Serum cTnI Research Articles

Comparison of Two Commercially Available Immunoassays for the Measurement of Bovine Cardiac Troponin I in Cattle With Induced Myocardial Injury

Background: Multiple cardiac troponin I (cTnI) immunoassays are commercially available. Overall, assays have not been standardized, and inter-assay differences in the detection of the analyte cardiac troponin I can be clinically relevant.Objective: To compare the diagnostic accuracy of the commercially available Abbott i-STAT®1 cTnI immunoassay (i-STAT) and the previously validated ADVIA Centaur TnI-Ultra immunoassay (Centaur) in cattle.Hypothesis: There will be significant differences in bovine serum cTnI results measured by the Centaur and i-STAT methods.Animals: Ten dairy cows with experimentally induced myocardial injury due to monensin administration. Thirty apparently healthy dairy cows with no history of monensin exposure served as controls.Methods: Blood was collected at various time points after administration of a single dose of monensin (20 to 50 mg/kg) via orogastric tube. A total of 112 blood samples were collected. Cardiac TnI concentration was analyzed with the two methods and the association between methods analyzed via linear regression. Bland-Altman analysis to evaluate agreement between methods was performed on samples divided into groups (cTnI < 1.0 ng/mL and cTnI ≥ 1.0 ng/mL).Results: Analyzer results were linearly correlated with each other (R2 = 0.931). Samples with cTnI concentrations <1.0 ng/mL had a bias of −0.13 ± 0.20 ng/mL and samples with cTnI concentrations >1.0 ng/mL had a bias of −9.81 ± 13.26 ng/mL.Conclusions and clinical importance: The results of this study reveal that cTnI concentrations determined with the i-STAT are systematically lower compared to the concentrations determined by the Centaur.

Correlations between cardiac troponin I and nonsustained ventricular tachycardia in hypertrophic obstructive cardiomyopathy.

BackgroundNonsustained ventricular tachycardia (NSVT) is an independent risk factor for sudden cardiac death (SCD) in patients with hypertrophic obstructive cardiomyopathy (HOCM). However, data concerning the correlations of cardiac biomarkers and NSVT in HOCM are rather limited.HypothesisOur study aimed to investigate the associations between the occurrence of NSVT and circulating biomarkers representing myocardial injury (cardiac troponin I, cTnI), cardiac function (N‐terminal pro‐brain natriuretic peptide, NT‐pro BNP), and inflammation (high‐sensitivity C‐reactive protein) in a large Chinese HOCM cohort.MethodsA total of 755 consecutive HOCM patients were recruited. Systematic cardiac evaluations and circulating biomarkers were examined routinely in all subjects under the clinically stable status. According to the results of 24‐hour Holter monitoring, patients were divided into the NSVT group (n = 138) and the nonventricular tachycardia (non‐VT) group (n = 617).ResultsCompared with the non‐VT group, circulating levels of both cTnI and NT‐pro BNP elevated significantly in patients with positive NSVT episodes (P < .001). Multivariable analyses demonstrated that cTnI was independently associated with the presence of NSVT (OR = 1.675, 95% CI: 1.406‐1.994, P < .001). Concentrations of cTnI increased progressively not only with the aggravation of ventricular arrhythmic events (P < .001), but also with the growing risk of SCD in HOCM patients (P < .001). Serum cTnI ≥ 0.0265 ng/mL indicated predictive value for the occurrence of NSVT in the HOCM cohort (area under the curve = 0.707, 95% CI: 0.660‐0.754, P < .001).ConclusionsElevated cTnI was an independent determinant of NSVT, and it seemed to be valuable for assessing the clinical status of ventricular arrhythmias and the risk of SCD in patients with HOCM.

Identifying Cardiac Diseases using Cardiac Biomarkers in Rhesus Macaques (Macaca mulatta).

Cardiac biomarkers are an important tool for diagnosing cardiac diseases in both human and veterinary patients. Serum concentrations of N-terminal probrain natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) have been used to indicate the presence of various cardiac diseases including hypertrophic cardiomyopathy (HCM) in various species including humans. However, these cardiac biomarkers have not been established as a diagnostic tool for detecting cardiac disease in rhesus macaques. In the rhesus macaque colony at the California National Primate Research Center, naturally occurring HCM and various other cardiac diseases have been identified. In this study, commercially available assays were used to measure serum cTnI and NT-proBNP concentrations to evaluate their utility as a diagnostic screening tool for cardiac diseases in rhesus macaques. This study revealed that the serum cTnI concentration was significantly higher in animals with echocardiographically apparent cardiac disease as compared with the animals that had no cardiac structural and functional changes (the control group). However, no significant differences were detected between animals with HCM and non-HCM cardiac disease. Because the area under the receiver operating characteristic curve was 0.81 when the serum cTnI was compared between the control and cardiac disease groups, serum cTnI was considered a moderately accurate test to predict the presence of cardiac disease. The optimal cut-off value of serum cTnI concentration for diagnosis of cardiac disease was 0.0085 ng/mL, with a sensitivity of 0.68 and specificity of 0.94. Significant but weak correlations were noted between the serum cTnI concentration and several echocardiographic parameters. Conversely, no significant differences in NT-proBNP concentrations were detected between animals with and without cardiac diseases. In conclusion, measurement of serum cTnI can be used to aid in diagnosing cardiac diseases in rhesus macaques. However, cTnI measurement does not replace echocardiographic evaluation to diagnose cardiac diseases in rhesus macaques due to the poor sensitivity of the assay and the weak correlation to with more established echocardiographic markers for cardiac disease.

Dual-mode of electrochemical-colorimetric imprinted sensing strategy based on self-sacrifice beacon for diversified determination of cardiac troponin I in serum

Diversified determination of cardiac troponin I (cTnI) in serum is of great significance for the clinical diagnose and daily monitoring of acute myocardial infarction. Herein, an electrochemical-colorimetric dual-mode imprinted sensing strategy was proposed. Firstly, the aptamer-functionalized Fe3+-polydopamine (Apt@Fe3+-PDA) was constructed as the self-sacrifice beacon. Furthermore, an epitope magnetic molecularly imprinted polymer was prepared to recognize cTnI. Once the cTnI was captured, the beacon was then bound to it through the aptamer, which formed a sandwich-like complex. Under acidic condition, the Apt@Fe3+-PDA was disintegrated to release large amount of Fe3+, and further converted to Prussian blue (PB). On one hand, the electrochemical response of the PB was sensitive to the cTnI amount. On the other hand, the addition of the yellow K3[Fe(CN)6] into different amounts of the produced PB was able to result in different colors, which enabled the visual detection of cTnI. Under the optimal condition, the sensing strategy exhibited a linear range from 1.0 × 10−2 to 1.0 × 103 ng mL−1, and the detection limits were 3.2 and 7.4 pg mL−1 for the electrochemical and colorimetric modes, respectively. Besides, It is demonstrated that the dual-mode strategy shows favorable selectivity and stability in the assays, indicating a diversified application prospect in both clinic analysis and daily care.

Elevated troponin levels are associated with early neurological worsening in ischemic stroke with atrial fibrillation

Serum cardiac troponin I (cTnI) is often elevated in patients with ischemic stroke, and is associated with their prognosis. Since cTnI is also closely related to atrial fibrillation (AF), cTnI may be a sensitive prognostic indicator in patients with AF-related stroke. This study aimed to evaluate the association between serum cTnI and early neurological deterioration (END) in patients with AF-related stroke. We included consecutive AF-related stroke patients between 2013 and 2015. END was defined as an increase ≥ 2 in the total NIHSS score or ≥ 1 in the motor NIHSS score within the first 72 h of admission. A total of 1,133 patients with AF-related stroke were evaluated. In multivariable analysis, cTnI [adjusted odds ratio (aOR) = 1.16, 95% confidence interval (CI) 1.00–1.34; P = 0.047] remained significant after adjusting for confounders. Initial NIHSS score (aOR = 1.03, 95% CI 1.00–1.06; P = 0.043) was also positively associated with END; meanwhile, the use of anticoagulants was negatively associated in both vitamin K antagonists (aOR = 0.35, 95% CI 0.23–0.54; P < 0.001) and new oral anticoagulants (aOR = 0.41, 95% CI 0.19–0.89; P = 0.024). In conclusion, higher serum cTnI was associated with END in patients with AF-related stroke.

Two different troponin isoforms for detecting early myocardial injury after curative resection of oesophageal cancer

BackgroundThe objective of this study was to explore the consistency and correlation of two troponin (cTn) subtypes, troponin I (cTnI) and high-sensitivity troponin T (hs-cTnT), which can be used to judge early myocardial injury after curative resection of oesophageal cancer.MethodsThis study is a secondary analysis of data obtained from a previous randomized controlled trial on postoperative myocardial injury in 70 patients undergoing elective curative resection of oesophageal cancer who were randomly assigned to undergo aggressive body temperature management (nasopharyngeal temperature 36.61 ± 0.18 °C) or standard body temperature management (35.80 ± 0.18 °C, n = 35 in each arm). The serum cTnI and hs-cTnT levels were measured in each patient at the 4 time points: before the operation and 6 h ~ 12 h, 24 h and 48 h after the operation. The diagnostic criteria of myocardial injury followed the third edition ESC/ACCF definition of myocardial infarction. The primary outcomes included the following: (1) the incidence of myocardial injury and the relationship between hs-cTnT and cTn and (2) the consistency and correlation of the two cTn subtypes.ResultsA total of 280 pairs of cTn samples were tested. The incidence of postoperative day 2 myocardial injury was 8.6% (3/35) among patients receiving aggressive body temperature management and 31.4% (11/35) among patients receiving standard body temperature management (P < 0.05). Among 3 patients who experienced myocardial injury in the aggressive body temperature management group, 2 met the diagnostic criteria for cTnI and hs-cTnT and only 1 met the diagnostic criteria for hs-cTnT. Among the 11 patients who experienced myocardial injury in the standard body temperature management group, 7 met the diagnostic criteria for cTnI and hs-cTnT and only 3 met the diagnostic criteria for hs-cTnT; only 1 met the diagnostic criteria for cTnI. The bias of cTnI and hs-cTnT was − 8.82 ± 31.91 ng/L. The consistency limit was − 71.37 ~ 53.73 ng/L. The proportion within the scope of the consistency of its corresponding boundary was 98.57%. The correlation coefficient of cTnI and hs-cTnT was 0.845 (P < 0.05).ConclusionsIn the evaluation of postoperative myocardial injury in patients undergoing curative resection of oesophageal cancer, cTnI and hs-cTnT exhibit high consistency and a good correlation. The combination of cTnI and hs-cTnT can improve the detection rate of myocardial injury, thus providing a better reference than a single measure alone for reducing the risk of perioperative myocardial injury in patients.Trial registrationChiCTR-INR-17011621. Registered June 10, 2017.

Detection of Early Myocardial Injury in Children with Ventricular Septal Defect Using Cardiac Troponin I and Two-Dimensional Speckle Tracking Echocardiography.

Children with ventricular septal defects (VSDs) are subjected to hemodynamic overload which causes myocardial injury and subsequent heart failure. Early stages of myocardial damage cannot be detected by conventional echocardiography. Two-dimensional speckle tracking echocardiography (2D-STE) and cardiac troponin I (cTnI) have been recently introduced as more accurate tools for early assessment of cardiovascular diseases. The purpose of this study is to evaluate the role of cardiac troponin I (cTnI) and 2D-STE in the early detection of VSD-induced myocardial injury. Thirty children with VSD (symptomatic and asymptomatic) and 30 controls were assessed serologically by measuring serum cTnI and by conventional echocardiography. STE was performed to measure the averaged global peak longitudinal systolic stain [G peak SL(AVG)]. Serum cTnI levels were significantly higher in patients when compared to controls (P < 0.05) and in the symptomatic group when compared to the asymptomatic group (P < 0.05). Serum cTn I level correlated positively with the left atrial (r = 0.37, P = 0.045) and left ventricular dimensions (r = 0.46, P = 0.01) and negatively with the G peak SL(AVG) (r = -0.39, P = 0.03). There were no statistically significant differences between patients and controls or between symptomatic and asymptomatic groups with regard to the G peak SL(AVG). The peak longitudinal systolic strain (measured by 2D-STE) is not affected despite the elevation of serum cTnI. Serum cTnI is a sensitive marker for early detection of myocardial injury in VSD patients even before the development of ventricular dilatation or dysfunction.

Nimbolide prevents myocardial damage by regulating cardiac biomarkers, antioxidantlevel, and apoptosis signaling against doxorubicin-induced cardiotoxicity in rats.

The current work planned to assess the protecting properties of nimbolide against doxorubicin (DOX)-treated myocardial damage. Myocardial damage was produced with2.5 mg/kg of DOX given onalternative days (14 days). Thiobarbituric acid reactive substances (TBARS) levels of alipid peroxidative marker were elevated, whereas reduced body weight, heart weight, blood pressure indices and reduced levels of antioxidants like glutathione-S-transferase, superoxide dismutase, catalase, glutathione peroxidase, glutathione, and glutathione reductase were observed in the heart tissue of DOX-treated animals. DOX-treated animalsshowedaugmented levels of cardiac markers likes monocyte chemotactic protein-1, interferon-gamma, aspartate transferase, creatine kinase, lactate dehydrogenase, creatine kinase-muscle/brain, heart-type fatty acid-binding protein, glycogen phosphorylase isoenzyme BB, transforming growth factor-β, brain natriuretic peptide, myoglobin, and cTnI in serum. Histopathological assessment confirmed the DOX-induced cardiotoxicity. Furthermore, DOX-induced rats showed augmented inflammatory mediators (nuclear factor-κB [NF-kB], tumor necrosis factor-α [TNF-α], and interleukin-1β [IL-1β]) and increased PI3K/Akt signaling proteins (PI3K, p-Bad/Bad, caspase-3, and p-Akt), whereas decreased oxidative markers (HO-1 and NQO-1) and p-PTEN were observed. Nimbolide-supplemented rats showed reduced activity/levels of cardiac markers and TBARS levels in serum and heart tissue. Levels of enzymatic and nonenzymatic antioxidants were augmented in the heart tissue of nimbolide-supplemented rats. Nimbolide influence decreased apoptosis, inflammation, and enhanced antioxidant markers through the modulation of p-Bad/Bad, caspase-3, PI3K, p-Akt, TNF-α, NF-kB, IL-1β, HO-1, NQO-1, and p-PTEN markers. The histopathological explanations were observed to be in line with biochemical analysis. Therefore, the findingof current work wasthat nimbolide has a defensiveeffect onthe myocardium against DOX-induced cardiac tissue damage.

Assessment of left ventricular systolic function in hypertrophic cardiomyopathy patients with myocardial injury: a study based on layer-specific speckle tracking echocardiaography.

We conducted this study to investigate left ventricle (LV) systolic function in endocardial, mid-myocardial, and epicardial layers by two-dimensional (2D) speckle tracking echocardiography (STE) in hypertrophic cardiomyopathy (HCM) patients with myocardial injury indexed by elevated serum cardiac troponin I (cTnI). Twenty-nine HCM patients with myocardial injury, thirty-five HCM patients without myocardial injury, and ninty-one healthy controls were enrolled in this study. Serum cTnI > 0.026ng/mL was defined as myocardial injury. LV longitudinal and circumferential strain (LS and CS) were assessed in endocardial, mid-myocardial and epicardial layers. Layer-specific LS and CS differed significantly (all P < 0.001) among all three groups in all three layers, in a descending order from healthy controls to HCM patients without myocardial injury to HCM patients with myocardial injury. Layer-specific LS and CS were decreased the most in HCM patients with myocardial injury indexed by elevated seum cTnI (all P < 0.05). In HCM patients with myocardial injury, layer-specific LS and CS were significantly lower in the segments with greater hypertrophy (segmental thickness ≥ 15mm) (all P < 0.001) except for endocardial CS (P > 0.05). Layer-specific evaluation of LV strain may improve understanding of impaired LV systolic function in HCM patients with myocardial injury, thus preventing further damage.

The impact of dietary tarragon (Artemisia dracunculus) on serum apelin, brain-derived neurotrophic factor, cardiac troponin concentrations and histopathology of liver tissue in laying hens housed at different stocking densities

Due to its association with several other stress factors (poultry house gases, inadequate ventilation, heat, cold and poor hygiene), the high stocking density is a major stress factor that adversely affects the health and performance of poultry and the quality of the poultry products. Therefore, this experimental study was aimed at analysing the impact of different doses of dietary tarragon (Artemisia dracunculus) on the serum apelin, plasma brain-derived neurotrophic factor (p-BDNF), and cardiac troponin I (cTnI) concentrations, and the correlation between these indicators in laying hens housed at different stocking densities. The aim of this study is to investigate the effects of adding tarragon in different ratios to laying hen rations in the 2&lt;sup&gt;nd&lt;/sup&gt; ovulation period on the cTnI, apelin, and BDNF hormone concentrations and the liver histopathology. The experiment was carried out over a period of eight weeks, with 192 Lohman Brown commercial hybrids at 50 weeks of age. Eight groups (four replicates each), composed of laying hens of equal body weight, which were housed at stocking densities of 580 cm&lt;sup&gt;2&lt;/sup&gt;/hen and 810 cm&lt;sup&gt;2&lt;/sup&gt;/hen and received 0, 1, 5 and 10 mmol/kg of tarragon (Artemisia dracunculus) in the feed, were established. At the end of the trial, 96 of the housed egg-laying hens (3 birds in each subgroup, a total of 12 birds in each group) were randomly selected and blood samples were taken from the vena subcutanea ulnaris. The samples collected were analysed for the apelin, p-BDNF, and cTnI contents. The analysis results demonstrated that tarragon supplementation had no effect on the serum apelin, p-BDNF and cTnI concentrations (P &amp;gt; 0.05). The Sub-Groups ST1, ST1.2, and ST6 presented with severe hyperaemia of the sinusoidal, portal and acinar blood vessels, whilst the hyperaemia of these blood vessels was moderate in Sub-Group ST12. Apelin, BDNF, and cTnI can act as protective factors against negative consequences of stress (e.g., stocking density or heat stress).

Ambulatory electrocardiography and serum cardiac troponin I measurement in 21 dogs envenomated by the European adder (Vipera berus).

BackgroundEnvenomation by the European adder (Vipera berus) is common in dogs in Europe. Cardiac arrhythmias occur but clinical studies of envenomated dogs are limited.ObjectivesTo describe arrhythmias in dogs within 48 hours of envenomation, and investigate associations between arrhythmia grade, serum troponin I (cTnI), and snakebite severity score (SS score).AnimalsTwenty‐one client‐owned dogs bitten by V berus.MethodsProspective cohort study of envenomated dogs. Ambulatory electrocardiograms were recorded from presentation to 48 hours after snakebite, and arrhythmias graded 0 to 3 based on frequency and severity. Serum cTnI was measured at presentation, 12 hours, 24 hours, 36 hours, and 14 days after bite. An SS score of 1 to 3 was recorded at admission and based on clinical examination.ResultsAll dogs survived. Twelve dogs (57%) developed arrhythmias, all of which were ventricular in origin. Severe complex ventricular arrhythmias (VAs) were observed in 6 dogs (29%). Eighty‐one percent of dogs (n = 17) had increased cTnI concentrations at 1 or more time points. Dogs that developed arrhythmias had significantly higher concentrations of cTnI at 12 hours (1.67 [0.04‐32.68] versus 0.03 [0.01‐0.052]; P = .002), 24 hours (1.88 [0.2‐14.23] versus 0.06 [0.01‐2.06]; P = .009), and 36 hours (3.7 [0.02‐16.62] versus 0.06 [0.01‐1.33]; P = .006) after bite compared to those that did not. Contingency table analysis showed that SS score was not significantly associated with arrhythmia grade (P = .9).Conclusions and Clinical ImportanceMyocardial cell injury, reflected by increased cTnI concentrations and VAs, is common after V berus envenomation in dogs. Prolonged electrocardiography monitoring is advised, particularly where cTnI is increased.

Investigation of the myocardial damage due to acute anemia in a rabbit model of acute normovolemic anemia

Myocardial damage and increased circulating cardiac troponin I (cTnI) concentrations have been shown in various diseases that cause anemia in animals. Whether the acute anemia that occurs during these diseases directly contributes to myocardial damage and to the release of cTnI to the circulation still remains unclear. The objective of this study was to investigate the effect of acute anemia on myocardial damage and serum cTnI concentration using experimentally-induced acute normovolemic anemia. New Zealand rabbits were randomly separated into 2 groups: an acute anemia group (AG, n = 8) and a control group (CG, n = 6). To induce acute anemia, repeated jugular phlebotomy was performed. Blood samples were collected before the experiment (0) and at 24, 48, 72, 96, and 120 h. Serum cTnI concentrations were measured using a human specific cTnI assay. After the last blood sample was taken, euthanasia was performed to evaluate the histopathological changes and the cTnI immunolabelling in cardiomyocytes. In the AG, the mean packed cell volume (PCV) was 13.1 ± 1.4% at 120 h. The median serum cTnI concentrations in the AG and the CG were 0.075 (IQR; 0.017?0.077) and 0.015 ng/mL (IQR; 0.01?0.02) at the 120-h mark, respectively (P < 0.01). There was a negative correlation between PCV and serum cTnI concentrations (r = -0.52, P < 0.001). In addition, serum cTnI concentrations were significantly correlated with both the histopathological score (r = 0.75, P < 0.001) and cTnI immunoreactivity (r= -0.79, P < 0.001). The results of this study showed that acute anemia caused histopathological lesions and loss of cTnI immunolabelling in cardiomyocytes, along with an increase in serum cTnI concentrations.

Predictive Role of Cardiac Troponin I, Creatine Kinase-Mb and Electrocardiogram in Early Assessment of Acute Cardiotoxicity in Patients Poisoned by Cardiotoxic Drugs and Toxins

Background: In spite speedy development of clinical toxicology researches and protocols cardiovascular failure in severe acute intoxication remains a leading cause of death. Early cardiovascular risk assessment in acutely intoxicated patients is a must nowadays.&#x0D; This study aims to evaluate the role of ECG, serum cardiac troponin I (cTnI) and creatine kinase myocardial band (CK-MB) for early detection of cardio-toxicity in acutely poisoned patients.&#x0D; Methods: Prospective study was carried on100 patients with acute cardiotoxicity by drugs and toxins known to cause cardiac injury admitted to Sohag University hospitals, informed written consent has been obtained from each patient; ECG and biochemical analysis of serum cTnI and CK-MB were estimated in all studied patients.&#x0D; Results: (90%) of studied patients had complete free recovery, (4%) discharged with complications and (6%) of patients died. ECG test can be used as a predictor of mortality and had sensitivity 100%, specificity 46.8% and negative predictive value (NPV) 100%. Serum cTnI was highly significantly increased with death hence could be used as predictors of outcome. While serum CK-MB couldn't be used as an outcome predictor. ROC curve analysis to assess serum cTnI as a predictor of mortality of acute cardiovascular toxicity with cut off &gt; 1.0 ng/ml had sensitivity 100%, specificity 89.4% and NPV 100% with excellent diagnostic characteristic (accuracy rate 96.4%). There is no significant difference of serum CK-MB and serum cTnI among cardiac drugs toxicity patients and non-cardiac toxins patients.&#x0D; Conclusion: the study concluded that ECG and serum cTnI can be used as a predictor of mortality. Also, the protocol of management will be same in acute cardiotoxicity by cardiac drugs and non-cardiac drugs and toxins.&#x0D; Recommendation: the study recommends combining of ECG changes and serum cTnI as they can early detect acute cardiovascular effects in acutely poisoned patients.

Oxycodone inhibits myocardial cell apoptosis after myocardial ischemia-reperfusion injury in rats via RhoA/ROCK1 signaling pathway.

The purpose of this study was to investigate the effect of oxycodone on myocardial ischemia-reperfusion injury in rats through the Ras homolog gene family member A (RhoA)/Rho-associated coiled-coil containing protein kinase 1 (ROCK1) signaling pathway. A total of 48 Sprague-Dawley (SD) rats were randomly divided into sham operation group, model group, oxycodone group, and inhibitor group, with 12 rats in each group. The rats in the sham operation group only underwent thoracotomy without ischemia-reperfusion injury, those in the model group were used to prepare the myocardial ischemia-reperfusion model with normal saline intervention, those in the oxycodone group were used to prepare the myocardial ischemia-reperfusion model with oxycodone intervention, and those in the inhibitor group were utilized to prepare the myocardial ischemia-reperfusion model with AG490 intervention. Then, the expressions of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (BAX) were detected by immunohistochemistry, the relative protein expressions of RhoA and ROCK1 were examined via Western blotting, and the messenger ribonucleic acid (mRNA) expressions of Bcl-2 and BAX were measured by quantitative Polymerase Chain Reaction (qPCR). Thereafter, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was adopted for apoptosis detection, and the levels of creatine kinase-muscle/brain (CK-MB), and cardiac Troponin I (cTnI) in serum were detected using an automatic biochemical analyzer. Immunohistochemistry results showed that compared with those in the sham operation group, the positive expression of BAX was remarkably increased (p<0.05), while that of Bcl-2 was significantly decreased (p<0.05) in the model group, oxycodone group, and inhibitor group. Compared with the model group, oxycodone group and inhibitor group had an evidently reduced positive expression of BAX (p<0.05) and an evidently raised positive expression of Bcl-2 (p<0.05). No differences were found in the positive expressions of BAX and Bcl-2 between oxycodone group and inhibitor group (p>0.05). According to Western blotting results, the relative protein expressions of RhoA and ROCK1 in the model group, oxycodone group, and inhibitor group were notably increased compared with those in the sham operation group (p<0.05). In comparison with those in the model group, the relative protein expressions of RhoA and ROCK1 in the oxycodone group and inhibitor group were predominantly reduced (p<0.05). There were no differences in the relative protein expressions of RhoA and ROCK1 between oxycodone group and inhibitor group (p>0.05). Moreover, it was discovered from qRT-PCR results that compared with those in the sham operation group, the mRNA expression of BAX was markedly raised (p<0.05), whereas that of Bcl-2 was decreased predominantly (p<0.05) in the model group, oxycodone group, and inhibitor group. Compared with the model group, oxycodone group, and inhibitor group had an evidently reduced mRNA expression of BAX (p<0.05) and a significantly raised mRNA expression of Bcl-2 (p<0.05). No differences were found in the mRNA expressions of BAX and Bcl-2 between oxycodone group and inhibitor group (p>0.05). In addition, TUNEL assay results manifested that compared with sham operation group, model group, oxycodone group, and inhibitor group had a markedly elevated apoptosis rate (p<0.05). In comparison with the model group, the apoptosis rate in oxycodone group and inhibitor group was remarkably reduced (p<0.05). There was no difference in the apoptosis rate between oxycodone group and inhibitor group (p>0.05). According to biochemical analysis results, the serum levels of CK-MB and cTnI in model group, oxycodone group, and inhibitor group were significantly increased compared with those in the sham operation group, with statistically significant differences (p<0.05). The levels of serum CK-MB and cTnI in the oxycodone group and inhibitor group were substantially lowered in comparison with those in the model group, displaying statistically significant differences (p<0.05). Besides, the levels of serum CK-MB and cTnI in the oxycodone group were not different from those in the inhibitor group (p>0.05). Oxycodone inhibits myocardial cell apoptosis after myocardial ischemia-reperfusion injury by suppressing the RhoA/ROCK1 signaling pathway.

Effects of electroacupuncture pretreatment on mitochondrial energy metabolism in the rats with myocardial ischemia reperfusion: 电针预处理对心肌缺血再灌注大鼠线粒体能量代谢的影响

ObjectiveTo explore the effects of electroacupuncture pretreatment on mitochondrial energy metabolism in the rats with myocardial ischemia reperfusion injury (MIRI). MethodsA total of 60 SPF Wistar rats were randomly divided into a sham-operation group (sham group), a myocardial ischemia reperfusion injury group (MIRI group) and an electroacupuncture pretreatment group (EA group), 20 rats in each one. The rats in the sham group and the MIRI group were binded for 7 days, once a day, 20 min each time. On the 8th day, the sample was collected after the heart exposed for 50 min in thoractomy in the sham group and the sample was collected after ischemia for 20 min and reperfusion for 30 min in thoractomy in the MIRI group. In the EA group, the pretreatment intervention with electroacupuncture was applied at "Nèiguān (内关PC6)", "Guānyuán (关元CV4)" and "Zúsānlĭ (足三里ST36)" in the rats for 7 days, once a day, 20 min each time. On the 8th day, after ischemia for 20 min and reperfusion for 30 min in thoractomy, the sample was collected in the EA group. The changes in STⅡ segment of electroacardiogram (ECG) were observed and measured. Using enzyme-linked immunosorbent assay (ELISA), the concentrations of cardiac troponin T (cTnT) and cardiac troponin I (cTnI)were detected. Using nitro blue tetrazolium chloride monohydrate (NBT) staining, the myocardial infarction weight percentage was measured. Using ELISA, the concentrations of mitochondrial adenosine monophosphate (AMP), adenosine diphosphate (ADP)and adenosine triphosphate (ATP)were detected. Results(1) STⅡ changes: in 20 min of ligation, compared with the sham group, the STⅡ segment of electrocardiograph (ECG) was elevated significantly in the MIRI group and EA group (both P < 0.01), but the elevation range in the EA group was lower than that of the MIRI group (P < 0.01). After reperfusion for 30 min, the STⅡ segment was fallen by over 50% in the MIRI group and the EA group. Simultaneously, the STⅡ segment in the EA group was lower than that of the MIRI group (P < 0.01). (2) Regarding myocardial infarction weight percentage, compared with the sham group, the infarction weight was larger in the MIRI group and the EA group (both P < 0.05) and the infarction weight in the EA group was lower than that of the MIRI group (P < 0.05). (3) Regarding the levels of serum cTnt and cTnI, compared with the sham group, the levels of serum cTnT and cTnI were higher in the MIRI group and the EA group (all P < 0.01) and the levels of cTnT and cTnI in the EA group were lower than that of the MIRI group (both P < 0.01). (4) Regarding the concentrations of AMP, ADP and ATP, compared with the sham group, ATP concentration was lower in the MIRI group and the EA group (both P < 0.01) and the concentrations of AMP and ADP were higher (P < 0.05, P < 0.01). Compared with the MIRI group, ATP concentration was higher in the EA group (P < 0.05) and the concentrations of AMP and ADP were lower (both P < 0.01). ConclusionsElectroacupuncture pretreatment reduces the elevation of ECG STⅡ segment, decreases the concentrations of myocardial injury markers, cTnT and cTnI and regulates the transfer among AMP, ATP and ADP. The protective effect of electroacupuncture pretreatment may result from the regulation of mitochondrial energy metabolism.

Evaluation of N-terminal prohormone of brain natriuretic peptide and cardiac troponin-I levels in cats with systolic anterior motion of the mitral valve in the absence of left ventricular hypertrophy

ObjectivesTo identify the prevalence of systolic anterior motion of the mitral valve (SAM) in apparently healthy cats in the absence of left ventricular hypertrophy (LVH) and examine the relationship between specific cardiac biomarker concentrations and echocardiographic parameters in these individuals. Animalseighty client-owned cats. Materials and methodsretrospective study; inclusion criteria were the presence of SAM on conscious echocardiography and concurrent measurement of plasma N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and serum cardiac troponin-I (cTnI). Cats were excluded if they had LVH, left atrial enlargement or systemic disease. The percentages of cats with NT-proBNP and cTnI concentrations above the normal reference range were calculated. The correlation between each biomarker concentration and left ventricular myocardial wall thickness, left atrial size and maximum left ventricular outflow tract velocity was evaluated. ResultsThirty-four of 80 patients with SAM showed no evidence of cardiac remodelling (LVH or left atrial enlargement). Of these patients, 30 of 34 had elevated NT-proBNP, and cTnI was elevated in 13 of 27 (48.1%) cats where this biomarker was measured in association with the NT-proBNP assay. A positive correlation was observed between concentration of plasma NT-proBNP and maximum left ventricular outflow tract velocity (rs = 0.67, p<0.0001). No significant correlations were found between the concentration of biomarkers and the remaining echocardiographic parameters. ConclusionsSAM is frequently observed in cats even in the absence of cardiac remodelling, and these individuals often demonstrate elevated plasma NT-proBNP and serum cTnI concentrations. Plasma NT-proBNP elevation is correlated with the severity of the left ventricular outflow obstruction caused by SAM.

Time-resolved fluorescence resonance energy transfer-based lateral flow immunoassay using a raspberry-type europium particle and a single membrane for the detection of cardiac troponin I

Herein, we report a novel lateral flow immunoassay (LFIA) system for detecting cardiac troponin I (cTnI) in serum using the time-resolved fluorescence resonance energy transfer (TR-FRET) technique and the fusion 5 membrane. The fusion 5 membrane is used as a strip for LFIA, and it is constructed without additional matrices (such as a sample or conjugation pad). Although this strategy for constructing the LFIA strip is quite simple and cost-effective, LFIA is still not suitable for the analysis of biomarkers that require high sensitivity, such as cTnI. Therefore, the highly sensitive TR-FRET technique is integrated with a fusion 5 membrane-based LFIA strip. To accomplish this, a microparticle covered with europium chelate-contained silica nanoparticles is synthesized as a raspberry-type particle and used as a fluorescence donor. A gold nanorod (GNR) is used as a fluorescence acceptor particle. In the TR-FRET-based LFIA system, the competitive immunoassay should be performed to satisfy the condition required for the FRET phenomenon to occur. Therefore, the fluorescence signal is proportional to the cTnI concentration, ensuring a quantitative analysis of cTnI can be accomplished by measuring the fluorescence signal between the raspberry-type europium particles and GNR. Using the developed TR-FRET-based LFIA system, sensitive detection of cTnI is successfully achieved with a limit of detection of 97 pg/mL in human serum. Moreover, because the result can be obtained using one matrix (the fusion 5 membrane), the developed LFIA system can be employed in cTnI diagnosis with a simple manufacturing process.

Protective effect of astragalus injection against myocardial injury in septic young rats via inhibition of JAK/STAT signal pathway and regulation of inflammation

Purpose: To investigate the protective effect of astragalus injection against myocardial injury in septic young rats, and the underlying mechanism of action.&#x0D; Methods: Seventy-two healthy Sprague Dawley (SD) rats were randomly selected and used to establish a young rat model of sepsis. The young rats were randomly divided into 3 groups: sham, model and astragalus injection groups. Each group had 24 young rats. Serum cardiac troponin I (cTnI), IL-10, IL-6, JAK2 and STAT3 were measured after op.&#x0D; Results: Compared with sham group, serum cTnI level in the model group was significantly higher, while serum cTnI level of the drug group was significantly lower than that of the model group (p &lt; 0.05). Compared with model group, the level of IL-10 in the myocardial tissue of the drug group was significantly elevated, while IL-6 level was lower (p &lt; 0.05). Relative to sham rats, myocardial JAK2 and STAT3 protein levels in model rats were high. However, myocardial JAK2 and STAT3 proteins in the drug-treated rats were significantly downregulated, relative to model rats (p &lt; 0.05).&#x0D; Conclusion: Astragalus injection upregulates IL-10 and IL-6 in rats by inhibiting the activation of JAK/STAT signal pathway, and via maintenance of pro-inflammation/anti-inflammation balance. Thus, astragalus exerts protective effect against myocardial injury in sepsis, and can potentially be developed for use as such in clinical practice.&#x0D; Keywords: Astragalus injection, JAK/STAT signal pathway, Pro-inflammatory/anti-inflammatory imbalance, Sepsis, Myocardial injury

Evaluation of Cardiac Troponin I as a Non Invasive Tool for Diagnosis of the Newborns and Infants Below 6 Months with Congenital Heart Diseases

Background Congenital heart diseases accounts for nearly one third of all major congenital anomalies. Different modalities for diagnosis of CHD are available, in spite of that only 73% can be diagnosed before discharge from hospital, while 27% discharged without diagnosis. There is an increasing need for new diagnostic modalities to help early diagnosis and screening of CHD, biomarkers as cardiac troponin I represents an excellent choice. Aim The aim of this study is to find new, easy and noninvasive diagnostic modalities for earlier detection of congenital heart diseases. Patients /Methods The study was case control study. The study involved 50 cases. cases will be divided into 2 main groups: group (1) 25 patients with congenital heart diseases confirmed by echocardiography, group (2) (control) 25 healthy newborns and infants, patients with CHD in group (1) was further divided into 2 subgroups: group (1a) patients with simple shunts, group (1b) patients with combined defects. Each case was subjected to complete history, physical examination, and peripheral blood samples were withdrawn and cardiac troponin I level was measured. Results Serum level of cardiac troponin I (cTnI) was higher in the diseased group compared to the control group, and is higher in patients with complex defects compared to patients with simple shunts. The sensitivity of the test was 72% and the specificity was 92%. Conclusion Serum cTnI level was found to have a statistically significant association with congenital heart disease, being higher in complex defects than simple shunts.

Heat Shock Protein 70 Protects the Heart from Ischemia/Reperfusion Injury through Inhibition of p38 MAPK Signaling.

Background Heat shock protein 70 (Hsp70) has been shown to exert cardioprotection. Intracellular calcium ([Ca2+]i) overload induced by p38 mitogen-activated protein kinase (p38 MAPK) activation contributes to cardiac ischemia/reperfusion (I/R) injury. However, whether Hsp70 interacts with p38 MAPK signaling is unclear. Therefore, this study investigated the regulation of p38 MAPK by Hsp70 in I/R-induced cardiac injury. Methods Neonatal rat cardiomyocytes were subjected to oxygen-glucose deprivation for 6 h followed by 2 h reoxygenation (OGD/R), and rats underwent left anterior artery ligation for 30 min followed by 30 min of reperfusion. The p38 MAPK inhibitor (SB203580), Hsp70 inhibitor (Quercetin), and Hsp70 short hairpin RNA (shRNA) were used prior to OGD/R or I/R. Cell viability, lactate dehydrogenase (LDH) release, serum cardiac troponin I (cTnI), [Ca2+]i levels, cell apoptosis, myocardial infarct size, mRNA level of IL-1β and IL-6, and protein expression of Hsp70, phosphorylated p38 MAPK (p-p38 MAPK), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase2 (SERCA2), phosphorylated signal transducer and activator of transcription3 (p-STAT3), and cleaved caspase3 were assessed. Results Pretreatment with a p38 MAPK inhibitor, SB203580, significantly attenuated OGD/R-induced cell injury or I/R-induced myocardial injury, as evidenced by improved cell viability and lower LDH release, resulted in lower serum cTnI and myocardial infarct size, alleviation of [Ca2+]i overload and cell apoptosis, inhibition of IL-1β and IL-6, and modulation of protein expressions of p-p38 MAPK, SERCA2, p-STAT3, and cleaved-caspase3. Knockdown of Hsp70 by shRNA exacerbated OGD/R-induced cell injury, which was effectively abolished by SB203580. Moreover, inhibition of Hsp70 by quercetin enhanced I/R-induced myocardial injury, while SB203580 pretreatment reversed the harmful effects caused by quercetin. Conclusions Inhibition of Hsp70 aggravates [Ca2+]i overload, inflammation, and apoptosis through regulating p38 MAPK signaling during cardiac I/R injury, which may help provide novel insight into cardioprotective strategies.