidney disease (CKD). Major adverse cardiovascular events (MACE) are prolific in CKD. The risk of MACE in GN cohorts is multifactorial. We investigated the prognostic significance of routine cardiac biomarkers, Troponin I and N-terminal pro-BNP (NT-proBNP) in predicting MACE within 5 years of GN diagnosis. Study Design: Retrospective cohort study. Setting & participants: Data were obtained from TriNetX, a global federated health research network of electronic health records (EHR). Exposure or predictor: Biomarker thresholds: Troponin I: 18 ng/L, NT-proBNP: 400 pg/mL. Outcomes: Primary outcome: Incidence of major adverse cardiovascular events (MACE). Secondary outcome: was the risk for each individual component of the composite outcome. Analytical Approach: 1:1 propensity score matching using logistic regression. Cox proportional hazard models were used to assess the association of cardiac biomarkers with the primary and secondary outcomes, reported as Hazard Ratio (HR) and 95% confidence intervals (CI). Survival analysis was performed which estimates the probability of an outcome over a 5-year follow-up from the index event. Results: Following PSM, 34,974 and 18,218 patients were analysed in the Troponin I and NTproBNP cohorts, respectively. In the Troponin I all cause GN cohort, 3,222 (9%) developed composite MACE outcome HR 1.79; (95% CI, 1.70, 1.88, p < 0.0001). In the NTproBNP GN cohort, 1,686 (9%) developed composite MACE outcome HR 1.99; (95% CI, 1.86, 2.14, p < 0.0001). Limitations: The data are derived from EHR for administrative purposes; therefore, there is the potential for data errors or missing data. Conclusions: In GN, routinely available cardiac biomarkers can predict incident MACE. The results suggest the clinical need for cardiovascular and mortality risk profiling in glomerular disease using a combination of clinical and laboratory variables. [ABSTRACT FROM AUTHOR]

Background and Aims Strategies to assess patients with suspected acute myocardial infarction (AMI) using a point-of-care (POC) high-sensitivity cardiac troponin I (hs-cTnI) assay may expedite emergency care. A 2-h POC hs-cTnI strategy for emergency patients with suspected AMI was derived and validated. Methods In two international, multi-centre, prospective, observational studies of adult emergency patients (1486 derivation cohort and 1796 validation cohort) with suspected AMI, hs-cTnI (Siemens Atellica® VTLi) was measured at admission and 2 h later. Adjudicated final diagnoses utilized the hs-cTn assay in clinical use. A risk stratification algorithm was derived and validated. The primary diagnostic outcome was index AMI (Types 1 and 2). The primary safety outcome was 30-day major adverse cardiac events incorporating AMI and cardiac death. Results Overall, 81 (5.5%) and 88 (4.9%) patients in the derivation and validation cohorts, respectively, had AMI. The 2-h algorithm defined 66.1% as low risk with a sensitivity of 98.8% [95% confidence interval (CI) 89.3%–99.9%] and a negative predictive value of 99.9 (95% CI 99.2%–100%) for index AMI in the derivation cohort. In the validation cohort, 53.3% were low risk with a sensitivity of 98.9% (95% CI 92.4%–99.8%) and a negative predictive value of 99.9% (95% CI 99.3%–100%) for index AMI. The high-risk metrics identified 5.4% of patients with a specificity of 98.5% (95% CI 96.6%–99.4%) and a positive predictive value of 74.5% (95% CI 62.7%–83.6%) for index AMI. Conclusions A 2-h algorithm using a POC hs-cTnI concentration enables safe and efficient risk assessment of patients with suspected AMI. The short turnaround time of POC testing may support significant efficiencies in the management of the large proportion of emergency patients with suspected AMI. [ABSTRACT FROM AUTHOR]

Introduction: Risk stratification scores such as the European Systematic COronary Risk Evaluation (SCORE) are used to guide individuals on cardiovascular disease (CVD) prevention. Adding high-sensitivity troponin I (hsTnI) to such risk scores has the potential to improve accuracy of CVD prediction. We investigated how applying hsTnI in addition to SCORE may impact management, outcome, and cost-effectiveness. Methods: Characteristics of 72,190 apparently healthy individuals from the Biomarker for Cardiovascular Risk Assessment in Europe (BiomarCaRE) project were included into a discrete-event simulation comparing two strategies for assessing CVD risk. The standard strategy reflecting current practice employed SCORE (SCORE); the alternative strategy involved adding hsTnI information for further stratifying SCORE risk categories (S-SCORE). Individuals were followed over ten years from baseline examination to CVD event, death or end of follow-up. The model tracked the occurrence of events and calculated direct costs of screening, prevention, and treatment from a European health system perspective. Cost-effectiveness was expressed as incremental cost-effectiveness ratio (ICER) in € per quality-adjusted life year (QALYs) gained during 10 years of follow-up. Outputs were validated against observed rates, and results were tested in deterministic and probabilistic sensitivity analyses. Results: S-SCORE yielded a change in management for 10.0% of individuals, and a reduction in CVD events (4.85% vs. 5.38%, p<0.001) and mortality (6.80% vs. 7.04%, p<0.001). S-SCORE led to 23 (95%CI: 20–26) additional event-free years and 7 (95%CI: 5–9) additional QALYs per 1,000 subjects screened, and resulted in a relative risk reduction for CVD of 9.9% (95%CI: 7.3–13.5%) with a number needed to screen to prevent one event of 183 (95%CI: 172 to 203). S-SCORE increased costs per subject by 187€ (95%CI: 177 € to 196 €), leading to an ICER of 27,440€/QALY gained. Sensitivity analysis was performed with eligibility for treatment being the most sensitive. Conclusion: Adding a person's hsTnI value to SCORE can impact clinical decision making and eventually improves QALYs and is cost-effective compared to CVD prevention strategies using SCORE alone. Stratifying SCORE risk classes for hsTnI would likely offer cost-effective alternatives, particularly when targeting higher risk groups. [ABSTRACT FROM AUTHOR]

Aims Methods and results Conclusions The aim of this study was to report safety and efficacy of aficamten in patients with non‐obstructive hypertrophic cardiomyopathy (nHCM) over 36 weeks in the ongoing FOREST‐HCM trial.Patients were started on aficamten 5 mg daily, with doses adjusted in 5‐mg increments (5–20 mg) at ≥2‐week intervals according to site‐read left ventricular ejection fraction (LVEF). Aficamten dose was increased if LVEF ≥55%, maintained if LVEF 50–54%, decreased if LVEF 40–<50%, and temporarily interrupted if LVEF <40%. Safety and efficacy were assessed over 36 weeks. Overall, 34 patients were enrolled (mean age 57.2 ± 15.3 years, 62% female, 41% in New York Heart Association [NYHA] class III). Over 36 weeks, 82.3% achieved 15–20 mg daily dose and there was a modest reduction in LVEF by −4.3% ± 5.2 from 70% ± 6.1 (p < 0.0001). At Week 36, NYHA class improved by ≥1 class in 27 (79.4%) patients. Mean Kansas City Cardiomyopathy Questionnaire clinical summary score improved by 13.8 ± 12.5 points relative to baseline. Median (interquartile range) levels of N‐terminal pro‐B‐type natriuretic peptide were significantly improved from baseline (−665.5 pg/ml [−1244.0, −232.0]; p < 0.0001), while high‐sensitivity cardiac troponin I was unchanged (−2.7 ng/L [−11.3, 1.6]; p = 0.25). There were no drug discontinuations due to adverse events. LVEF <50% occurred in 2 (5.9%) patients, one following pulmonary vein isolation and one associated with atrial fibrillation.Over 36 weeks, aficamten appeared safe and effective in the studied patients with nHCM. [ABSTRACT FROM AUTHOR]

Background/Objectives: Persistent cardiovascular issues are common in COVID-19 survivors, making the detection of subtle myocardial injuries critical. This study evaluates myocardial work (MW) indices in patients recently recovering from mild-to-moderate COVID-19. Methods: A total of 105 recently recovered COVID-19 patients (who had a mean age of 52 years) underwent comprehensive laboratory testing and advanced echocardiographic assessments. The median time since their COVID-19 infections was 56 days (IQR: 42–71). The cohort was stratified based on high-sensitive troponin I (hs-TnI) levels: undetectable versus detectable. The echocardiographic analysis utilized pressure-strain loops to evaluate MW indices. Results: Detectable hs-TnI levels were observed in 42% of patients. The median values of MW indices for the entire group were slightly below normal values: global work index (GWI)—1834 mmHg% (IQR 1168–2054 mmHg%), global constructive work (GCW)—2130 mmHg% (IQR 2010–2398 mmHg%), global wasted work (GWW)—119 mmHg% (IQR 78–175 mmHg%), and global work efficiency (GWE)—94% (IQR 92–96%). Patients with detectable hs-TnI had higher GWW (168 vs. 97 mmHg%, p < 0.005) and lower GWE (93% vs. 95%, p < 0.005). In multiple regression analysis, strain dispersion (PSD) was the sole predictor for GWW (β = 0.67, p < 0.001), while for GWE, PSD (β = −0.67, p < 0.001) and LVEF (β = 0.16, p = 0.05) were significant predictors. Conclusions: Among patients recently recovering from mild-to-moderate COVID-19, elevated hs-TnI levels are linked with a reduction in GWE and an increase in GWW. PSD is an important predictor of myocardial inefficiency and wasted work. In this group, disruptions in the timing and coordination of cardiac muscle contractions may play a key pathophysiological role in reducing the efficiency of the heart's performance. [ABSTRACT FROM AUTHOR]

Background: high-sensitive cardiac TroponinI (hs-cTnI) is widely used for diagnosis of acute coronary syndromes. The latest recommendation for hs-cTnI determination is the protocol 0–1 h finalized to improve the rule out accuracy of the test. A Point of Care Testing able to guarantee these performances could be very useful due to reducing the turnaround time and ruling out patients suspected of ACS, especially by using biological matrices that are not required for centrifuge. The aim of our work is to compare the results for hs-cTnI obtained using different biological matrices and anticoagulants, obtained between Atellica® VTLi hs-cTnI POCT and Access AccuTnI+3 DxI800 performances, in order to establish a possible bias derived directly from these pre-analytical conditions. Methods: Li-heparinized pool samples were primary employ for hs-cTnI with Atellica® VTLi as whole blood, then centrifuged and tested on Atellica® VTLi and DxI800. K3EDTA pool samples were centrifuged and measured on DxI800 too. A comparison of methods was performed according to CLSI_EP-09A2 protocol. Constant and proportional errors were investigated with Deming regression. Bias between methods was evaluated with the Bland Altman test. Results: comparing whole blood lithium heparin results obtained with Atellica versus lithium heparin and K3EDTA plasma tested on DxI 800, the Deming regression revealed a proportional error, whereas in both cases Bland Altman highlighted a minimal underestimation. A similar performance was revealed when considering plasma lithium heparin tested on Atellica versus lithium heparin and K3EDTA plasma obtained with DxI800, confirming the same underestimation. Considering values close to the cut off, no significant differences were found. Conclusions: in the laboratory, the estimation of the bias of two different analyzers is pivotal. Once more this is crucial when different biological matrices and anticoagulants are employed for the analysis. Our study demonstrates that no significant differences among the two matrices are present when comparing Atellica and DxI800 performances. [ABSTRACT FROM AUTHOR]