cTnI Concentrations Research Articles

Cardiac Troponin I and Electrocardiographic Evaluation in Hospitalized Cats with Systemic Inflammatory Response Syndrome.

Several studies conducted on humans demonstrate the increase in cardiac troponins and the onset of arrhythmias in the course of systemic inflammatory response syndrome (SIRS). The aim of the current study was to assess the blood concentration of cardiac troponin I (cTnI) and electrocardiographic findings in SIRS-affected cats. Seventeen shorthair cats hospitalized with SIRS were enrolled (Group 1). SIRS diagnosis was performed based on the detection of at least two of the four criteria such as abnormal body temperature, abnormal heart rate (i.e., tachycardia or bradycardia), abnormal respiratory rate (i.e., tachypnea or bradypnea), and alterations of white blood cell number (i.e., leukocytes or band neutrophils). Ten cats screened for elective surgery such as neutering or dental procedures were evaluated as a control population (Group 2). They were considered healthy based on history, physical examination, hematological and biochemical profile, urinalysis, coprological exam, thyroxine assay, blood pressure measurement, and echocardiography. A physical examination, complete blood cell count, biochemistry test (including an electrolyte panel), electrocardiographic examination, and cTnI assay were carried out in each cat enrolled. Traumatic events, gastrointestinal, neoplastic, respiratory, and neurological disorders were identified as causes of SIRS in Group 1. In Group 1, a significantly higher concentration of cTnI than that in Group 2 was recorded (p = 0.004). In 37.5% of cats with SIRS, ventricular premature complexes occurring in couplets with multiform configuration were detected. Similarly, to humans, data herein reported would indicate possible cardiac damage present in cats with SIRS diagnosis.

Association between troponin level and medium-term mortality in 20 000 hospital patients

IntroductionCardiac troponin (cTn) concentrations above the manufacturer recommended upper limit of normal (ULN) are frequently seen in hospital patients without a clinical presentation consistent with type 1 myocardial infarction, and...

Analytical validation, sample stability, and clinical evaluation of a new high-sensitivity cardiac troponin I immunoassay for use in dogs, with comparison to a previous ultrasensitive assay.

Cardiac troponin I (cTnI) is considered the gold standard biomarker for myocardial injury and shows a high degree of homology between humans and dogs. The ADVIA Centaur XP High-Sensitivity Troponin I (AC-cTnI-HS) assay has been validated for use in humans but not dogs. The study objectives were to analytically validate the AC-cTnI-HS assay in dogs, to assess correlation between the AC-cTnI-HS and a previous ADVIA Centaur TnI-Ultra (AC-cTnI-U) assay, to assess cTnI sample storage stability, and to clinically evaluate the AC-cTnI-HS assay in healthy dogs and dogs with cardiac disease. Canine serum samples were used for analytical validation. Intra- and inter-assay variability, dilutional parallelism, and spiking recovery were assessed. Samples from 196 client-owned dogs were evaluated (healthy dogs (n = 39) or dogs with congenital heart disease (n = 54), myxomatous mitral valve disease (n = 68), dilated cardiomyopathy (n = 15), or myocarditis (n = 20)). Inter- and intra-assay coefficient of variation (%CV) was between 2.8-41.4% and 3.8-30.2%, respectively, with pools with concentrations >20 pg/mL all having %CVs <10%. The observed to expected ratios for dilutional parallelism and spiking recovery experiments ranged between 92.3 and 266.7.0% and 84.3 and 108%, respectively. A strong correlation between the AC-cTnI-HS and AC-cTnI-U assays was observed (Spearman's ρ = 0.927), though a proportional bias existed, with AC-cTnI-HS assay concentrations being proportionally lower than AC-cTnI-U assay concentrations. Serum samples stored at -80°C had stable cTnI measurements for up to 2.7 years and after a single freeze-thaw cycle. Healthy dogs and dogs with congenital heart disease had significantly lower cTnI concentrations than dogs in the other three groups. The AC-cTnI-HS assay precisely, reproducibly, and accurately measures cTnI concentrations in dog serum with cTnI concentrations >20 pg/mL.

Atipamezole Reverses Cardiovascular Changes Induced by High-Dose Medetomidine in Cats Undergoing Sedation for Semen Collection.

This study aimed at describing the change in echocardiographic variables after high-dose medetomidine and the reversal with atipamezole in six cats undergoing sedation for semen collection. Further cardiac Troponin I (cTnI) concentration and the effect of repeated sedation were assessed. Echocardiography was performed before and 20 min after sedation with 0.1 mg/kg medetomidine intramuscularly (IM) for urethral catheterisation. Prior to epididymectomy, S-ketamine was administered intravenously. Twenty minutes after reversal with 0.5 mg/kg atipamezole IM, the third echocardiography was performed. Sedation with medetomidine and reversal with atipamezole was repeated on day 7, 14, 21 and 28. Heart rate (HR) and rhythm were monitored throughout all sedations. On day 0 and 28 cTnI concentrations were measured before and after the procedure. After normality testing, the values were compared over time. The administration of medetomidine led to a marked reduction in HR, cardiac output and ventricular systolic function and a significant increase in left ventricular dimensions. Rhythm abnormalities, such as ventricular premature complexes and idioventricular rhythm, could be observed. The administration of atipamezole completely reversed sedation and the changes in haemodynamic variables. No significant increase in cTnI concentrations could be detected, although two out of six cats showed values above the reference range.

Patterns of Cardiac Troponin I Concentrations as Risk Predictors of Cardiovascular Disease and Death: The Trøndelag Health Study

BackgroundConcentrations of cardiac troponin predict risk of cardiovascular disease and death in the general population. There is limited evidence on changing patterns of cardiac troponin in the years preceding cardiovascular events. MethodsWe analyzed cardiac troponin I (cTnI) with a high-sensitivity assay in 3272 participants in the Trøndelag Health (HUNT) Study at study visit 4 (2017-2019). Of these, 3198 had measurement of cTnI at study visit 2 (1995-1997), 2661 at study visit 3, and 2587 at all 3 study visits. We assessed the trajectories of cTnI concentrations in the years prior to cardiovascular events using a generalized linear mixed model, with adjustment for age, sex, cardiovascular risk factors, and comorbidities. ResultsAt HUNT4 baseline, median age was 64.8 (range 39.4-101.3) years, and 55% were women. Study participants who were admitted because of heart failure or died from cardiovascular cause on follow-up had a steeper increase in cTnI compared with study participants with no events (P < .001). The average yearly change in cTnI was 0.235 (95% confidence interval, 0.192-0.289) ng/L for study participants with heart failure or cardiovascular death, and −0.022 (95% confidence interval, −0.022 to −0.023) ng/L for study participants with no events. Study participants who experienced myocardial infarction, ischemic stroke, or noncardiovascular mortality exhibited similar cTnI patterns. ConclusionsFatal and nonfatal cardiovascular events are preceded by slowly increasing concentrations of cardiac troponin, independently of established cardiovascular risk factors. Our results support the use of cTnI measurements to identify at-risk subjects who progress to subclinical and later overt cardiovascular disease.

Cardiac Magnetic Resonance Imaging Detects Myocardial Abnormalities in Naturally Infected Dogs with Chronic Asymptomatic Chagas Disease.

Trypanosoma cruzi infection causes inflammation and fibrosis, resulting in cardiac damage in dogs. The objectives of this study were to describe cardiac magnetic resonance imaging (CMR) in naturally infected dogs with chronic Chagas disease and the frequency of abnormalities for CMR and cardiac diagnostic tests. Ten asymptomatic, client-owned dogs seropositive for T. cruzi were prospectively enrolled in an observational study evaluating echocardiography, ECG (standard and ambulatory), cardiac troponin I (cTnI), and CMR. Standard ECG measurements (3/10) and cTnI concentration (1/10) outside the reference range were uncommon. Ambulatory ECG abnormalities were documented more frequently (6/10 dogs) than with standard ECG and included ventricular arrhythmias (4), supraventricular premature beats (3), second-degree atrioventricular block (2), and sinus arrest (1). Echocardiographic abnormalities were documented in 6/10 dogs including mildly increased left ventricular internal dimension in diastole (1) and decreased right ventricular (RV) systolic function based on reductions in tricuspid annular plane systolic excursion (3) and RV S' (4). Abnormalities were detected with CMR in 7/10 dogs including delayed myocardial enhancement in 5 of which 2 also had increased extracellular volume, abnormal wall motion in 5, and loss of apical compact myocardium in 1. In conclusion, CMR abnormalities were common, and the results of this study suggest CMR can provide useful information in dogs with T. cruzi infection and may support naturally infected dogs for future clinical investigation as an animal model for Chagas disease.

N‐terminal brain natriuretic peptide, cardiactroponin‐I, and point‐of‐care ultrasound in dogs with cardiac and noncardiac causes of nonhemorrhagic ascites

Nonhemorrhagic ascites (NHA) can be caused by cardiac diseases (cNHA) and noncardiac diseases (ncNHA). N-terminal brain natriuretic peptide (NT-proBNP), cardiac troponin-I (cTnI), and point-of-care ultrasound (POCUS) may differentiate between cNHA and ncNHA. We compared NT-proBNP and cTnI concentrations as well as POCUS findings in dogs presented with cNHA and ncNHA. Dogs (n = 60) were enrolled based on identification of NHA with an effusion packed cell volume < 10%. Blood samples were collected and POCUS was performed on all dogs. Dogs were diagnosed with cNHA (n = 28) or ncNHA (n = 32) based on echocardiography. The cNHA group was subdivided into cardiac non-pericardial disease (n = 17) and pericardial disease (n = 11). The NT-proBNP concentration (median; range pmol/L) was significantly higher in the cNHA group (4510; 250-10 000) compared to the ncNHA group (739.5; 250-10 000; P = .01), with a sensitivity of 53.8% and specificity of 85.7% using a cut-off of 4092 pmol/L. The NT-proBNP concentrations were significantly higher in the cardiac non-pericardial disease group (8339; 282-10 000) compared with the pericardial disease group (692.5; 250-4928; P = .002). A significant difference in cTnI concentration (median; range ng/L) between the cNHA group (300; 23-112 612) and ncNHA group (181; 17-37 549) was not detected (P = .41). A significantly higher number of dogs had hepatic venous and caudal vena cava distension in the cNHA group compared to the ncNHA group, respectively (18/28 vs 3/29, P < .0001 and 13/27 vs 2/29, P < .001). Gall bladder wall edema was not significantly different between groups (4/28 vs 3/29, P = .74). NT-proBNP concentration and POCUS help distinguish between cNHA and ncNHA.

A novel DNAzyme-driven walker-walkers serial amplified electrochemical aptasensor for ultrasensitive detection of cardiac troponin I

Sensitive and accurate detection of Cardiac troponin I (cTnI) plays an instrumental role in the prevention and management of acute myocardial infarction. Herein, a novel electrochemical aptasensor was designed for cTnI ultrasensitive detection based on DNAzyme-driven walker-walkers serial amplified strategy. The Au/NiCo2S4 nanocomposites, which possess excellent conductivity and a high specific surface area, were used to assemble on the modified electrode for the first time. The Hairpin probe I (HPI) and hairpin probe II (HP II) were self-assembled onto an Au/NiCo2S4 electrode surface through the interaction of Au-S bond. In the present of cTnI, the walker-walkers strategy was activated. After the hybridization between cTnI and HP I, the DNA walker shears the specific sequence of HP II and releases triggered DNA. Since the triggered DNA corresponds to the HP I complementary sequence, which could trigger multiple recycling and release DNA walkers. By the joint action of cTnI and triggered DNA, HP I was opened and released more DNA walkers. With the use of cDNA, capturing methylene blue (MB), resulting in the significant electrochemical signal in differential pulse voltammetry (DPV). The proposed strategy can effectively avoid problems of the insufficient distance or limited available driving force that general exist in unipedal DNA walkers. Under optimal conditions, the change of current was linearly related to the negative logarithm of cTnI concentration in the detection range of 0.01–60 ng/mL with a low detection limit of 0.26 pg/mL. Moreover, the proposed aptasensor was successfully applied in detection of human serum samples.

Optical and dielectric realisation of biomolecular detection using gold nanoparticles bio-conjugate with liquid crystal

Dielectric biosensor based on nematic liquid crystal platform has been fabricated using sandwich immunoassay technique for the detection of a biomolecule, human cardiac troponin I (cTnI). The optical response of Liquid crystal (LC) biosensor and its corresponding frequency-dependent dielectric properties have been investigated as a function of cTnI concentration. Gold nanoparticles conjugate with detection antibody (AB-GNP) is used for the enhancement of both the optical and dielectric signal of the biosensor. AB-GNP binding with cTnI alter the surface energy of the substrate causing disturbances in LC alignment resulting in a change in transmission. The transmission of the LC cell has been found to be varying from dark to bright texture under polarized microscope as a function of cTnI concentration. A change in low-frequency permittivity with increasing cTnI concentration that forms an increasing order of sandwich immunocomplex with AB-GNP revealed an interfacial surface phenomenon. A positive shift in the onset frequency of permittivity is observed due accumulation of immunocomplex with increasing concentration of cTnI at electrode/LC interface. The dielectric response ε′ of the biosensor is fitted with Hill-Langmuir equation over a concentration range of 0.01 to 10 ng mL−1 cTnI. The dissociation constant ‘Kd’ of 1.02 ± 0.24 ng/mL−1 indicates strong cTnI binding affinity for substrate antibody. A nearby value of 1, calculated for Hill coefficient ‘n’ revealed no co-operativity characteristic of cTnI binding to the primary capture antibody, wherein each binding site of the antibody functions independently at the electrode surface, causing accumulation of charged species revealing LC interfacial surface electrical property.

LncRNA JPX targets SERCA2a to mitigate myocardial ischemia/reperfusion injury by binding to EZH2

Long non-coding RNAs (lncRNAs) are pivotal regulators in heart disease, including myocardial ischemia/reperfusion (I/R) injury. LncRNA just proximal to XIST (JPX) is a molecular switch for X-chromosome inactivation. Enhancer of zeste homolog 2 (EZH2) is a core catalytic subunit of the polycomb repressive complex 2 (PRC2), which is involved in chromatin compaction and gene repression. This study aims to explore the mechanism of JPX regulating the expression of Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) by binding to EZH2 and preventing cardiomyocyte I/R damage in vivo and in vitro.First, we constructed mouse myocardial I/R and HL1 cell hypoxia/reoxygenation models, and found that JPX was low expressed in both models. JPX overexpression alleviated cardiomyocyte apoptosis in vivo and in vitro, reduced the I/R-induced infarct size in mouse hearts, lowered the serum cTnI concentration, and promoted mouse cardiac systolic function. The evidence implies that JPX can alleviate I/R-induced acute cardiac damage. Mechanistically, the FISH and RIP assays showed that JPX could bind to EZH2. The ChIP assay revealed EZH2 enrichment at the promoter region of SERCA2a. Both the EZH2 and H3K27me3 levels at the promoter region of SERCA2a were reduced in the JPX overexpression group compared to those in the Ad-EGFP group (P < 0.01).In summary, our results suggested that LncRNA JPX directly bound to EZH2 and reduced the EZH2-mediated H3K27me3 in the SERCA2a promoter region, protecting the heart from acute myocardial I/R injury. Therefore, JPX might be a potential therapeutic target for I/R injury.

Heat-related biomarkers: Focus on the correlation of troponin I and 70 kDa heat shock protein

Heat-related biomarkers: Focus on the correlation of troponin I and 70 kDa heat shock protein Abstract Introduction: There is intensive research related to the forensic importance of biomarkers that would be the standard for postmortem damage to cardiomyocytes and the mechanism of the resulting damage. The aim of the research was to examinate the forensic-medical significance of serum levels of biomarkers as detectors of terminal hyperthermic damage to the myocardium. Material and Method: 40 laboratory animals were divided into groups: the first group was the control (n = 8) exposed to a physiological temperature of 37 °C, the second group was divided into two subgroups: antemortem (n = 8) and postmortem (n = 8), which included a exposure temperature of 41 °C and the third group was divided into two subgroups: antemortem (n = 8) and postmortem (n = 8), which included a exposure temperature of 44 °C. The concentration of cardiac TnI and Hsp70 was resoluted in serum by immunochemical enzyme-labeled immunoabsorption method. Results: A positive correlation was found between the temperature measured at the time of death and the serum values of cTnI (p = 0.02), in G41, and Hsp70 values did not significantly correlate with the core temperature in this group, p > 0.005. A positive correlation was significant between the concentration of Hsp 70 and the body temperature of rats in the group of rats with a fatal outcome was determined, p = 0.03. Conclusion: Changes in the concentration of cTnI and Hsp70 in rat serum may indicate hyperthermic damage to the myocardium in the Wistar rat model of heat stroke.

The Pulse of It: Dietary Inclusion of Up to 45% Whole Pulse Ingredients with Chicken Meal and Pea Starch in a Complete and Balanced Diet Does Not Affect Cardiac Function, Fasted Sulfur Amino Acid Status, or Other Gross Measures of Health in Adult Dogs

BackgroundPulses are an attractive alternative protein source for all mammals; however, recent reports suggest that these ingredients may be related to developing dilated cardiomyopathy in dogs. ObjectivesThe primary objective of this study was to quantify the effects of dietary pulse intake by adult dogs on cardiac function using echocardiographic measurements and cardiac biomarkers N-terminal pro-B-type natriuretic peptide and cardiac troponin I (cTnI). Second, to investigate the effects of pulse consumption on plasma sulfur amino acid (SAA) concentrations as pulses are generally low in SAA and may limit taurine synthesis. Last, to assess the general safety and efficacy of feeding pulse-containing diets on canine body composition and hematological and biochemical indices. MethodsTwenty-eight privately-owned domestic Siberian Huskies (13 females; 4 intact, and 15 males; 6 intact) with a mean age of 5.3 ± 2.8 y (± SD) were randomly assigned to 1 of 4 dietary treatments (n = 7/treatment), with equal micronutrient supplementation and increasing whole pulse ingredient inclusion (0%, 15%, 30%, and 45%) with pea starch used to balance protein and energy. ResultsAfter 20 wks of feeding, there were no differences (P > 0.05) in echocardiographic parameters, N-terminal pro-B-type natriuretic peptide, and cTnI concentrations among treatments or across time within treatment (P > 0.05), indicating no differences in cardiac function among treatments. Concentrations of cTnI remained below the safe upper limit of 0.2 ng/mL for all dogs. Plasma SAA status, body composition, and hematological and biochemical indices were similar among treatments and over time (P > 0.05). ConclusionsThe results from this study suggest that increasing the inclusion of pulses up to 45% with the removal of grains and equal micronutrient supplementation does not impact cardiac function concurrent with dilated cardiomyopathy, body composition, or SAA status and is safe for healthy adult dogs to consume when fed for 20 wks.

Long-term outcome and troponin I concentrations in Great Danes screened for dilated cardiomyopathy: an observational retrospective epidemiological study

IntroductionDilated cardiomyopathy (DCM) is common in Great Danes (GDs) but screening for this condition can be challenging. We hypothesised that cardiac troponin-I (cTnI) concentration is elevated in GDs with DCM and/or ventricular arrhythmias (VAs), and is associated with reduced survival time in GDs. AnimalsOne hundred and twenty-four client-owned GDs assigned echocardiographically as normal (n = 53), equivocal (n = 37), preclinical DCM (n = 21), or clinical DCM (n = 13). Materials and methodsA retrospective epidemiological study. Echocardiographic diagnosis, VAs, and contemporaneous cTnI concentrations were recorded. Diagnostic accuracy and cTnI cut-offs were determined with receiver operating characteristic analyses. Effects of the cTnI concentration and disease status on survival and cause of death were explored. ResultsMedian cTnI was greater in clinical DCM (0.6 ng/mL [25th–75th percentiles: 0.41–1.71 ng/mL]) and GDs with VAs (0.5 ng/mL [0.27–0.80 ng/mL], P<0.001). Elevated cTnI detected these dogs with good accuracy (area under the curve: 0.78–0.85; cut-offs 0.199–0.34 ng/mL). Thirty-eight GDs (30.6%) suffered a cardiac death (CD); GDs suffering CD (0.25 ng/mL [0.21–0.53 ng/mL]) and specifically sudden cardiac death (SCD) (0.51 ng/mL [0.23–0.72 ng/mL]) had higher cTnI than GDs dying of other causes (0.20 ng/mL [0.14–0.35 ng/mL]; P<0.001). Elevated cTnI (>0.199 ng/mL) was associated with shorter long-term survival (1.25 years) and increased risk of SCD. Great Danes with VAs had shorter survival times (0.97 years). ConclusionsA cardiac troponin-I concentration is a useful adjunctive screening tool. Elevated cTnI is a negative prognostic indicator.

Photoelectrochemical Determination of Cardiac Troponin I as a Biomarker of Myocardial Infarction Using a Bi2S3 Film Electrodeposited on a BiVO4-Coated Fluorine-Doped Tin Oxide Electrode.

A sensitive and selective label-free photoelectrochemical (PEC) immunosensor was designed for the detection of cardiac troponin I (cTnI). The platform was based on a fluorine-doped tin oxide (FTO)-coated glass photoelectrode modified with bismuth vanadate (BiVO4) and sensitized by an electrodeposited bismuth sulfide (Bi2S3) film. The PEC response of the Bi2S3/BiVO4/FTO platform for the ascorbic acid (AA) donor molecule was approximately 1.6-fold higher than the response observed in the absence of Bi2S3. The cTnI antibodies (anti-cTnI) were immobilized on the Bi2S3/BiVO4/FTO platform surface to produce the anti-cTnI/Bi2S3/BiVO4/FTO immunosensor, which was incubated in cTnI solution to inhibit the AA photocurrent. The photocurrent obtained by the proposed immunosensor presented a linear relationship with the logarithm of the cTnI concentration, ranging from 1 pg mL-1 to 1000 ng mL-1. The immunosensor was successfully employed in artificial blood plasma samples for the detection of cTnI, with recovery values ranging from 98.0% to 98.5%.

Serial measurement of cardiac troponin I in hospitalised dogs with canine parvoviral enteritis: Association with outcome and canine pancreas-specific lipase concentration

The aim of this study was to serially evaluate serum cardiac troponin I (cTnI) concentrations in dogs with parvoviral enteritis (CPVE), and investigate the association with outcome and serum pancreas-specific lipase (Spec cPL) concentrations. Dogs with CPVE that were hospitalised for at least 5 days were included. cTnI and Spec cPL concentrations were measured on days 1, 3 and 5 of hospitalisation. Twenty-nine dogs (20 survivors, 9 non-survivors) were included. Spec cPL was indicative of pancreatitis (>400 μg/L) on at least one day in 10/29 (34.5%) dogs. Serum median (range) cTnI concentration was higher (P = 0.021) in non-survivors on day 5 [0.032 (0.001–0.395) ng/mL] compared to day 1 [0.012 (0.003–0.196) ng/mL]. Non-survivors had higher (P = 0.014) cTnI concentrations on day 5 [0.032 (0.001–0.395) ng/mL] compared to survivors [0.001 (0.001–0.042) ng/mL], but not at admission or on day 3 (P > 0.05). Serum cTnI concentrations were not significantly different (P = 0.465) between the three Spec cPL groups [group 1 (Spec cPL ≤ 200 μg/L): 0.007 (0.001–0.527) ng/mL; group 2 (Spec cPL: 201-399 μg/L): 0.0045 (0.001–0.196) ng/mL; group 3 (Spec cPL ≥ 400 μg/L): 0.011 (0.001–0.278) ng/mL]. cTnI and Spec cPL concentrations were not significantly correlated (rho = −0.043, P = 0.703). Serial measurement of cTnI had prognostic value in the examined cohort. However, cTnI was not correlated with spec cPL.

Preclinical evaluation of triiodothyronine nanoparticles as a novel therapeutic intervention for resuscitation from cardiac arrest

BackgroundGiven emerging evidence of rapid non-genomic cytoprotective effects of triiodothyronine (T3), we evaluated the resuscitative efficacy of two nanoparticle formulations of T3 (T3np) designed to prolong cell membrane receptor-mediated signaling. MethodsSwine (n = 40) were randomized to intravenous vehicle (empty np), EPI (0.015 mg/kg), T3np (0.125 mg/kg), or T3np loaded with phosphocreatine (T3np + PCr; 0.125 mg/kg) during CPR following 7-min cardiac arrest (n = 10/group). Hemodynamics and biomarkers of heart (cardiac troponin I; cTnI) and brain (neuron-specific enolase; NSE) injury were assessed for up to 4-hours post-ROSC, at which time the heart and brain were collected for post-mortem analysis. ResultsCompared with vehicle (4/10), the rate of ROSC was higher in swine receiving T3np (10/10; p < 0.01), T3np + PCr (8/10; p = 0.08) or EPI (10/10; p < 0.01) during CPR. Although time to ROSC and survival duration were comparable between groups, EPI was associated with a ∼2-fold higher post-ROSC concentration of cTnI vs T3np and T3np + PCr and the early post-ROSC rise in NSE and neuronal injury were attenuated in T3np-treated vs EPI-treated animals. Analysis of hippocampal ultrastructure revealed deterioration of mitochondrial integrity, reduced active zone length, and increased axonal vacuolization in EPI-treated animals vs controls. However, the frequency of these abnormalities was diminished in animals resuscitated with T3np. ConclusionsT3np achieved a ROSC rate and post-ROSC survival that was superior to vehicle and comparable to EPI. The attenuation of selected biomarkers of cardiac and neurologic injury at individual early post-ROSC timepoints in T3np-treated vs EPI-treated animals suggests that T3np administration during CPR may lead to more favorable outcomes in cardiac arrest.

Analytical performance comparing siemens whole blood point of care Atellica VTLi to the central laboratory plasma Atellica IM high-sensitivity cardiac troponin I assays

IntroductionThis study examined the analytical performance of a whole blood (WB) point of care (POC) hs-cTnI assay compared to a plasma central laboratory hs-cTnI assay in patients presenting with ischemic symptoms to a US emergency department. MethodsFresh WB specimens collected at 0 and 2 h from 1089 consecutive patients (2152 total from 1076 matched specimens) were analyzed for hs-cTnI using WB on POC Siemens Atellica VTLi assay and plasma on central laboratory Siemens Atellica IM assay. Concordances were determined based on concentrations ranging from < limit of detection (LoD), LoD to overall and sex specific 99th percentiles from both the IFCC manufacturer package inserts and Universal Sample Bank (USB) data, and > 99th percentiles. Method comparisons were calculated using Passing Bablok regression and Bland Altmann plots, and linear regression determined by Pearson correlation coefficient. ResultsBaseline concentration comparisons showed: POC VTLi < LoD 4–5 %, ≥ LoD 95 %; Atellica IM < LoD 5–7 %, and ≥ LoD 94–95 %. From the 2152 paired 0 and 2-hour samples, based on 99th percentiles, overall concordance was 91–92 % (kappa 0.72–0.77) and discordance 8 %. Passing Bablok regression analysis using 1924 specimens between LoD to 500 ng/L showed: slopes 0.469–0.490; y-intercepts 1.753–2.028; r values 0.631–0.817. Pearson correlation coefficient showed moderate to strong correlation strength, even with up to 53 % cTnI concentrations variance (Passing Bablok slopes) vs 27.0–40.1 % (Bland-Altmann plots). ConclusionsUp to 95 % of measured samples were > LoD for both the POC (Atellica VTLi) and central laboratory (Atellica IM) hs-cTnI assays. Moderate to strong concordance and correlation were observed between assays, despite up to 53 % variances in cTnI concentration.

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.

Evaluation of cardiac troponin I as a predictor of death in critically ill cats.

Abnormally high serum cardiac troponin I (cTnI) concentration, reflecting leakage from or necrosis of cardiomyocytes, is a negative prognosticator for death in dogs. To investigate in critically ill cats whether serum cTnI concentration is abnormally high, identify conditions associated with abnormally high cTnI concentrations, and evaluate cTnI as an independent prognosticator for death and a potential coprognosticator to the acute patient physiologic and laboratory evaluation (APPLE) score in cats. One hundred nineteen cats admitted to intensive care units (ICU) and 13 healthy cats at 2 university teaching hospitals. Prospective study. Clinical examinations were performed, APPLE scores calculated, and serum cTnI and serum amyloid A (SAA) measured within 24 hours after admission. Outcome was defined as death/euthanasia or survival to discharge, 28 and 90 days after ICU-admission. Prognostic capacity of cTnI, APPLE scores and models combining cTnI and scores were evaluated by receiver-operator-characteristic analyses. Median (IQR) serum cTnI concentration was higher in ill (0.63 [0.18-2.65] ng/mL) compared to healthy (0.015 [0.005-0.041] ng/mL) cats (P < .001) and higher in subgroups with structural cardiac disease (2.05 [0.54-16.59] ng/mL; P < .001) or SAA >5mg/L (0.84 [0.23-2.81] ng/mL; P=.009) than in cats without these characteristics (0.45 [0.12-1.70] and 0.35 [0.015-0.96] ng/mL). The in-hospital case fatality rate was 29%. Neither serum cTnI concentration for all critically ill cats (area-under-the-curve 0.567 [95% CI 0.454-0.680], n=119) or subgroups (0.625 [0.387-0.863], n=27; 0.506 [0.360-0.652], n=86), nor APPLE scores (fast 0.568 [0.453-0.682], full 0.585 [0.470-0.699], n=100), were significant prognosticators for death. Abnormally high serum cTnI concentration was common in critically ill cats. Unlike in dogs, cTnI did not confer prognostic information regarding death.

EVALUATION OF PLASMA CARDIAC TROPONIN I IN ASIAN ELEPHANTS (ELEPHAS MAXIMUS) USING TWO CLINICAL ANALYZERS.

Cardiac troponin I (cTnI) is specific to myocardial tissue, highly conserved across taxa, and a reliable indicator of myocardial disease in human and veterinary medicine. Biomarkers, like cTnI, may be useful for cardiac evaluation of elephants because the application of other modalities is complicated by the size of the animal. The goal of this study was to establish observed ranges for plasma cTnI in Asian elephants (Elephas maximus) measured by two point-of-care analyzers. Blood was collected from captive juvenile (≤15 yr; n = 9), adult (16-50 yr; n = 42), and geriatric (>50 yr; n = 16) elephants. Following centrifugation, heparinized plasma was stored at 5°C prior to and in between analyses on iSTAT (Abbott Point of Care Inc, Princeton, NJ 08540, USA) and HUBI-QUANpro (Humiasis Co, Ltd, Anyang-si 14042, South Korea) analyzers. With the exception of two results, plasma concentrations of cTnI were below the limit of quantification (LOQ < 0.05 ng/ml) for the HUBI-QUANpro (n = 64), which prohibited comparison between the two analyzers. Observed ranges were determined for plasma cTnI concentrations reported by the iSTAT for the entire population sampled (n = 58; mean 0.011 ng/ml; SD ± 0.013 ng/ml; range 0.00-0.07 ng/ml; 95% CI 0.008-0.015 ng/ml; median 0.01 ng/ml) and with outliers excluded (n = 50; mean 0.007 ng/ml; SD ± 0.007 ng/ml; range 0.00-0.02 ng/ml; 95% CI 0.005-0.009 ng/ml; median 0.01 ng/ml). No significant differences were observed between age classes (P = 0.70) or sexes (P = 0.34). Higher cTnI concentrations were significantly correlated with increasing age (Pearson's r = 0.426; P = 0.002). Future studies are warranted to investigate the diagnostic potential of plasma cTnI in Asian elephants.