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The toxicity of methylmercury (MeHg) during embryonic development is a relevant issue that remains unclear and deserves investigation. In this sense, there is evidence that links the intake of contaminated food with cardiovascular pathologies in human adults and children. Thus, this study aimed to verify the impact of MeHg on the structure and integrity of extraembryonic and cardiac blood vessels and the contractile function of cardiomyocytes, also evaluating embryonic weight and the cardiosomatic index (CSI). Thus, chicken embryos, used as an experimental model, were exposed to a single dose of 0.1 μg MeHg/50 μl saline at E1.5 and analyzed at E10. After exposure, an increase in the number of extraembryonic blood vessels and the veins of the cardiac tissue was observed. These increases were accompanied by a reduction in the content of VEGF and VCAM proteins related to vessel growth and adhesiveness. Together, these results were related to reduced nitrite (NOx) levels. Furthermore, MeHg reduces the number of sarcomeres and increases the content of cardiac troponin I (cTnI), a protein that regulates contraction. In general, exposure to MeHg affected the integrity of extraembryonic and cardiac vessels and the contractile function of cardiomyocytes, which had a systemic impact evidenced by the reduction in embryonic weight gain and CSI. Ingestion of MeHg through contaminated food is associated with cardiovascular problems. This study assessed MeHg effects on extraembryonic and cardiac blood vessels, cardiomyocyte function, embryonic weight, and cardiosomatic index (CSI). Gallus domesticus embryos received a single dose 0.1 μg MeHg/50 μl saline at E1.5, analyzed at E10. MeHg exposure increased extraembryonic and cardiac vessel numbers, reduced VEGF and VCAM proteins, and lowered NOx levels. MeHg also decreased sarcomeres and increased cTnI, impacting cardiomyocyte function, embryonic weight, and CSI. [ABSTRACT FROM AUTHOR]

Background and purpose Methods Results Conclusions Sparse information is available on the correct interpretation of elevated high‐sensitivity cardiac troponin (hs‐cTn) in confirmed muscular dystrophies.Serum concentrations of hs‐cTn T (hs‐cTnT) and hs‐cTn I (hs‐cTnI) were determined in 35 stable outpatients with confirmed skeletal muscle dystrophies. We calculated sensitivities, specificities, and positive and negative predictive values of hs‐cTnT and hs‐cTnI for identification of cardiac involvement using a comprehensive definition that included diastolic left ventricular and right ventricular function, strain analysis using two‐dimensional transthoracic echocardiogram and magnetic resonance imaging, myocardial biopsies, and consideration of a variety of triggers for cardiac injury, including arrhythmias, conduction disorders, and hypoxemia due to respiratory failure.Cardiac involvement was diagnosed in 34 of 35 cases. Specificities of hs‐cTnT increased from 12.5% to 100% (p = 0.0006) applying the comprehensive definition compared to a definition based on electrocardiography and echocardiography alone. At the recommended 99th percentile upper limit of normal, sensitivities were significantly lower for hs‐cTnI than for hs‐cTnT (29.4% vs. 100%, p = 0.0164). Conversely, the specificities of hs‐cTnT and hs‐cTnI increased to 100% when using the comprehensive definition criteria for diagnosing cardiac involvement.Elevated hs‐cTnT but not hs‐cTnI discriminates cardiac involvement in cases with confirmed skeletal muscle dystrophies with very high sensitivity and 100% specificity. Prior reports on worse performance may be explained by the use of less sensitive imaging methods or incomplete assessment of cardiac involvement. [ABSTRACT FROM AUTHOR]

Objectives. This study aimed to analyze an indication of physical exercise on the increase of cardiac troponin (cTn) levels as a marker of myocardial infarction from the physiological perspective. Materials and methods. A search of journal databases including MEDLINE-Pubmed, Web of Science, Scopus, and Science Direct was used in this systematic review study. The inclusion criteria were papers that addressed cardiac troponin (cTn), physical activity, and myocardial infarction, and were published within the last five years. Using the databases Science Direct, Pubmed, and Web of Science, 83 recognized publications were found. For this systematic review, finally ten publications that fulfilled the requirements for inclusion were chosen and examined. This study evaluated standard operating procedures using the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA). Results. This systematic review reports that physical exercise has been found to increase cardiac troponin (cTn) levels as a marker of myocardial infarction, but this increase is triggered by the body’s physiological response during exercise and is not considered as a pathological response. Conclusions. According to the findings of the study, physical exercise has been proven to elevate the risk of heart muscle damage by triggering an increase in cardiac troponin (cTn). However, this feature occurs in a physiological state and represents an exercise adaptation process. An analysis of the relevant articles reveals that this increase in cardiac troponin (cTn) has not been shown to have a negative influence on developing cardiovascular disease.

Aim. We present two cases with clearly discrepant results of clinical examination and cardiac troponin I (cTnI) and cardiac troponin T (cTnT) concentrations. In similar cases with discrepant results, the possibility of interference should be considered. Methods. Due to the suspicion of the presence of macrotroponin I in both of the presented cases, the patients were invited to our laboratory and both cTnI (Architect i1000, Abbott) and cTnT (Cobas 8000, Roche) concentrations were analysed. The samples were treated by preincubation in a heterophilic antibodies blocking tube (HBT) and analysed. Precipitation with polyethylene glycol solution (PEG) and molecular weight separation by gel filtration on Sephadex G100 was performed and concentrations of cTnI were analysed. Results. In the same blood sample, the cTnT and cTnI concentrations were 7 and 1782 ng/L, respectively, in Case 1, and 6 and 96 ng/L, respectively, in Case 2. Incubation of samples in HBT had no significant effect. CTnI concentrations after precipitation with PEG - presented as the percentage of initial concentrations - were 7.4% in Case 1 (and 26.8% in the control sample) and 1.4% in Case 2 (and 56.0% in the control sample). These results indicate a significant decrease in both cases, supporting presence of macrotroponin I. Finally, analyses of cTnI concentrations after gel filtration also supported the presence of macrotroponin I. Conclusion. The present cases show that the presence of macrotroponin can lead to unnecessary investigation of the patient. When the possibility of interference is suspected, cooperation with laboratory staff to help with interpretation or to perform more detailed analysis is crucial.

Objective To improve the detection ability and to know the current situation of Chongqing point of care testing (POCT) of cardiac troponin by analyzing the external quality assessment (EQA) of cardiac troponin POCT from 2018 to 2023 in Chongqing. Methods The results of troponin POCT EQA laboratory in Chongqing Center for Clinical Laboratory from 2018 to 2023 were collected and statistically analyzed. Results From 2018 to 2023, the number of laboratories participating in Chongqing's troponin POCT EQA increased from 36 to 88, the number of instrument brand groupings used increased from none to 8, and the qualified rate of each batch of laboratories increased from the lowest 26. 32% to the highest 89.77%. However, there was still a large difference in the target values of each instrument brand grouping. The variable coefficients of grouped target value for each batch varied from 44.72% to 105.69% in 2023. Conclusion The participation rate and detection level of Chongqing cardiac troponin POCT EQA needs to be improved and troponin POCT should be continuously included in EQA plan to regularly monitor the detection quality of this project in the whole city, so as to provide rapid and reliable guarantee for clinical diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Objectives. This study aimed to analyze an indication of physical exercise on the increase of cardiac troponin (cTn) levels as a marker of myocardial infarction from the physiological perspective. Materials and methods. A search of journal databases including MEDLINE-Pubmed, Web of Science, Scopus, and Science Direct was used in this systematic review study. The inclusion criteria were papers that addressed cardiac troponin (cTn), physical activity, and myocardial infarction, and were published within the last five years. Using the databases Science Direct, Pubmed, and Web of Science, 83 recognized publications were found. For this systematic review, finally ten publications that fulfilled the requirements for inclusion were chosen and examined. This study evaluated standard operating procedures using the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA). Results. This systematic review reports that physical exercise has been found to increase cardiac troponin (cTn) levels as a marker of myocardial infarction, but this increase is triggered by the body’s physiological response during exercise and is not considered as a pathological response. Conclusions. According to the findings of the study, physical exercise has been proven to elevate the risk of heart muscle damage by triggering an increase in cardiac troponin (cTn). However, this feature occurs in a physiological state and represents an exercise adaptation process. An analysis of the relevant articles reveals that this increase in cardiac troponin (cTn) has not been shown to have a negative influence on developing cardiovascular disease. [ABSTRACT FROM AUTHOR]

Background: There is an unmet medical need for the early detection of immune checkpoint inhibitor (ICI)-induced cardiovascular (CV) adverse events due to a lack of adequate biomarkers. This study aimed to provide insights on the incidence of troponin elevations and echocardiographic dynamics during ICI treatment in cancer patients and their role as potential biomarkers for submyocardial damage. In addition, it is the first study to compare hs-TnT and hs-TnI in ICI-treated patients and to evaluate their interchangeability in the context of screening. Results: Among 59 patients, the mean patient age was 68 years, and 76% were men. Overall, 25% of patients received combination therapy. Although 10.6% [95% CI: 5.0–22.5] of the patients developed troponin elevations, none experienced a CV event. No significant changes were found in 3D left ventricular (LV) ejection fraction nor in global longitudinal strain f (56 ± 6% vs. 56 ± 6%, p = 0.903 and −17.8% [−18.5; −14.2] vs. −17.0% [−18.8; −15.1], p = 0.663) at 3 months. There were also no significant changes in diastolic function and right ventricular function. In addition, there was poor agreement between hs-TnT and hs-TnI. Methods: Here, we present a preliminary analysis of the first 59 patients included in our ongoing prospective clinical trial (NCT05699915) during the first three months of treatment. All patients underwent electrocardiography and echocardiography along with blood sampling at standardized time intervals. This study aimed to investigate the incidence of elevated hs-TnT levels within the first three months of ICI treatment. Elevations were defined as hs-TnT above the upper limit of normal (ULN) if the baseline value was normal, or 1.5 ≥ times baseline if the baseline value was above the ULN. Conclusions: Hs-TnT elevations occurred in 10.6% of the patients. However, no significant changes were found on 3D echocardiography, nor did any of the patients develop a CV event. There were also no changes found in NT-proBNP. The study is still ongoing, but these preliminary findings do not show a promising role for cardiac troponins nor for echocardiographic dynamics in the prediction of CV events during the early stages of ICI treatment. [ABSTRACT FROM AUTHOR]

The selection of an appropriate transducer is a key element in biosensor development. Currently, a wide variety of substrates and working electrode materials utilizing different fabrication techniques are used in the field of biosensors. In the frame of this study, the following three specific material configurations with gold-finish layers were investigated regarding their efficacy to be used as electrochemical (EC) biosensors: (I) a silicone-based sensor substrate with a layer configuration of 50 nm SiO/50 nm SiN/100 nm Au/30–50 nm WTi/140 nm SiO/bulk Si); (II) polyethylene naphthalate (PEN) with a gold inkjet-printed layer; and (III) polyethylene terephthalate (PET) with a screen-printed gold layer. Electrodes were characterized using electrochemical impedance spectroscopy (EIS) and cyclic voltammetry (CV) to evaluate their performance as electrochemical transducers in an aptamer-based biosensor for the detection of cardiac troponin I using the redox molecule hexacyanoferrade/hexacyaniferrade (K3[Fe (CN)6]/K4[Fe (CN)6]. Baseline signals were obtained from clean electrodes after a specific cleaning procedure and after functionalization with the thiolate cardiac troponin I aptamers "Tro4" and "Tro6". With the goal of improving the PEN-based and PET-based performance, sintered PEN-based samples and PET-based samples with a carbon or silver layer under the gold were studied. The effect of a high number of immobilized aptamers will be tested in further work using the PEN-based sample. In this study, the charge-transfer resistance (Rct), anodic peak height (Ipa), cathodic peak height (Ipc) and peak separation (∆E) were determined. The PEN-based electrodes demonstrated better biosensor properties such as lower initial Rct values, a greater change in Rct after the immobilization of the Tro4 aptamer on its surface, higher Ipc and Ipa values and lower ∆E, which correlated with a higher number of immobilized aptamers compared with the other two types of samples functionalized using the same procedure. [ABSTRACT FROM AUTHOR]

Aim. We present two cases with clearly discrepant results of clinical examination and cardiac troponin I (cTnI) and cardiac troponin T (cTnT) concentrations. In similar cases with discrepant results, the possibility of interference should be considered. Methods. Due to the suspicion of the presence of macrotroponin I in both of the presented cases, the patients were invited to our laboratory and both cTnI (Architect i1000, Abbott) and cTnT (Cobas 8000, Roche) concentrations were analysed. The samples were treated by preincubation in a heterophilic antibodies blocking tube (HBT) and analysed. Precipitation with polyethylene glycol solution (PEG) and molecular weight separation by gel filtration on Sephadex G100 was performed and concentrations of cTnI were analysed. Results. In the same blood sample, the cTnT and cTnI concentrations were 7 and 1782 ng/L, respectively, in Case 1, and 6 and 96 ng/L, respectively, in Case 2. Incubation of samples in HBT had no significant effect. CTnI concentrations after precipitation with PEG -- presented as the percentage of initial concentrations -- were 7.4% in Case 1 (and 26.8% in the control sample) and 1.4% in Case 2 (and 56.0% in the control sample). These results indicate a significant decrease in both cases, supporting presence of macrotroponin I. Finally, analyses of cTnI concentrations after gel filtration also supported the presence of macrotroponin I. Conclusion. The present cases show that the presence of macrotroponin can lead to unnecessary investigation of the patient. When the possibility of interference is suspected, cooperation with laboratory staff to help with interpretation or to perform more detailed analysis is crucial. [ABSTRACT FROM AUTHOR]

The cardiac troponin complex (cTn) is a regulatory component of sarcomere. cTn consists of three subunits: cardiac troponin C (cTnC), which confers Ca2+ sensitivity to muscle; cTnI, which inhibits the interaction of cross-bridge of myosin with thin filament during diastole; and cTnT, which has multiple roles in sarcomere, such as promoting the link between the cTnI-cTnC complex and tropomyosin within the thin filament and influencing Ca2+ sensitivity of cTn and force development during contraction. Conditions that interfere with interactions within cTn and/or other thin filament proteins can be key factors in the regulation of cardiac contraction. These conditions include alterations in myofilament Ca2+ sensitivity, direct changes in cTn function, and triggering downstream events that lead to adverse cardiac remodeling and impairment of heart function. This review describes gene expression and post-translational modifications of cTn as well as the conditions that can adversely affect the delicate balance among the components of cTn, thereby promoting contractile dysfunction.

Background Acute myocardial injury is associated with poor outcomes in patients with acute ischemic stroke, but its prognostic significance in patients with spontaneous intracerebral hemorrhage remains unclear. We investigated whether acute myocardial injury and the direction of the cardiac troponin I (cTnI) change (rising versus falling) affect post‐intracerebral hemorrhage outcomes. Methods and Results We re‐analyzed the FAST (Factor‐Seven‐for‐Acute‐Hemorrhagic‐Stroke) trial. Acute myocardial injury was defined as at least 1 cTnI value above the upper reference limit with a rise/fall of >20%. Logistic regression tested for associations (1) between acute myocardial injury (presence versus absence) and poor outcome (modified Rankin Scale 4–6) and mortality at 15 and 90 days; (2) among 3 groups (rising versus falling versus no acute myocardial injury) and outcomes. Among the 841 FAST participants, 785 patients were included. Acute myocardial injury was detected in 29% (n=227); 170 had rising cTnI. At 15 and 90 days, respectively, those with acute myocardial injury had higher odds of poor outcome (adjusted odds ratio) ([aOR] 2.3 [95% CI, 1.3–3.9]); and adjusted odds ratio 2.5 [95% CI, 1.6–3.9];, and higher odds of mortality (adjusted odds ratio 2.4 [95% CI, 1.4–4.3]; and adjusted odds ratio 2.2 [CI, 1.3–3.6]) than patients without. There was no interaction between FAST group assignment and myocardial injury, and associations between myocardial injury and outcomes were consistent across group assignments. Rising cTnI was associated with the highest risk of poor outcomes and mortality. Conclusions In this secondary analysis of the FAST trial, acute myocardial injury was common and associated with poor outcomes. The direction of the cTnI change might provide additional risk stratification after intracerebral hemorrhage.

Abstract Introduction Use of doxorubicin, an anthracycline chemotherapeutic agent has been associated with late-occurring cardiac toxicities. Detection of early-occurring cardiac effects of cancer chemotherapy is essential to prevent occurrence of adverse events including toxicity, myocardial dysfunction, and death. Objective To investigate the prevalence of elevated cardiac troponin T (cTnT) and associated factors of myocardial injury in children on doxorubicin cancer chemotherapy. Methods Design: A cross-sectional study. Setting and subjects: A hospital-based study conducted on children aged 1-month to 12.4-years who had a diagnosis of cancer and were admitted at Kenyatta National Hospital (KNH). Interventions and outcomes: The patients underwent Echocardiography (ECHO) before their scheduled chemotherapy infusion. Twenty-four (24) hours after the chemotherapy infusion the patients had an evaluation of the serum cardiac troponin T (cTnT) and a repeat ECHO. Myocardial injury was defined as cTnT level > 0.014 ng/ml or a Fractional Shortening (FS) of 175 mg/m2 was significantly associated with and elevated cTnT (OR, 10.76; 95% CI, 1.18–97.92; p = 0.035). Diagnosis of nephroblastoma was also associated with an elevated cTnT (OR, 3.0; 95% CI, 1.23–7.26) but not statistically significant (p = 0.105). Nine percent (9%) of the participants had echocardiographic evidence of myocardial injury. Conclusion When compared to echocardiography, elevated levels of cTnT showed a higher association with early-occurring chemotherapy-induced myocardial injury among children on cancer treatment at a tertiary teaching and referral hospital in Kenya.

Objective To investigate the effect of moxibustion on Neiguan acupoint in preventing myocardial damage caused by anthracycline-based chemotherapy in breast cancer patients, and to explore the feasibility of moxibustion on Neiguan acupoint in reducing cardiotoxicity induced by chemotherapy. Methods A total of 80 breast cancer patients who underwent adjuvant chemotherapy with EC-T (pirarubicin + cyclophosphamide followed by docetaxel) regimen after surgery in the Department of Breast Cancer, Shaanxi Provincial Cancer Hospital from May 2020 to May 2021 were selected and divided into control group (n=40) and experimental group (n=40) randomly. During the first four cycles of chemotherapy, both groups received dexrazoxane on the same day as pirarubicin. The experimental group received moxibustion on Neiguan acupoint for three consecutive days starting one day before chemotherapy. The electrocardiograms, cardiac function, levels of cardiac troponin I (cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), and Karnofsky Performance Status (KPS) score were observed before and after four cycles of chemotherapy. Results After four cycles of chemotherapy, the incidences of arrhythmia ［22.5%(9/40) vs 50.0%(20/40), χ2=6.545, P=0.011］ and QRS wave voltage decrease［27.5%(11/40) vs 55.0%(22/40), χ2=6.241, P=0.012］ in the experimental group were lower than those in the control group. The cardiac function classification in the experimental group was better than that in the control group ( Z=2.388，P＜0.017). After four cycles of chemotherapy, left ventricular ejection fraction (LVEF) decreased and left ventricular end-diastolic diameter (LVEDD) increased in the control group, while LVEF and LVEDD changes were not significant in the experimental group. The cTnI levels, NT-proBNP levels, and KPS scores increased in both groups, and LVEF, LVEDD, cTnI, NT-proBNP levels, and KPS scores were better in the experimental group than those in the control group (P＜0.05). Conclusion Moxibustion on Neiguan acupoint has a significant protective effect on myocardial damage caused by chemotherapy in breast cancer patients, and can further improve myocardial function on the basis of dexrazoxane.

Introduction: Use of doxorubicin, an anthracycline chemotherapeutic agent has been associated with late-occurring cardiac toxicities. Detection of early-occurring cardiac effects of cancer chemotherapy is essential to prevent occurrence of adverse events including toxicity, myocardial dysfunction, and death. Objective: To investigate the prevalence of elevated cardiac troponin T (cTnT) and associated factors of myocardial injury in children on doxorubicin cancer chemotherapy. Methods: Design: A cross-sectional study. Setting and subjects: A hospital-based study conducted on children aged 1-month to 12.4-years who had a diagnosis of cancer and were admitted at Kenyatta National Hospital (KNH). Interventions and outcomes: The patients underwent Echocardiography (ECHO) before their scheduled chemotherapy infusion. Twenty-four (24) hours after the chemotherapy infusion the patients had an evaluation of the serum cardiac troponin T (cTnT) and a repeat ECHO. Myocardial injury was defined as cTnT level > 0.014 ng/ml or a Fractional Shortening (FS) of < 29% on ECHO. Results: One hundred (100) children were included in the final analysis. Thirty-two percent (32%) of the study population had an elevated cTnT. A cumulative doxorubicin dose of > 175 mg/m2 was significantly associated with and elevated cTnT (OR, 10.76; 95% CI, 1.18–97.92; p = 0.035). Diagnosis of nephroblastoma was also associated with an elevated cTnT (OR, 3.0; 95% CI, 1.23–7.26) but not statistically significant (p = 0.105). Nine percent (9%) of the participants had echocardiographic evidence of myocardial injury. Conclusion: When compared to echocardiography, elevated levels of cTnT showed a higher association with early-occurring chemotherapy-induced myocardial injury among children on cancer treatment at a tertiary teaching and referral hospital in Kenya. [ABSTRACT FROM AUTHOR]

Myocardial infarction can be ruled out in patients with a single cardiac troponin measurement. Whether use of a uniform rule-out threshold has resulted in sex differences in care remains unclear. The purpose of this study was to evaluate implementation of a uniform rule-out threshold in females and males with possible myocardial infarction, and to derive and validate sex-specific thresholds. The implementation of a uniform rule-out threshold (<5 ng/L) with a high-sensitivity cardiac troponin I assay was evaluated in consecutive patients presenting with possible myocardial infarction. The proportion of low-risk patients discharged from the emergency department and incidence of myocardial infarction or cardiac death at 30 days were determined. Sex-specific thresholds were derived and validated, and proportion of female and male patients were stratified as low-risk compared with uniform threshold. In 16,792 patients (age 58 ± 17 years; 46% female) care was guided using a uniform threshold. This identified more female than male patients as low risk (73% vs 62%), but a similar proportion of low-risk patients were discharged from the emergency department (81% for both) with fewer than 5 (<0.1%) patients having a subsequent myocardial infarction or cardiac death at 30 days. Compared with a uniform threshold of <5 ng/L, use of sex-specific thresholds would increase the proportion of female (61.8% vs 65.9%) and reduce the proportion of male (54.8% vs 47.8%) patients identified as low risk. Implementation of a uniform rule-out threshold for myocardial infarction was safe and effective in both sexes. Sex-specific rule-out thresholds should be considered, but their impact on effectiveness and safety may be limited. [Display omitted] [ABSTRACT FROM AUTHOR]

The relationship between exercise‐induced troponin elevation and non‐obstructive coronary artery disease (CAD) is unclear. This observational study assessed non‐obstructive CAD's impact on exercise‐induced cardiac Troponin I (cTnI) elevation in middle‐aged recreational athletes. cTnI levels of 40 well‐trained recreational athletes (73% males, 50 ± 9 years old) were assessed by a high‐sensitive cTnI assay 24 h before, and at 3 and 24 h following two high‐intensity exercises of different durations; a cardiopulmonary exercise test (CPET), and a 91‐km mountain bike race. Workload was measured with power meters. Coronary computed tomography angiography was used to determine the presence or absence of non‐obstructive (<50% obstruction) CAD. A total of 15 individuals had non‐obstructive CAD (Atherosclerotic group), whereas 25 had no atherosclerosis (normal). There were higher post‐exercise cTnI levels following the race compared with CPET, both at 3 h (77.0 (35.3–112.4) ng/L vs. 11.6 (6.4–22.5) ng/L, p < 0.001) and at 24 h (14.7 (6.7–16.3) vs. 5.0 (2.6–8.9) ng/L, p < 0.001). Absolute cTnI values did not differ among groups. Still, the association of cTnI response to power output was significantly stronger in the CAD versus Normal group both at 3 h post‐exercise (Rho = 0.80, p < 0.001 vs. Rho = −0.20, p = 0.33) and 24‐h post‐exercise (Rho = 0.87, p < 0.001 vs. Rho = −0.13, p = 0.55). Exercise‐induced cTnI elevation was strongly correlated with exercise workload in middle‐aged athletes with non‐obstructive CAD but not in individuals without CAD. This finding suggests that CAD influences the relationship between exercise workload and the cTnI response even without coronary artery obstruction. [ABSTRACT FROM AUTHOR]

Background: This study assesses how ambulance paramedics using the modified HEART-score with a point-of-care cardiac troponin (cTn) compare to the emergency physicians using the modified HEART-score with a high-sensitive cTn (hs-cTn) in patients with suspected non-ST-elevation acute coronary syndrome (NSTE-ACS), focusing on interobserver agreement and diagnostic performance. Methods: In this prospective multicenter cohort, we compare four cTn testing strategies (serial point of care and hs-cTn cTn measurement) with and without the HEART-score. Outcomes include the HEART-score's interobserver agreement, NSTE-ACS at discharge, major adverse cardiovascular events (MACE) after 30 days, and diagnostic accuracy of the different strategies. Conclusion: The POPular HEART study aims to improve NSTE-ACS diagnostic pathways, promoting pre-hospital detection and ruling out of NSTE-ACS to minimize unnecessary hospitalizations and associated costs. Clinical Trial Registration:NCT04851418 (ClinicalTrials.gov) Many people visit the emergency department (ED) due to chest pain, often worried about the possibility of a heart attack. While acute heart attacks can often be detected through an electrocardiogram (ECG; a test of the heart's electrical activity), a significant number of patients with a heart attack have a normal ECG. These patients require further testing to measure cardiac troponin (cTn; an indicator of heart damage) in the hospital to rule out a heart attack, known as non-ST-elevation acute coronary syndrome (NSTE-ACS). To improve diagnosis and care for these patients, we compared two approaches: ambulance paramedics using a quick bedside cTn test and the HEART-score, versus hospital doctors using a more sensitive cTn test with the HEART-score. The HEART score combines factors like the patient's medical history, ECG results, age, risk factors, and cTn levels to assess the risk of heart problems. In this comparison, the key difference lies in how cTn levels are measured – either through a quick finger prick test in an ambulance using a point-of-care device or a more detailed analysis in a hospital laboratory. We focused on patients visited by emergency medical services for chest pain suspected of a heart attack and transported to the hospital. We assessed the quick bedside test by paramedics and the detailed hospital test by doctors, alongside the use of the HEART score in both settings. Our evaluation looked at the agreement between these methods and their effectiveness in identifying or excluding an NSTE-ACS. Our research, known as the POPular HEART study, seeks to simplify the early identification or rule-out of an NSTE-ACS in patients with chest pain directly by ambulance. This approach aims to decrease unnecessary hospital admissions and reduce healthcare costs. We're exploring innovative methods to safely identify patients with a very low risk of NSTE-ACS in individuals with chest pain outside the hospital. Our objective is to safely minimize hospital admissions that may not be necessary, thereby saving resources. By doing so, we aim to alleviate the pressure on EDs and contribute to more cost-effective healthcare. Article highlights Background The study investigates the use of the HEART-score with point-of-care (POC) cTn testing by ambulance paramedics compared with HEART-score assessments with high-sensitive cTn (hs-cTn) by emergency physicians in patients suspected of having non-ST-elevation acute coronary syndrome (NSTE-ACS). Focuses on evaluating the interobserver agreement and diagnostic performance using the (modified) HEART-score. Methods A prospective, multicenter cohort study design. Comparison of four cTn testing strategies involving serial POC and hs-cTn measurements, with and without the modified HEART score. Including patients presenting with chest pain, visited by an ambulance, and transported to a hospital under a working diagnosis of NSTE-ACS. Primary outcomes measured were the HEART-score's interobserver agreement, the final diagnosis of NSTE-ACS at discharge, major adverse cardiovascular events (MACE) within 30 days, and the diagnostic accuracy of the testing methods. Conclusion The POPular HEART study aims to refine the diagnostic approach for NSTE-ACS, allowing for the early detection and exclusion of NSTE-ACS in the pre-hospital phase. The study seeks to reduce unnecessary hospital admissions and associated healthcare costs by improving the accuracy and reliability of NSTE-ACS diagnosis in the pre-hospital setting. Key findings The use of POC troponin testing by paramedics, when combined with the HEART score, can potentially streamline the diagnostic process for NSTE-ACS in the pre-hospital setting. High interobserver agreement suggests that the modified HEART-score is a reliable tool for assessing NSTE-ACS risk both pre-hospital and in-hospital. Early identification and exclusion of NSTE-ACS could significantly reduce unnecessary hospital stays, promoting more efficient use of healthcare resources. Implications for practice Implementing POC cTn testing and the HEART-score assessment in ambulance services could enhance the early diagnosis and management of NSTE-ACS. This approach may lead to a shift in how patients with suspected NSTE-ACS are triaged and managed, emphasizing the importance of accuracy and speed in the diagnostic process. Healthcare systems could see a reduction in the burden on emergency departments and in the overall costs associated with the care of patients with chest pain. Future directions Further research is needed to explore the scalability of implementing POC cTn testing and the HEART-score in diverse healthcare settings. Long-term studies could evaluate the impact of these diagnostic strategies on patient outcomes, healthcare costs, and system efficiency. Innovation in POC testing technology, reimbursement by health insurers and training for pre-hospital care providers will be critical to the widespread adoption of these strategies. [ABSTRACT FROM AUTHOR]

Background: The characterization of the different pathophysiological mechanisms involved in normotensive versus hypertensive acute heart failure (AHF) might help to develop individualized treatments. Methods: The extent of hemodynamic cardiac stress and cardiomyocyte injury was quantified by measuring the B-type natriuretic peptide (BNP), N-terminal proBNP (NT-proBNP), and high-sensitivity cardiac troponin T (hs-cTnT) concentrations in 1152 patients presenting with centrally adjudicated AHF to the emergency department (ED) (derivation cohort). AHF was classified as normotensive with a systolic blood pressure (SBP) of 90–140 mmHg and hypertensive with SBP > 140 mmHg at presentation to the ED. Findings were externally validated in an independent AHF cohort (n = 324). Results: In the derivation cohort, with a median age of 79 years, 43% being women, 667 (58%) patients had normotensive and 485 (42%) patients hypertensive AHF. Hemodynamic cardiac stress, as quantified by the BNP and NT-proBNP, was significantly higher in normotensive as compared to hypertensive AHF [1105 (611–1956) versus 827 (448–1419) pg/mL, and 5890 (2959–12,162) versus 4068 (1986–8118) pg/mL, both p < 0.001, respectively]. Similarly, the extent of cardiomyocyte injury, as quantified by hs-cTnT, was significantly higher in normotensive AHF as compared to hypertensive AHF [41 (24–71) versus 33 (19–59) ng/L, p < 0.001]. A total of 313 (28%) patients died during 360 days of follow-up. All-cause mortality was higher in patients with normotensive AHF vs. patients with hypertensive AHF (hazard ratio 1.66, 95%CI 1.31–2.10; p < 0.001). Normotensive patients with a high BNP, NT-proBNP, or hs-cTnT had the highest mortality. The findings were confirmed in the validation cohort. Conclusion: Biomarker profiling revealed a higher extent of hemodynamic stress and cardiomyocyte injury in patients with normotensive versus hypertensive AHF. [ABSTRACT FROM AUTHOR]

Assay-specific increases in circulating cardiac troponin are observed in 20–40% of patients after noncardiac surgery, depending on patient age, type of surgery, and comorbidities. Increased cardiac troponin is consistently associated with excess morbidity and mortality after noncardiac surgery. Despite these findings, the underlying mechanisms are unclear. The majority of interventional trials have been designed on the premise that ischaemic cardiac disease drives elevated perioperative cardiac troponin concentrations. We consider data showing that elevated circulating cardiac troponin after surgery could be a nonspecific marker of cardiomyocyte stress. Elevated concentrations of circulating cardiac troponin could reflect coordinated pathological processes underpinning organ injury that are not necessarily caused by ischaemia. Laboratory studies suggest that matching of coronary artery autoregulation and myocardial perfusion–contraction coupling limit the impact of systemic haemodynamic changes in the myocardium, and that type 2 ischaemia might not be the likeliest explanation for cardiac troponin elevation in noncardiac surgery. The perioperative period triggers multiple pathological mechanisms that might cause cardiac troponin to cross the sarcolemma. A two-hit model involving two or more triggers including systemic inflammation, haemodynamic strain, adrenergic stress, and autonomic dysfunction might exacerbate or initiate acute myocardial injury directly in the absence of cell death. Consideration of these diverse mechanisms is pivotal for the design and interpretation of interventional perioperative trials. [ABSTRACT FROM AUTHOR]

Acute coronary syndrome (ACS) includes myocardial infarction (MI) and unstable angina (UA). MI is defined by elevated necrosis markers, preferably high-sensitivity cardiac troponins (hs-cTn). However, it takes hours for cTn to become elevated after coronary occlusion; therefore, difficulties are associated with diagnosing early post-onset MI or UA. The aim of this prospective cohort study was to examine the diagnostic ability of serum nardilysin (NRDC) for the early detection of ACS. This study consisted of two sequential cohorts, the Phase I cohort, 435 patients presenting to the emergency room (ER) with chest pain, and the Phase II cohort, 486 patients with chest pain who underwent coronary angiography. The final diagnosis was ACS in 155 out of 435 patients (35.6%) in the phase I and 418 out of 486 (86.0%) in the phase II cohort. Among 680 patients who presented within 24 h of onset, 466 patients (68.5%) were diagnosed with ACS. Serum NRDC levels were significantly higher in patients with ACS than in those without ACS. The sensitivity of NRDC in patients who presented within 6 h after the onset was higher than that of hsTnI, and the AUC of NRDC within 1 h of the onset was higher than that of hsTnI (0.718 versus 0.633). Among hsTnI-negative patients (300 of 680 patients: 44.1%), 136 of whom (45.3%) were diagnosed with ACS, the sensitivity and the NPV of NRDC were 73.5 and 65.7%, respectively. When measured in combination with hsTnI, NRDC plays auxiliary roles in the early diagnosis of ACS. [ABSTRACT FROM AUTHOR]

The troponin complex—consisting of three subunits: troponin C (TnC), cardiac troponin I (cTnI) and cardiac troponin T (cTnT)—plays a key role in the regulation of myocardial contraction. Troponins are preferentially localized in the cytoplasm and bind to myofibrils. However, numerous, albeit scattered, studies have shown the presence of troponins in the nuclei of muscle cells. There is increasing evidence that the nuclear localization of troponins may be functionally important, making troponins an important nuclear player in the pathogenesis of various diseases including cancer and myopathies. Further studies in this area could potentially lead to the development of treatments for certain pathologies. In this review, we collected and discussed recent data on the properties of non-canonically localized cardiac troponins, the molecular mechanisms leading to this non-canonical localization, and the possible functions or pathological effects of these non-canonically localized troponins. [ABSTRACT FROM AUTHOR]

Cardiac troponin serum concentration is the primary marker used for the diagnosis of acute coronary syndrome. Moreover, the measurement of cardiac troponin concentration is important for risk stratification in patients with pulmonary embolism. The cardiac troponin level is also a general marker of myocardial damage, regardless of etiology. The purpose of this study is to conduct a literature review and present the most important information regarding the current state of knowledge on the cardiac troponin serum concentration in patients with chronic cardiovascular disease (CVD), as well as on the relationships between cardiac troponin serum concentration and features of subclinical cardiovascular dysfunction. According to research conducted to date, patients with CVDs, such as chronic coronary syndrome, chronic lower extremities' ischemia, and cerebrovascular disease, are characterized by higher cardiac troponin concentrations than people without a CVD. Moreover, the literature data indicate that the concentration of cardiac troponin is correlated with markers of subclinical dysfunction of the cardiovascular system, such as the intima–media thickness, pulse wave velocity, ankle–brachial index, coronary artery calcium index (the Agatston score), and flow-mediated dilation. However, further research is needed in various patient subpopulations and in different clinical contexts. [ABSTRACT FROM AUTHOR]

A selective fluorescence turn-on immunosensor for the specific detection of cardiac troponin I (cTnI), the potent biomarker for myocardial infarction diagnosis, was developed with a nano couple comprised of protein-stabilized gold nanocluster and gold nanoparticle. The red fluorescence of cTnI-specific antibody tagged bovine serum albumin stabilized gold nanoclusters was quenched with gold nanoparticles (AuNP) via the intensive interaction between amine and hydroxyl functionalities of BSA and AuNP. Through this, the adsorption of gold nanoclusters at the surface of AuNP, resulting in a core-satellite assembly, was assumed to quench the fluorescence emission. While in the presence of cTnI antigen, this gets disturbed due to the formation of immunocomplex between cTnI antigen and antibody, which restricts the close interaction between gold clusters and nanoparticles, thereby restoring quenched fluorescence. The enhancement in fluorescence signal is directly related to the concentration of cTnI, and this facilitates the selective detection of cTnI in the linear concentration range 0.7 to 10 ng/mL without any interference from other potentially interfering co-existing biomolecules. An appreciable limit of detection of 0.51 ng/mL and a limit of quantification of 0.917 ng/mL for cTnI is comparable to that of the previous report. [ABSTRACT FROM AUTHOR]

Background Biomarkers simplifying the diagnostic workup by discriminating between non–ST‐segment–elevation myocardial infarction (NSTEMI) and infarct‐like myocarditis are an unmet clinical need. Methods and Results A total of 105 subjects were categorized into groups as follows: ST‐segment−elevation myocardial infarction (n=36), NSTEMI (n=22), infarct‐like myocarditis (n=19), cardiomyopathy‐like myocarditis (n=18), and healthy control (n=10). All subjects underwent cardiac magnetic resonance imaging, and serum concentrations of matrix metalloproteinase‐1 (MMP‐1) and procollagen type I carboxy terminal propeptide (PICP) were measured. Biomarker concentrations in subjects presenting with acute coronary syndrome and non‐ST‐segment‐elevation, for example NSTEMI or infarct‐like myocarditis, categorized as the non−ST‐segment−elevation acute coronary syndrome−like cohort, were of particular interest for this study. Compared with healthy controls, subjects with myocarditis had higher serum concentrations of MMP‐1 and PICP, while no difference was observed in individuals with myocardial infarction. In the non−ST‐segment−elevation acute coronary syndrome−like cohort, MMP‐1 concentrations discriminated infarct‐like myocarditis and NSTEMI with an area under the receiver operating characteristic curve (AUC) of 0.95 (95% CI, 0.89−1.00), whereas high‐sensitivity cardiac troponin T performed inferiorly (AUC, 0.74 [95% CI, 0.58−0.90]; P=0.012). Application of an optimal MMP‐1 cutoff had 94.4% sensitivity (95% CI, 72.7%−99.9%) and 90.9% specificity (95% CI, 70.8%−98.9%) for the diagnosis of infarct‐like myocarditis in this cohort. The AUC of PICP in this context was 0.82 (95% CI, 0.68−0.97). As assessed by likelihood ratio tests, incorporating MMP‐1 or PICP with age and C‐reactive protein into composite prediction models enhanced their diagnostic performance. Conclusions MMP‐1 and PICP could potentially be useful biomarkers for differentiating between NSTEMI and infarct‐like myocarditis in individuals with non−ST‐segment−elevation acute coronary syndrome‐like presentation, though further research is needed to validate their clinical applicability.

Objective and rationale: This study aimed to develop a highly sensitive and selective single-stranded DNA (ssDNA) aptamer targeting cardiac troponin I (cTnI), a crucial biomarker for acute myocardial infarction (AMI). The objective was to fabricate a novel aptamer electrochemical sensor using a composite material of cobalt-nickel metal-organic framework (CoNi-MOF) on screen-printed carbon electrodes (SPCE), leveraging the composite's large surface area and excellent electrical conductivity alongside the aptamer's high affinity for cTnI. Methods: The aptamer electrochemical sensor was fabricated using the CoNi-MOF composite on SPCE and characterized its properties. They conducted electrochemical measurements to assess the sensor's performance in detecting cTnI. The sensor's stability, reproducibility, and electro-catalytic activity were evaluated. Results: The sensor demonstrated linear detection of cTnI over a concentration range of 5–75 pg/mL, with a low limit of detection (LOD) of 13.2 pM. Remarkable stability and reproducibility were observed in cTnI detection. The sensor exhibited exceptional electro-catalytic activity, enabling accurate quantification of cTnI levels in various solutions. Conclusions: This research presents a significant advancement towards the development of reliable, cost-effective, and easily deployable cTnI sensors for clinical applications. The sensor's versatility in detecting cTnI across different concentration ranges highlights its potential utility in diverse clinical settings, particularly for early detection and monitoring of cardiac conditions.

Cardiac troponin is extensively used as a biomarker in modern medicine due to its diagnostic capability for myocardial injury, as well as its predictive and prognostic value for cardiac diseases. However, heterophile antibodies, antitroponin antibodies, and macrotroponin complexes can be observed both in seemingly healthy individuals and patients with cardiac diseases, potentially leading to false positive or disproportionate elevation of cTn (cardiac troponin) assay results and introducing discrepancies in clinical interpretations with impact on medical management. In this review article, we describe the possible mechanisms of cTn release and the sources of variations in the assessment of circulating cTn levels. We also explore the pathophysiological mechanisms underlying antitroponin antibody development and discuss the influence exerted by macrotroponin complexes on the results of immunoassays. Additionally, we explore approaches to detect these complexes by presenting various clinical scenarios encountered in routine clinical practice. Finally, unsolved questions about the development, prevalence, and clinical significance of cardiac autoantibodies are discussed.

Background. Periprocedural myocardial injury (PMI) is an acute complication of percutaneous coronary interventions (PCI) in patients with stable coronary artery disease. Its frequency and relationship with the prognosis of the disease are especially important in elective interventions due to the low risk of ischemic events in this cohort of patients. However, according to the literature, there are significant differences in the criteria for PMI and type 4a myocardial infarction (MI), and, accordingly, their frequency and their prognostic value. Aim. To study the frequency and magnitude of PMI during elective PCI in terms of the level of periprocedural increase in cardiospecific biomarkers, as well as to determine the relationship of PMI with long-term adverse events in patients with chronic coronary artery disease. Materials and methods. A single-center open retrospective cohort study was conducted, which included 435 patients (367/84.4 % men, mean age 58.3±8.6 years) from the elective PCI registry. PMI was diagnosed with an increase in the level of creatine phosphokinase MB fraction (CK-MB) or or cardiac troponin I (cTn I) >1×99 percentile URL (Upper Reference Limit), while the level of increase in biomarkers >1, 2, 3, 4 or >5×99 percentile URL was recorded. An increase in biomarkers >5x99 URL percentile was assessed as a large PMI, and in the presence of clinical and imaging evidence of new loss of viable myocardium, as periprocedural MI type 4a. Depending on the level of periprocedural increase in biomarkers, the relative risk (RR) of developing long-term (within 5 years after index PCI) adverse cardiovascular events, death, as well as clinically significant bleeding and newly diagnosed malignant oncological diseases was calculated. In addition, the correlation between PMI and the above endpoints was summarized using Kaplan-Meier analysis. Results. The frequency of periprocedural PMI diagnosed by increased biomarkers >1×99 percentile URL was 40.2 %, >2×99 percentile URL — 9.7 %, >3×99 percentile URL — 6.7 %, >4×99 percentile URL — 4.8 %, >5×99 percentile URL — 3.5 %, type 4a MI — in 2 patients (0.46 %). An association of “major” PMI (>5x99 percentile URL) with cardiovascular complications within 3 years after elective PCI, including fatal ones, was revealed: for acute myocardial infarction (AMI), RR — 6.516, confidence interval (CI) [2.375-17.881]; for death from cardiovascular causes RR — 6.538, CI [1.695-25.227]. An association of “moderate” PMI (>3, but 1, but 1, but

Abstract Background Whether distributions and prognostic values of high-sensitivity cardiac troponin (hs-cTn) T and I are different across normoglycemic, prediabetic, and diabetic populations is unknown. Methods 10127 adult participants from the National Health and Nutrition Examination Survey 1999–2004 with determined glycemic status and measurement of at least one of hs-cTn assays were included, from whom healthy participants and presumably healthy diabetic and prediabetic participants were selected to investigate pure impacts of glycemic status on distributions of hs-cTn. The nonparametric method and bootstrapping were used to derive the 99th upper reference limits of hs-cTn and 95% CI. Participants with available follow-up and hs-cTn concentrations of all 4 assays were included in prognostic analyses. Associations of hs-cTn with all-cause and cardiac-specific mortality were modeled by Cox proportional hazard regression under the complex survey design. The incremental value of hs-cTn to an established risk score in predicting cardiac-specific mortality was assessed by the 10-year area under time-dependent receiver operating characteristic curve (AUC) using the Fine-Grey competing risk model. Results Among 9714 participants included in prognostic analyses, 5946 (61.2%) were normoglycemic, 2172 (22.4%) prediabetic, and 1596 (16.4%) diabetic. Hyperglycemic populations were older than the normoglycemic population but sex and race/ethnicity were similar. During the median follow-up of 16.8 years, hs-cTnT and hs-cTnI were independently associated with all-cause and cardiac-specific mortality across glycemic status. In the diabetic population, adjusted hazard ratios per 1-standard deviation increase of log-transformed hs-cTnT and hs-cTnI (Abbott) concentrations were 1.77 (95% CI 1.48–2.12; P

Unstable angina (UA) is a type of acute coronary syndrome (ACS) without ischemic myocardial damage. The main criterion for the diagnosis of UA in ACS is the absence of changes in the concentration of cardiac troponin in the patient’s blood. When the volume of myocardial damage is small, it may be difficult to detect myocardial infarction in a patient using low-sensitivity tests for determining of cardiac troponin in the blood. This issue may lead to overdiagnosis of UA in patients with non-STE ACS. Optimal drug therapy and revascularization of the coronary arteries significantly reduce the risk of death and the development of myocardial infarction both in the hospital and in the long-term period in patients with UA. Outpatient follow-up and provision of free of charge medications to patients may reduce long-term mortality after an episode of UA.

ABSTRACTBackground Elevated brain natriuretic peptide (BNP) is crucial to detect perioperative adverse cardiovascular events in patients with cardiac risk, even at low elevation of BNP level or when myocardial necrosis has not been already established. This study aims to compare between two anaesthesia methods in preventing perioperative myocardial infarction for patients having cardiac risk undergoing total knee arthroplasty (TKA).Patients and methods Fifty adult patients planned for TKA with risk factors as ischemic heart disease, diabetics, hypertensive, heavy smokers or body mass index ≥ 35 were categorized randomly into two groups. Group (S): received spinal anaesthesia followed by continuous ultrasound guided femoral nerve block once spinal motor blockade had been resolved. Group (G): received combined general and lumber epidural anaesthesia. BNP, cardiac troponins, pain severity, analgesic consumption, patients’ satisfaction and adverse cardiac events were observed preoperatively and extended to 2 days postoperatively.Results Baseline readings of BNP and cardiac troponins were comparable in both members. At 24 and 48 hours postoperatively, it decreased significantly in group S compared to group G. Mean Visual analogue score was significantly lower in group S comparative to group G at all times except at 40 and 48 hours postoperatively. Morphine utilization was significantly lower in group S. Patients in group S were significantly more satisfied than those in group G.Conclusions The use of spinal anaesthesia with continuous femoral nerve block can reduce the prevalence of perioperative myocardial infarction in patients with cardiac risk undergoing TKA.

Background: Whether distributions and prognostic values of high-sensitivity cardiac troponin (hs-cTn) T and I are different across normoglycemic, prediabetic, and diabetic populations is unknown. Methods: 10127 adult participants from the National Health and Nutrition Examination Survey 1999–2004 with determined glycemic status and measurement of at least one of hs-cTn assays were included, from whom healthy participants and presumably healthy diabetic and prediabetic participants were selected to investigate pure impacts of glycemic status on distributions of hs-cTn. The nonparametric method and bootstrapping were used to derive the 99th upper reference limits of hs-cTn and 95% CI. Participants with available follow-up and hs-cTn concentrations of all 4 assays were included in prognostic analyses. Associations of hs-cTn with all-cause and cardiac-specific mortality were modeled by Cox proportional hazard regression under the complex survey design. The incremental value of hs-cTn to an established risk score in predicting cardiac-specific mortality was assessed by the 10-year area under time-dependent receiver operating characteristic curve (AUC) using the Fine-Grey competing risk model. Results: Among 9714 participants included in prognostic analyses, 5946 (61.2%) were normoglycemic, 2172 (22.4%) prediabetic, and 1596 (16.4%) diabetic. Hyperglycemic populations were older than the normoglycemic population but sex and race/ethnicity were similar. During the median follow-up of 16.8 years, hs-cTnT and hs-cTnI were independently associated with all-cause and cardiac-specific mortality across glycemic status. In the diabetic population, adjusted hazard ratios per 1-standard deviation increase of log-transformed hs-cTnT and hs-cTnI (Abbott) concentrations were 1.77 (95% CI 1.48–2.12; P <.001) and 1.83 (95% CI 1.33–2.53; P <.001), respectively, regarding cardiac-specific mortality. In the diabetic but not the normoglycemic population, adding either hs-cTnT (difference in AUC: 0.062; 95% CI 0.038–0.086; P < 0.001) or hs-cTnI (Abbott) (difference in AUC: 0.071; 95% CI 0.046–0.097; P < 0.001) would significantly increase the discriminative ability of the risk score; AUC of the score combined with hs-cTnT would be further improved by incorporating hs-cTnI (0.018; 95%CI 0.006–0.029; P = 0.002). The 99th percentile of hs-cTnT of the presumably healthy diabetic population was higher than the healthy population and had no overlap in 95% CIs, however, for hs-cTnI 99th percentiles of the two populations were very close and 95% CIs extensively overlapped. Conclusions: Hs-cTnT and hs-cTnI demonstrated consistent prognostic associations across glycemic status but incremental predictive values in hyperglycemic populations only. The susceptibility of hs-cTnT 99th percentiles to diabetes plus the additive value of hs-cTnI to hs-cTnT in diabetic cardiovascular risk stratification suggested hs-cTnI and hs-cTnT may be differentially associated with glycemic status, but further research is needed to illustrate the interaction between hyperglycemia and hs-cTn. [ABSTRACT FROM AUTHOR]

Cardiac surgery may lead to myocardial damage and release of cardiac biomarkers through various mechanisms such as cardiac manipulation, systemic inflammation, myocardial hypoxia, cardioplegic arrest and ischaemia caused by coronary or graft occlusion. Defining perioperative myocardial infarction (PMI) after cardiac surgery presents challenges, and the association between the current PMI definitions and postoperative outcomes remains uncertain. To address these challenges, the European Association of Cardio-Thoracic Surgery (EACTS) facilitated collaboration among a multidisciplinary group to evaluate the existing evidence on the mechanisms, diagnosis and prognostic implications of PMI after cardiac surgery. The review found that the postoperative troponin value thresholds associated with an increased risk of mortality are markedly higher than those proposed by all the current definitions of PMI. Additionally, it was found that large postoperative increases in cardiac biomarkers are prognostically relevant even in absence of additional supportive signs of ischaemia. A new algorithm for PMI detection after cardiac surgery was also proposed, and a consensus was reached within the group that establishing a prognostically relevant definition of PMI is critically needed in the cardiovascular field and that PMI should be included in the primary composite outcome of coronary intervention trials. [ABSTRACT FROM AUTHOR]

End-stage renal disease is associated with a high risk of cardiovascular disease. We compared the concentration and prognostic ability of high sensitivity cardiac troponin T (hs-cTnT) and I (hs-cTnI) and cardiac myosin-binding protein C (cMyC) among stable hemodialysis patients. Patients were sampled before and after hemodialysis. We measured hs-cTnI, hs-cTnT and cMyC and used Cox regressions to assess the association between quartiles of concentrations and all-cause mortality and a combination of cardiovascular events and all-cause mortality during follow-up. A total of 307 patients were included, 204 males, mean age 66 years (SD 14). Before dialysis, 299 (99 %) had a hs-cTnT concentration above the 99th percentile, compared to 188 (66 %) for cMyC and 35 (11 %) for hs-cTnI. Hs-cTnT (23 %, p<0.001) and hs-cTnI (15 %, p=0.049) but not cMyC (4 %, p=0.256) decreased during dialysis. Follow-up was a median of 924 days (492–957 days); patients in the 3rd and 4th quartiles of hs-cTnT (3rd:HR 3.0, 95 % CI 1.5–5.8, 4th:5.2, 2.7–9.8) and the 4th quartile of hs-cTnI (HR 3.8, 2.2–6.8) had an increased risk of mortality. Both were associated with an increased risk of the combined endpoint for patients in the 3rd and 4th quartiles. cMyC concentrations were not associated with risk of mortality or cardiovascular event. Hs-cTnT was above the 99th percentile in almost all patients. This was less frequent for hs-cTnI and cMyC. High cTn levels were associated with a 3-5-fold higher mortality. This association was not present for cMyC. These findings are important for management of hemodialysis patients. [ABSTRACT FROM AUTHOR]

Background: The European Society of Cardiology (ESC) guidelines recommend a dynamic (0-1h) cardiac troponin (cTn) determination for non-ST elevation myocardial infarction diagnosis. For patients with low cTn levels, a discharge from emergency can be considered. Nevertheless, cTn cutoffs for discharge are lower than the limits of quantification proposed by laboratory reagent suppliers. Aim: Validate cTn assay on the Elecsys STAT kit. Materials and methods: Precision, trueness, repeatability and within-laboratory variability were calculated from internal quality control and plasma pooled at 5.78 and 10.73 ng/L. Accuracy was calculated from external quality control. Uncertainty of measurement was calculated from (i) the uncertainty of the standard and control values and (ii) by precision from pooled plasma. Distribution of precision results from pooled plasma has been evaluated by bootstrap simulations. Dilution linearity tests with patient plasma were performed to evaluate the method for values near 5 ng/L. Results: Precision and trueness ranged from 1.35 to 4.45% and from 0.14 to −3.74%, respectively. Accuracy results ranged from 101.40 to 104.90%. Within laboratory variability was 2.91%. Uncertainty ranged from 3.66% to 19.90% for higher (2188) to lower values (5.78 ng/L). Bootstrap simulations allowed utilization of precision data from pooled plasma to evaluate cTn assay. The method was linear from 4.48 to 39.80 ng/L. A linear regression model best described the data. Conclusion: Elecsys STAT method provides accurate cTn results, including patients with cTn results categorizing them as 'rule-out' in the ESC guidelines. [ABSTRACT FROM AUTHOR]

Type II myocardial injury following surgical procedures is associated with adverse outcomes. The prognostic value of high-sensitivity cardiac troponin (hs-cTn) due to type II myocardial injury in surgical patients admitted to intensive care unit (ICU) remains unclear. The aim of this study was to assess prognostic value of hs-cTn in type II acute myocardial injury in non-cardiac surgical patients requiring post-operative ICU admission. Retrospective analysis of patients admitted to two level III ICUs following surgery and had hs-cTn measured on the day of ICU admission. Patients who had type I acute myocardial infarction (AMI) during their admission were excluded from the study. The primary outcome was hospital mortality. Secondary outcomes included ICU mortality, ICU length of stay (LOS) and hospital LOS. A total of 420 patients were included. On univariable analysis, higher hs-cTn was associated with increased hospital mortality (14.6% vs 6.3%, p = 0.008), ICU LOS (41.1 h, vs 25 h, p = 0.004) and hospital LOS (253 h vs 193 h, p = 0.02). On multivariable analysis, hs-cTn was not independently associated with increased risk of hospital mortality. However, in patients who had elective surgery, hs-cTn was associated with increased risk (OR 1.048; 95% CI 1.004–1.094; p = 0.031) of hospital mortality with area under the receiver operating characteristic curve of 0.753 (95% CI 0.598–0.908). In elective surgical patients, hs-cTn was associated with increased risk of mortality. Larger multicentre studies are required to confirm this association that may assist in risk stratification of elective surgical patients requiring ICU admission. [ABSTRACT FROM AUTHOR]

The effect of Eucalyptus globulus in diabetic cardiac dysfunction and the possible mechanisms involved have not been explored. To evaluate the effect of ethanol leaf extract of E. globulus (NEE) on the cardiac function of fructose/streptozotocin-induced diabetic rats. Type-2 diabetes was induced in rats with 10% fructose feeding for 14 days and an intraperitoneal administration of 40 mg/kg streptozotocin. Diabetic animals were treated with NEE (100–400 mg/kg) or 5 mg/kg glibenclamide orally for 21 days. Biochemical assays, histopathological examination and analyses of PCSK9, Rho kinase and Cardiac troponin expression were performed. The untreated diabetic group showed decreased expression of the genes, oxidative stress, dyslipidemia, increased activities of creatine kinase MB and lactate dehydrogenase, reduced nitric oxide level, and depletion of cardiomyocytes, which were reversed in NEE treated groups. Eucalyptus globulus ameliorated diabetic cardiac dysfunction through increased PCSK9, Rho kinase and Cardiac troponin expression. [ABSTRACT FROM AUTHOR]

Objectives. Perioperative myocardial injury (PMI) is increasingly recognised as an important complication of non-cardiac surgery, with often clinically silent presentation, but detrimental prognosis. Active screening for PMI, involving the detection of dynamic and elevated levels of cardiac troponin, has recently been advocated by an increasing number of guidelines; however, active PMI screening has not been reflected in clinical practice. Design. As consensus on a common screening and management pathway is lacking, we synthesise the current evidence to provide suggestions on the selection of patients for screening, organisation of a screening program, and a potential management pathway, building upon a recently published perioperative screening algorithm. Results. Screening should be performed using high-sensitivity assays both preoperatively and postoperatively (postoperative Days 1 and 2) in patients at high-risk of experiencing perioperative complications. Conclusion. This expert opinion piece by an interdisciplinary group of predominantly Norwegian clinicians aims to assist healthcare professionals planning to implement guideline-recommended PMI screening at a local level in order to improve patient outcomes following non-cardiac surgery. [ABSTRACT FROM AUTHOR]

Background: Elevated brain natriuretic peptide (BNP) is crucial to detect perioperative adverse cardiovascular events in patients with cardiac risk, even at low elevation of BNP level or when myocardial necrosis has not been already established. This study aims to compare between two anaesthesia methods in preventing perioperative myocardial infarction for patients having cardiac risk undergoing total knee arthroplasty (TKA). Patients and methods: Fifty adult patients planned for TKA with risk factors as ischemic heart disease, diabetics, hypertensive, heavy smokers or body mass index = 35 were categorized randomly into two groups. Group (S): received spinal anaesthesia followed by continuous ultrasound guided femoral nerve block once spinal motor blockade had been resolved. Group (G): received combined general and lumber epidural anaesthesia. BNP, cardiac troponins, pain severity, analgesic consumption, patients' satisfaction and adverse cardiac events were observed preoperatively and extended to 2 days postoperatively. Results: Baseline readings of BNP and cardiac troponins were comparable in both members. At 24 and 48 hours postoperatively, it decreased significantly in group S compared to group G. Mean Visual analogue score was significantly lower in group S comparative to group G at all times except at 40 and 48 hours postoperatively. Morphine utilization was significantly lower in group S. Patients in group S were significantly more satisfied than those in group G. Conclusions: The use of spinal anaesthesia with continuous femoral nerve block can reduce the prevalence of perioperative myocardial infarction in patients with cardiac risk undergoing TKA. [ABSTRACT FROM AUTHOR]

Background Subclinical myocardial injury expressed as higher cardiac troponin concentrations may represent an important intermediary between hypertension and the risk of cardiovascular disease. The study aimed to assess the relative strength of associations between systolic blood pressure (BP), diastolic BP, and pulse pressure, and subclinical myocardial injury, and how change in BP variables over time associates with subclinical myocardial injury. Methods and Results cTnl (cardiac troponin I) was measured in 32 968 participants of the fourth wave of the population‐based cohort HUNT4 (Trøndelag Health Study) without a history of cardiovascular disease. An additional longitudinal analysis included participants from HUNT4 with BP measurements from HUNT3 (n=18 681). Associations between BP variables and cTnI concentrations were assessed by linear and logistic regression analyses. The median cTnI concentration was 1.6 ng/L (25th–75th percentiles, 0.6–3.1 ng/L), median age was 52 years (39.1–65.6 years), and 57% were female subjects. Cross‐sectionally, only systolic BP categories ≥130 mm Hg associated with higher cTnI concentrations, compared with a reference systolic BP of

Background Subclinical myocardial injury in form of hs‐cTn (high‐sensitivity cardiac troponin) levels has been associated with cognitive impairment and imaging markers of cerebral small vessel disease (SVD) in population‐based and cardiovascular cohorts. Whether hs‐cTn is associated with domain‐specific cognitive decline and SVD burden in patients with stroke remains unknown. Methods and Results We analyzed patients with acute stroke without premorbid dementia from the prospective multicenter DEMDAS (DZNE [German Center for Neurodegenerative Disease]‐Mechanisms of Dementia after Stroke) study. Patients underwent neuropsychological testing 6 and 12 months after the index event. Test results were classified into 5 cognitive domains (language, memory, executive function, attention, and visuospatial function). SVD markers (lacunes, cerebral microbleeds, white matter hyperintensities, and enlarged perivascular spaces) were assessed on cranial magnetic resonance imaging to constitute a global SVD score. We examined the association between hs‐cTnT (hs‐cTn T levels) and cognitive domains as well as the global SVD score and individual SVD markers, respectively. Measurement of cognitive and SVD‐marker analyses were performed in 385 and 466 patients with available hs‐cTnT levels, respectively. In analyses adjusted for demographic characteristics, cardiovascular risk factors, and cognitive status at baseline, higher hs‐cTnT was negatively associated with the cognitive domains “attention” up to 12 months of follow‐up (beta‐coefficient, −0.273 [95% CI, −0.436 to −0.109]) and “executive function” after 12 months. Higher hs‐cTnT was associated with the global SVD score (adjusted odds ratio, 1.95 [95% CI, 1.27–3.00]) and the white matter hyperintensities and lacune subscores. Conclusions In patients with stroke, hs‐cTnT is associated with a higher burden of SVD markers and cognitive function in domains linked to vascular cognitive impairment. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT01334749.

Background Sex differences in presentation, treatment, and prognosis of cardiovascular disorders are well recognized. Although an association between acute myocardial injury and mortality after ischemic stroke has been demonstrated, it is unclear whether prevalence and outcome of poststroke acute myocardial injury differ between women and men. Methods and Results We prospectively screened consecutive patients with acute ischemic stroke and serial high‐sensitivity cardiac troponin T measurements admitted to our center. Acute myocardial injury was defined as at least 1 high‐sensitivity cardiac troponin T value above the upper reference limit (14 ng/L) with a rise/fall of >20%. Rates of acute myocardial injury were also calculated using sex‐specific high‐sensitivity cardiac troponin T cutoffs (women upper reference limit, 9 ng/L; men upper reference limit, 16 ng/L). Logistic regression analyses were performed to evaluate the association between acute myocardial injury and outcomes. Of 1067 patients included, 494 were women (46%). Women were older, had a higher rate of known atrial fibrillation, were more likely to be functionally dependent before admission, had higher stroke severity, and more often had cardioembolic strokes (all P values

Objectives Troponins are classically raised in acute coronary syndrome (ACS) although other cardiovascular and non-cardiovascular causes are recognized. We aimed to see the association of high sensitivity (Hs) Troponin I values exceeding the sex-specific 99th percentile upper reference limit (URL) with diagnoses, emergency department (ED) outcomes, 30-day outcomes of admitted patients and predictors of ACS in both genders.

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Background: There is an unmet medical need for the early detection of immune checkpoint inhibitor (ICI)-induced cardiovascular (CV) adverse events due to a lack of adequate biomarkers. This study aimed to provide insights on the incidence of troponin elevations and echocardiographic dynamics during ICI treatment in cancer patients and their role as potential biomarkers for submyocardial damage. In addition, it is the first study to compare hs-TnT and hs-TnI in ICI-treated patients and to evaluate their interchangeability in the context of screening. Results: Among 59 patients, the mean patient age was 68 years, and 76% were men. Overall, 25% of patients received combination therapy. Although 10.6% [95% CI: 5.0–22.5] of the patients developed troponin elevations, none experienced a CV event. No significant changes were found in 3D left ventricular (LV) ejection fraction nor in global longitudinal strain f (56 ± 6% vs. 56 ± 6%, p = 0.903 and −17.8% [−18.5; −14.2] vs. −17.0% [−18.8; −15.1], p = 0.663) at 3 months. There were also no significant changes in diastolic function and right ventricular function. In addition, there was poor agreement between hs-TnT and hs-TnI. Methods: Here, we present a preliminary analysis of the first 59 patients included in our ongoing prospective clinical trial (NCT05699915) during the first three months of treatment. All patients underwent electrocardiography and echocardiography along with blood sampling at standardized time intervals. This study aimed to investigate the incidence of elevated hs-TnT levels within the first three months of ICI treatment. Elevations were defined as hs-TnT above the upper limit of normal (ULN) if the baseline value was normal, or 1.5 ≥ times baseline if the baseline value was above the ULN. Conclusions: Hs-TnT elevations occurred in 10.6% of the patients. However, no significant changes were found on 3D echocardiography, nor did any of the patients develop a CV event. There were also no changes found in NT-proBNP. The study is still ongoing, but these preliminary findings do not show a promising role for cardiac troponins nor for echocardiographic dynamics in the prediction of CV events during the early stages of ICI treatment.

The selection of an appropriate transducer is a key element in biosensor development. Currently, a wide variety of substrates and working electrode materials utilizing different fabrication techniques are used in the field of biosensors. In the frame of this study, the following three specific material configurations with gold-finish layers were investigated regarding their efficacy to be used as electrochemical (EC) biosensors: (I) a silicone-based sensor substrate with a layer configuration of 50 nm SiO/50 nm SiN/100 nm Au/30–50 nm WTi/140 nm SiO/bulk Si); (II) polyethylene naphthalate (PEN) with a gold inkjet-printed layer; and (III) polyethylene terephthalate (PET) with a screen-printed gold layer. Electrodes were characterized using electrochemical impedance spectroscopy (EIS) and cyclic voltammetry (CV) to evaluate their performance as electrochemical transducers in an aptamer-based biosensor for the detection of cardiac troponin I using the redox molecule hexacyanoferrade/hexacyaniferrade (K3[Fe (CN)6]/K4[Fe (CN)6]. Baseline signals were obtained from clean electrodes after a specific cleaning procedure and after functionalization with the thiolate cardiac troponin I aptamers “Tro4” and “Tro6”. With the goal of improving the PEN-based and PET-based performance, sintered PEN-based samples and PET-based samples with a carbon or silver layer under the gold were studied. The effect of a high number of immobilized aptamers will be tested in further work using the PEN-based sample. In this study, the charge-transfer resistance (Rct), anodic peak height (Ipa), cathodic peak height (Ipc) and peak separation (∆E) were determined. The PEN-based electrodes demonstrated better biosensor properties such as lower initial Rct values, a greater change in Rct after the immobilization of the Tro4 aptamer on its surface, higher Ipc and Ipa values and lower ∆E, which correlated with a higher number of immobilized aptamers compared with the other two types of samples functionalized using the same procedure.