Release Of Cardiac Troponin Research Articles

Composition of cardiac troponin release differs after marathon running and myocardial infarction

ObjectivesElevations of cardiac troponin T (cTnT) levels are common after strenuous exercise. We assessed whether the composition of cTnT release after marathon race differs from that of acute myocardial infarction (MI).MethodsTroponin composition was analysed in plasma samples taken from 45 runners after marathon race and from 84 patients with type 1 MI. The concentration of long cTnT (intact and mildly fragmented cTnT) was measured with a novel upconversion luminescence immunoassay, total cTnT with a commercial high-sensitivity cTnT assay, and the ratio of long to total cTnT (troponin ratio) was determined as a measure of troponin fragmentation.ResultsTotal cTnT exceeded the upper reference limit (>14 ng/L) in 37 (82%) runners. Troponin ratio was lower in runners ((IQR) 0.17 (0.11–0.24) vs 0.62 (0.29–0.96), p<0.001). With increasing troponin release the troponin ratio decreased (r=−0.497, p<0.001) in marathon runners and the concentration of long cTnT remained in all runners below 8.4 ng/L. In contrast to marathon runners, troponin ratio increased (r=0.565, p<0.001) with the increase of cTnT release in patients with MI. The median total and long cTnT concentrations were lower in marathon runners than in patients with MI (25 ng/L vs 835 ng/L and 4.1 vs 385 ng/L, p<0.001 for both).ConclusionIn contrast to type 1 MI, only a small fraction of circulating cTnT exists as intact cTnT or long molecular forms after strenuous exercise and the difference in troponin composition is more pronounced in runners with higher troponin release.Trial registration numberNCT06000930.

The Role of High-Sensitivity Troponin T Regarding Prognosis and Cardiovascular Outcome across Heart Failure Spectrum.

Background: Cardiac troponin release is related to the cardiomyocyte loss occurring in heart failure (HF). The prognostic role of high-sensitivity cardiac troponin T (hs-cTnT) in several settings of HF is under investigation. The aim of the study is to assess the prognostic role of intrahospital hs-cTnT in patients admitted due to HF. Methods: In this observational, single center, prospective study, patients hospitalized due to HF have been enrolled. Admission, in-hospital peak, and discharge hs-cTnT have been assessed. Patients were followed up for 6 months. Cardiovascular (CV) death, HF hospitalization (HFH), and worsening HF (WHF) (i.e., urgent ambulatory visit/loop diuretics escalation) events have been assessed at 6-month follow up. Results: 253 consecutive patients have been enrolled in the study. The hs-cTnT median values at admission and discharge were 0.031 ng/mL (IQR 0.02-0.078) and 0.031 ng/mL (IQR 0.02-0.077), respectively. The risk of CV death/HFH was higher in patients with admission hs-cTnT values above the median (p = 0.02) and in patients who had an increase in hs-cTnT during hospitalization (p = 0.03). Multivariate Cox regression analysis confirmed that hs-cTnT above the median (OR: 2.06; 95% CI: 1.02-4.1; p = 0.04) and increase in hs-cTnT during hospitalization (OR:1.95; 95%CI: 1.006-3.769; p = 0.04) were predictors of CV death/HFH. In a subgroup analysis of patients with chronic HF, hs-cTnT above the median was associated with increased risk of CV death/HFH (p = 0.03), while in the subgroup of patients with HFmrEF/HFpEF, hs-cTnT above the median was associated with outpatient WHF events (p = 0.03). Conclusions: Inpatient hs-cTnT levels predict CV death/HFH in patients with HF. In particular, in the subgroup of chronic HF patients, hs-cTnT is predictive of CV death/HFH; while in patients with HFmrEF/HFpEF, hs-cTnT predicts WHF events.

The biological equivalent and prognostic relevance of c-reactive protein (CRP) velocity in ST segment elevation myocardial infarction

Abstract Funding Acknowledgements None. Background The rate of increase, i.e. the velocity, of circulating C-reactive protein (CRP) concentrations during myocardial infarction has been associated with left ventricular dysfunction. However, the prognostic yield of this biomarker as well as the underlying biological process that links high CRP velocity (CRPv) with increased myocardial injury are not clear. Therefore, we sought to determine the associations between CRPv early during STEMI with short- and long-term mortality and its correlation to myocardial necrosis. Methods We retrospectively examined 1,155 patients with the diagnosis of acute STEMI, who had at least two successive CRP measurements (up to 48 hours apart) and at least one echocardiographic evaluation, all within the first 96 hours of admission. We calculated CRPv and examined its correlation with myocardial injury, measured by cardiac troponin and overall mortality over a median follow-up period of 5.2 years [IQR 3.7-6.5]. Results Patients with high CRPv values (above 90th percentile, > 1 mg/L/h) had higher concentrations of cardiac troponin upon presentation regardless of their left ventricular systolic function (EF above or below 40%; Figure 1). Patients with high CRPv had increased 30-day and long-term mortality rates; OR= 4.6, 95% CI 2.3-9.2, p<0.001 for 30-day mortality and HR= 2.2, 95% CI 1.5-3.2, p<0.001 for long-term mortality. Furthermore, CRPv was associated with increased 30 –day and long term mortality rates even among patients with similar systolic function (EF above or below 40%; Figure 2). Conclusions High levels of CRPv early during STEMI are associated with increased mortality rates and elevated cardiac troponin release across all levels of left ventricular function. The higher mortality risk might be explained by an aggravated systemic inflammatory response to STEMI.CRP velocity and troponinCRP velocity and mortality

Diagnosis of acute coronary syndrome

Acute coronary syndrome is one of the most important differential diagnostic considerations in emergency medicine. It describes the constellation of newly occurring clinical symptoms, often accompanied by typical 12-lead ECG changes and the release of cardiac troponins. The spectrum includes unstable angina pectoris, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). It is important to consistently carry out the diagnostic steps that are crucial for further therapeutic procedures to avoid delaying life-saving invasive coronary diagnostics, without losing sight of the diverse, sometimes time-critical differential diagnoses. Anamnesis and clinical examination form the basis of the further procedure. Further developments of biomarker assays with personalized limit values, new imaging modalities with ever higher resolution and faster imaging methods as well as advances in automated ECG analysis with integration of all findings through artificial intelligence will continue to offer many optimization options in the future diagnosis of acute coronary syndrome.

Exercise-induced cardiac troponin release in athletes with versus without coronary atherosclerosis.

The magnitude of exercise-induced cardiac troponin (cTn) elevations is dependent on cardiovascular health status, and previous studies have shown that occult coronary atherosclerosis is highly prevalent among amateur athletes. We tested the hypothesis that middle-aged and older athletes with coronary atherosclerosis demonstrate greater cTn elevations following a controlled endurance exercise test compared with healthy peers. We included 59 male athletes from the Measuring Athletes' Risk of Cardiovascular events 2 (MARC-2) study and stratified them as controls [coronary artery calcium score (CACS) = 0, n = 20], high CACS [≥300 Agatston units or ≥75th Multi-Ethnic Study of Atherosclerosis (MESA) percentile, n = 20] or significant stenosis (≥50% in any coronary artery, n = 19). Participants performed a cycling test with incremental workload until volitional exhaustion. Serial high-sensitivity cTn (hs-cTn) T and I concentrations were measured (baseline, after 30-min warm-up, and 0, 30, 60, 120, and 180 min postexercise). There were 58 participants (61 [58-69] yr) who completed the exercise test (76 ± 14 min) with a peak heart rate of 97.7 [94.8-101.8]% of their estimated maximum. Exercise duration and workload did not differ across groups. High-sensitivity cardiac troponin T (Hs-cTnT) and high-sensitivity cardiac troponin I (hs-cTnI) concentrations significantly increased (1.55 [1.33-2.14]-fold and 2.76 [1.89-3.86]-fold, respectively) over time, but patterns of cTn changes and the incidence of concentrations >99th percentile did not differ across groups. Serial sampling of hs-cTnT and hs-cTnI concentrations during and following an exhaustive endurance exercise test did not reveal differences in exercise-induced cTn release between athletes with versus without coronary atherosclerosis. These findings suggest that a high CACS or a >50% stenosis in any coronary artery does not aggravate exercise-induced cTn release in middle-aged and older athletes.NEW & NOTEWORTHY Exercise-induced cardiac troponin (cTn) release is considered to be dependent on cardiovascular health status. We tested whether athletes with coronary atherosclerosis demonstrate greater exercise-induced cTn release compared with healthy peers. Athletes with coronary atherosclerosis did not differ in cTn release following exercise compared with healthy peers. Our findings suggest that a high CACS or a >50% stenosis in any coronary artery does not aggravate exercise-induced cTn release in middle-aged and older athletes.

Relation of ECG Abnormalities to Clinical Severity and Troponin I Changes in Patients with Subarachnoid Hemorrhage

Relation of ECG Abnormalities to Clinical Severity and Troponin I Changes in Patients with Subarachnoid Hemorrhage

Postoperative cardiac biomarker release is not associated with myocardial mass in computer tomography scans.

Myocardial hypertrophy results in increased levels of cardiac biomarkers in healthy individuals and in patients suffering from acute myocardial infarction. The influence of cardiac mass on postoperative cardiac biomarkers release remains unclear. This study investigated the correlation between myocardial mass and the release of high-sensitivity cardiac Troponin T (hs-cTnT) and creatine kinase-myocardial band (CK-MB) after isolated aortic valve replacement (AVR) or bypass surgery. Myocardial mass of a consecutive retrospective series of patients was measured automatically using preoperative computer tomography scans (636 patients, AVR = 251; bypass surgery = 385). Levels of cardiac biomarkers were measured before and serially after surgery. Spearman and Pearson correlation and a multivariate regression model was performed to measure the degree of association between myocardial mass and the release of hs-cTnT and CK-MB. Patients were divided into 3 tertiles according to their myocardial mass index. Higher biomarker levels were measured preoperatively in the upper tertile of patients undergoing AVR (P = 0.004) or bypass surgery (P < 0.001). Patients with different heart sizes showed no differences in postoperative biomarker release neither after AVR nor bypass surgery. No statistical significant correlation was observed between myocardial mass index and postoperative release of hs-cTnT or CK-MB in any subgroup (ρ maximum 0.106). Postoperative biomarker release is not correlated with myocardial mass. Patient factors leading to increased postoperative biomarker levels need to be elucidated in future studies.

Cardiac Troponin Release after Exercise in Healthy Young Athletes: A Systematic Review.

Cardiac troponin (cTn) is a recognized marker used to assess damage to the heart muscle. Actual research has indicated that the levels of cTn increase after doing exercise in individuals who are in good health, and this is believed to be a result of a normal cellular process rather than a pathological one. The main goal of this study was to investigate the evidence of a postexercise release of cTn in child and adolescent athletes (6-17.9 years old) of different ages, sex, and sports disciplines. The Web of Science, MEDLINE, and Scopus databases were used to conduct the research up to March 2023. Three hundred and twenty-eight records were identified from the databases, however, only twenty-three studies were included in the review after being screened and quality-assessed by two independent authors. The gender, age of the participants, maturational status, and training level of the participants, the timing of sample collection, the exercise modality, and the number of participants with values above the cut-off reference were the data analyzed. Males, older young people, and individual sports seemed to have higher levels of serum cTn after practice exercise. Different methodologies, analyzers, and cut-off reference values make it difficult to compare the data among studies.

Accelerated -Rule-Out of acute Myocardial Infarction using prehospital copeptin and in-hospital troponin: The AROMI study.

The present acute myocardial infarction (AMI) rule-out strategies are challenged by the late temporal release of cardiac troponin. Copeptin is a non-specific biomarker of endogenous stress and rises early in AMI, covering the early period where troponin is still normal. An accelerated dual-marker rule-out strategy combining prehospital copeptin and in-hospital high-sensitivity troponin T could reduce length of hospital stay and thus the burden on the health care systems worldwide. The AROMI trial aimed to evaluate if the accelerated dual-marker rule-out strategy could safely reduce length of stay in patients discharged after early rule-out of AMI. Patients with suspected AMI transported to hospital by ambulance were randomized 1:1 to either accelerated rule-out using copeptin measured in a prehospital blood sample and high-sensitivity troponin T measured at arrival to hospital or to standard rule-out using a 0 h/3 h rule-out strategy. The AROMI study included 4351 patients with suspected AMI. The accelerated dual-marker rule-out strategy reduced mean length of stay by 0.9 h (95% confidence interval 0.7-1.1 h) in patients discharged after rule-out of AMI and was non-inferior regarding 30-day major adverse cardiac events when compared to standard rule-out (absolute risk difference -0.4%, 95% confidence interval -2.5 to 1.7; P-value for non-inferiority = 0.013). Accelerated dual marker rule-out of AMI, using a combination of prehospital copeptin and first in-hospital high-sensitivity troponin T, reduces length of hospital stay without increasing the rate of 30-day major adverse cardiac events as compared to using a 0 h/3 h rule-out strategy.

Impact of cardiac troponin release and fluid resuscitation on outcomes of patients with sepsis

BackgroundSeptic patients are predisposed to myocardial injury manifested as cardiac troponin release (TnR). Prognostic significance and management implications of TnR and its relationship to fluid resuscitation and outcomes in the intensive care unit (ICU) setting has not been fully elucidated. MethodsA total of 24,778 patients with sepsis from eICU-CRD, MIMIC-III and MIMIC-IV databases were included in this retrospective study. In-hospital mortality and one-year survival were examined using multivariable regression analysis and Kaplan-Meier survival analysis with overlap weighting adjustment, as well as generalized additive models for fluid resuscitation. ResultsTnR on admission was associated with higher in-hospital mortality [adjusted odds ratios (OR) = 1.33; 95% confidence interval (CI) = 1.23–1.43; p < 0.001 in unweighted analysis and adjusted OR = 1.39; 95% CI = 1.29–1.50; P < 0.001 with overlap weighting]. One-year mortality was higher in patients with admission TnR (P = 0.002). A trend was noted for association between admission TnR and 1-year mortality [adjusted OR = 1.16; 95% CI = 0.99–1.37; P = 0.067 in unweighted analysis] while the association was statistically significant after overlap weighting (adjusted OR = 1.25; 95% CI = 1.06–1.47; P = 0.008). Patients with admission TnR were less likely to benefit from more liberal fluid resuscitation. Adequate fluid resuscitation (80 ml/kg in the first 24 h of ICU stay) was associated with lower in-hospital mortality in septic patients without TnR but not in those with admission TnR. ConclusionsAdmission TnR is significantly associated with higher in-hospital mortality and 1-year mortality among septic patients. Adequate fluid resuscitation improves in-hospital mortality in septic patients without but not with admission TnR.

Soluble Urokinase Plasminogen Activator Receptor (suPAR) Promotes Cardioprotective Intracellular Signalling in Myocardial Ischaemia

Soluble urokinase Plasminogen Activator Receptor (suPAR) is an emerging biomarker of inflammation capable of predicting cardiovascular outcomes. However, the biological activity of suPAR on the heart is poorly understood. Potential cardiac intracellular signalling pathways triggered by suPAR were explored. Isolated Langendorff rat hearts undergoing global ischaemia received treatment with either suPAR infusion or perfusion buffer (controls). Proteins were extracted from hearts for each treatment group, and Troponin T in rat outflow perfusates following ischaemia were measured. The phosphorylation status of each kinase was characterised using a phospho-specific antibody and a ratio of phosphorylation to the total protein was calculated. Analysis between treatment groups was performed with unpaired t-test with Welch’s correction. Hearts receiving suPAR treatment after ischaemia showed a 1.4-fold increase in Akt phosphorylation, and a 1.6-fold increase in Akt phosphorylation if suPAR was given before ischaemia. The ratio of p-Akt/Akt was 1.83±0.14 (n=7) in the post-ischaemic suPAR treatment group vs 1.3±0.04 (n=6) in controls (p=0.007). Pre-ischaemic suPAR treatment gave a p-Akt/Akt ratio of 1.08±0.03 (n=8) vs 0.67±0.11 (n=5) in controls (p=0.01). Upstream signalling ERK1 and ERK2 phosphorylation also increased at 2.6-fold (p=0.009) and 1.9-fold (p=0.01), respectively, in suPAR treated heart vs controls. Finally, suPAR treated hearts obtained lower Troponin T values compared with controls after recovery from ischaemia (p<0.001). suPAR infusion promoted the phosphorylation of ERK and Akt kinases in isolated rat heart tissue and reduced related cardiac troponin release after a period of global no-flow ischaemia. These actions suggest that suPAR is a novel activator of the reperfusion injury salvage kinase (RISK) pathway.

Myocardial protection in paediatric cardiac surgery: building an evidence-based strategy.

Cardioplegia is fundamental to the surgical repair of congenital heart defects by protecting the heart against ischaemia/reperfusion injury, characterised by low cardiac output and troponin release in the early postoperative period. The immature myocardium exhibits structural, physiological and metabolic differences from the adult heart, with a greater sensitivity to calcium overload-mediated injury during reperfusion. Del Nido cardioplegia was designed specifically to protect the immature heart, is widely used in North America and may provide better myocardial protection in children; however, it has not been commercially available in the UK, where most centres use St Thomas' blood cardioplegia. There are no phase 3 clinical trials in children to support one solution over another and this lack of evidence, combined with variations in practice, suggests the presence of clinical equipoise. The best cardioplegia solution for use in children, and the impact of age and other clinical factors remain unknown. In this Hunterian lecture, I propose an evidence-based strategy to improve myocardial protection during cardiac surgery in children through: (1) conducting multicentre clinical trials of established techniques; (2) improving our knowledge of ischaemia/reperfusion injury in the setting of cardioplegic arrest; (3) applying this to drive innovation, moving beyond current cardioplegia solutions; (4) empowering personalised medicine, through combining clinical and genomic data, including ethnic diversity; and (5) understanding the impact of cardioplegic arrest on the late outcomes that matter to patients and their families.

A Comparison between Postoperative Troponin Elevation in An Off-pump Versus Conventional Coronary Artery Bypass Graft in Predicting The Short-term Outcome

Background: Although, advancements in techniques and perioperative management in coronary artery bypass surgery the elevation of postoperative troponin still occurs commonly. In this regard, we aimed to assess the degree of myocardial injury by measuring and comparing the levels of cardiac troponin I in the postoperative period of conventional versus off-pump coronary artery bypass graft and identify the most associated factors. Patients and methods: This prospective cohort study included the patients who underwent conventional coronary artery bypass surgery (46 patients) and off-pump coronary artery bypass surgery (34 patients), at Azadi heart Center in Duhok province during the period between 25th November 2021 and 25th May 2022. Results: The total amount of cardiac troponin release was significantly higher in the conventional than in the off-pump group. At one hour, the conventional means was 7.13 ng/ml while the off-pump was 1.56 ng/ml, p &lt; 0.0001and at 24 hours, the convention mean was 5.51 ng/ml while the off-pump was 1.24 ng/ml, p &lt; 0.001. The most associated factors in the conventional compared to the off-pump were advanced age, male gender, hypertension, renal impairment, Previous myocardial infarction, and timing of surgery. the main independent factors associated with cardiac troponin I elevation within 24 hours following conventional coronary artery bypass surgery were overweight, chronic renal failure, Smoking, and urgent procedure status. Conclusion: This study showed that the patients who underwent the conventional group had significantly higher levels of troponin I at 1 hour and 24 hrs, postoperatively. The higher postoperative troponin I among patients who underwent the conventional group was associated with being overweight, smoking, having chronic renal failure, and using urgent procedure status

Repeated bout effect of exercise on cardiac troponin release is lost in individuals with cardiovascular disease: a cause for concern?

Editorial FocusCall for Papers: Exercise, Physical Activity, and Cardiovascular Health"Repeated Bout" Effect of Exercise on Cardiac Troponin Release Is Lost in Individuals with Cardiovascular Disease: A Cause for Concern?Brady J. HolmerBrady J. Holmer* Corresponding Author; email: [email protected]1Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, Florida, United States*Published Online:10 Mar 2023https://doi.org/10.1152/ajpheart.00114.2023MoreSectionsPDF (92 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation CollectionsAJP-Heart CollectionsExercise, Physical Activity, and Cardiovascular Health More from this issue > Articles in PressPublished 3/10/23 9:09 AM Crossmark Copyright & PermissionsCopyright © 2023, American Journal of Physiology-Heart and Circulatory Physiologyhttps://doi.org/10.1152/ajpheart.00114.2023PubMed36897747History Received 27 February 2023 Accepted 9 March 2023 Published online 10 March 2023 Keywordscardiovascular diseaseexercisecardiac troponinexercise-induced cardioprotectionaerobic exercise Metrics

Exercise-induced release of cardiac troponin is attenuated with repeated bouts of exercise: impact of cardiovascular disease and risk factors.

Prolonged exercise can induce cardiac troponin release. As single bouts of exercise may protect against cardiac injury, we explored the hypothesis that the magnitude of exercise-induced release of troponin attenuates upon successive days of exercise. We also examined whether effects of successive exercise bouts differ between healthy participants and individuals with cardiovascular risk factors (CVRFs) and established cardiovascular disease (CVD). We examined cardiac troponin I (cTnI) concentrations from whole venous blood samples collected from the antecubital vein (10 mL) in 383 participants (61 ± 14 yr) at rest and immediately following four consecutive days of long-distance walking (30-50 km/day). Participants were classified as either healthy (n = 222), CVRF (n = 75), or CVD (n = 86). Baseline cTnI concentrations were significantly higher in participants with CVD and CVRF compared with healthy (P < 0.001). Exercise-induced elevations in cTnI were observed in all groups following all days of walking compared with baseline (P < 0.001). Tobit regression analysis on absolute cTnI concentrations revealed a significant day × group interaction (P = 0.04). Following day 1 of walking, post hoc analysis showed that exercise-induced elevations in cTnI attenuated on subsequent days in healthy and CVRF, but not in CVD. Odds ratios for incident cTnI concentrations above the upper reference limit were significantly higher compared with baseline on day 1 for healthy participants (4.90 [95% CI, 1.58-15.2]) and participants with CVD (14.9 [1.86-125]) and remained significantly higher than baseline on all subsequent days in CVD. The magnitude of postexercise cTnI concentrations following prolonged walking exercise significantly declines upon repeated days of exercise in healthy individuals and those with CVRF, whereas this decline is not present in patients with CVD.NEW & NOTEWORTHY We show the magnitude of postexercise cardiac troponin concentrations following prolonged walking exercise significantly declines upon repeated days of exercise in healthy individuals and those with cardiovascular risk factors, while this decline is not present in patients with established cardiovascular disease.

Effects of high-intensity interval exercise on cardiac troponin elevation when comparing with moderate-intensity continuous exercise: a systematic review and meta-analysis.

This systematic review and meta-analysis aimed to compare the effects of high-intensity interval exercise (HIIE) with different recovery modes versus moderate-intensity continuous exercise (MICE) on cardiac troponin (cTn) elevation. A literature search was conducted in four databases: Scopus, PubMed, EBSCO and Web of Science from January 2010 to June 2022. The articles were screened, evaluated for quality before data were extracted. The review protocol was registered at PROSPERO (CRD42021245649). Standardized mean differences (SMD) of peak cTn were analyzed with a 95% confidence interval (95% CI) using Revman 5.4 software. Six studies satisfied the inclusion criteria with a total of 92 and 79 participants for HIIE and MICE, respectively. Overall, there was no significant difference between HIIE and MICE in the elevation of cardiac troponin T (SMD: 0.41 [95% CI [-0.21, 1.03]], p=0.20, I 2=77%, p for heterogeneity <0.01). In subgroup analysis, HIIE with passive recovery elicits greater release of cardiac troponin T than MICE (SMD: 0.85 [95% CI [0.44, 1.27]], p<0.01, I 2=32%, p for heterogeneity = 0.22). Changes of cardiac troponin T (SMD: 0.41 [95% CI [-0.21, 1.03]], p=0.20, I 2=77%, p for heterogeneity < 0.01) after HIIE with active recovery were not significantly different from those of MICE. There was no significant difference between HIIE and MICE in the elevation of cardiac troponin T. However, HIIE with passive recovery elicited more cardiac troponin T elevation than MICE, which should be considered when developing exercise programs.

ESMOLOL PROTECTS AGAINST LPS-INDUCED CARDIAC INJURY VIA THE AMPK/mTOR/ULK1 PATHWAY IN RAT.

Aim: The purpose of this study was to investigate the effect of esmolol (ES) on LPS-induced cardiac injury and the possible mechanism. Methods: Sepsis was induced by i.p. injection of LPS (10 mg/kg) in male Sprague-Dawley rats pretreated with ES, 3-methyladenine or rapamycin. The severity of myocardial damage was analyzed by hematoxylin-eosin staining, and myocardial damage scores were calculated. The concentration of cardiac troponin was measured by enzyme-linked immunosorbent assay. The expression of autophagy-related proteins (beclin-1, LC3-II, p-AMPK, p-ULK1, p-mTOR) in myocardial tissue was detected by Western blotting. Autophagosome formation and the ultrastructural damage of mitochondria were assessed using transmission electron microscopy. Results: LPS induced an increase in myocardial damage score in a time-dependent manner, accompanied with an increase in autophagy at 3 h and decrease in autophagy at 6, 12, and 24 h. Pretreatment of LPS-treated rats with ES or rapamycin reduced myocardial injury (release of cardiac troponin, myocardial damage score) and increased autophagy (LC3-II, beclin-1, p-AMPK, and p-ULK1 levels and autophagosome numbers) at 12 and 24 h. In contrast, 3-methyladenine showed no effect. Conclusion: Esmolol alleviates LPS-induced myocardial damage through activating the AMPK/mTOR/ULK1 signal pathway-regulated autophagy.

Moderní představy o mechanismech uvolňování srdečních troponinů a jejich diagnostické roli

Hlavním, ke dnešnímu dni dokázaným mechanismem uvolňování srdečních troponinů (cTnT a cTnI) je ischemická nekróza buněk myokardu, která vede k uvolnění všech intracelulárních molekul, včetně cTnT a cTnI, do krevního oběhu při akutním infarktu myokardu (AIM). V reálné klinické praxi se však lékaři často setkávají s mnoha dalšími (kromě AIM) patologickými stavy, při kterých jsou koncentrace cTnT a cTnI v krevním řečišti zvýšené, ale známky ischemie myokardu nejsou pozorovány. To jasně ukazuje na existenci dalších (neischemických) mechanismů poškození kardiomyocytů a uvolňování cTnT a cTnI do krevního řečiště. Pochopení všech mechanismů uvolňování srdečních troponinů umožní zlepšit diagnostiku a diferenciální diagnostiku AIM, rozšířit záběr cTnT a cTnI (pro diagnostiku a stratifikaci rizika u dalších onemocnění, která mají negativní vliv na buňky myokardu). V tomto přehledu jsou systematizované aktuální informace o mechanismech uvolňování srdečních troponinů, podrobně diskutovány diagnostické role jednotlivých mechanismů uvolňování cTnT a cTnI. &#169; 2022, ČKS.

Inflammatory activation biomarker profile after marathon running and its impact on cardiovascular stress in amateur middle-aged male runners.

Cardiovascular safety of marathon running middle-aged amateurs remains unclear. We previously hypothesized that transient release of cardiac troponin I (cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), in addition to an acute inflammatory response to exercise, may be the cause. To evaluate the effects of running a marathon on inflammatory biomarkers, and its impact on cardiovascular function. Thirty-three healthy male amateur runners aged ≥50 (mean age: 57 ±7 years) were enrolled in the study. Venous blood samples were obtained before the marathon, just after the race, and 2-4 days and 7 days after the marathon. Using novel single molecule counting (SMC) technology, we measured plasma concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). White blood cell (WBC) count was measured using a certified hematology analyzer. The results were related to previous analyses on cardiovascular stress and endothelial function biomarkers. Transthoracic echocardiography (TTE) and cardiac magnetic resonance (CMR) were used to determine myocardial function. We observed a sharp rise of all studied biomarkers after the race, which subsequently normalized after 2-4 days and stayed within the normal range 7 days after the race. We found no correlation between inflammatory and cardiovascular stress biomarkers. Transthoracic echocardiography and CMR did not show ischemic or inflammatory myocardial damage. Marathon running is associated with a sharp and significant rise in inflammatory and cardiovascular stress biomarkers. We found no connection between immune activation and cardiac biomarker release. Cardiovascular imaging showed no myocardial damage due to ischemia or inflammation.

Abstract 10085: Troponin Release is Associated With Mortality and Poor Fluid Resuscitation in Patients With Sepsis

Introduction: Septic patients are predisposed to myocardial injury manifested as cardiac troponin release (TnR). Prognostic significance and management implications of TnR in this setting has not been fully elucidated. We aimed to determine the impact of admission TnR and fluid resuscitation on outcomes of patients with sepsis admitted to intensive care units (ICU). Methods: A total of 24,778 patients with sepsis from eICU-CRD (n=11,992), MIMIC-III (n=6,638) and MIMIC-IV (n=6,148) databases were examined for mortality and 1-year survival by multivariable logistic, Cox regression analysis, or Kaplan-Meier survival analysis with overlap weighting adjustment, as well as generalized additive models for fluid resuscitation. Results: TnR on admission was associated with higher in-hospital mortality [adjusted odds ratios (aOR)=1.33; 95% confidence interval (CI)=1.23-1.43; p&lt; 0.001 in unweighted analysis and aOR=1.39; 95% CI=1.29-1.50; p&lt; 0.001 with overlap weighting]. One-year survival was lower in patients with admission TnR (Kaplan-Meier survival analysis; p=0.002). A trend was noted for association between admission TnR and 1-year mortality [aOR=1.16; 95% CI, 0.99-1.37; p = 0.067 in unweighted analysis] while the association was statistically significant after overlap weighting (aOR=1.25; 95% CI=1.06-1.47; p=0.008). We also found that patients with admission TnR were less likely to benefit from more liberal fluid resuscitation. Adequate fluid resuscitation within a range of 70 to 90 ml/kg in the first 24 hours of ICU stay was associated with lower in-hospital mortality in septic patients without TnR but not in those with admission TnR. Conclusions: Admission TnR was significantly associated with higher in-hospital mortality and worse 1-year survival among septic patients. Adequate fluid resuscitation improved in-hospital mortality in septic patients without but not with admission TnR.