cTnI Concentrations Research Articles

CTnI diagnosis in myocardial infarction using G-quadruplex selective Ir(Ⅲ) complex as effective electrochemiluminescence probe

In this work, strong electrochemiluminescence (ECL) emission was achieved by using one type of the G-quadruplex selective iridium (III) complex as an efficient ECL signal probe. Based on the typical sandwich immunoreaction between the cardiac troponin-I antigen (cTnI) and its corresponding antibody, iridium (III) complex was introduced according to its specific interaction with G-quadruplex DNA that modified on the surface of negatively charged gold nanoparticles ((−)AuNPs), inducing an increased ECL signal, which was proportional to cTnI concentration. Based on of this, quantitative detection of cTnI could be realized in the range of 5.0 fg/mL-100 ng/mL, with a detection limit of 1.67 fg/mL. Moreover, the proposed immunosensor was successfully applied for the diagnosis of cTnI in human serums from healthy individuals and acute myocardial infarction (AMI) patients, suggesting a great potential application value in the early diagnosis of AMI.

Ultrasensitive photoelectrochemical immunosensor based on Dual-Photosensitive electrodes

In the study, a photoelectrochemical (PEC) immunosensor based on dual-photosensitive electrodes was developed for cardiac troponin I (cTnI) detection. The sensing photocathode with biometric functions was prepared by CuInS2 and narrow band gap semiconductor In2S3 as the counter electrode. In this way, the separation of photoanode and biometric events was realized, and the ability of stability of the immunosensor could be effectively improved. Moreover, the attraction to the photogenerated electrons (e-) from photoanode would be increased by the abundant holes (h+) of photocathode, under the radiation of light. This tremendously improves the photoelectric response, which further improves the sensitivity of the immunosensor. The controllable-synthesis uncomplicated photoelectric material not only accords with the principle of simplicity of electrode modification but also makes the immunosensor more conducive to the practical application. Additionally, even in the case of zero bias voltage, the constructed PEC immunosensor can operate with high efficiency, namely, self-powered. The immunosensor could provide the quantitative readout photocurrent to a concentration of cTnI in the range of 0.10 pg/mL to 1.00 μg/mL and the detection limit was 0.0113 pg/mL under the optimal experimental conditions. With favorable performance in terms of anti-interference, stability, specificity and reproducibility, this immunosensor will provide new prospects for general PEC bioanalysis development.

A sensitive ratiometric biosensor for determination cardiac troponin I of myocardial infarction markers based on N, Zn-GQDs

A sensitive unlabeled ratiometric biosensor was developed to the detection of cardiac troponin I (cTnI). This biosensor was established by using the glassy carbon electrode coated with graphene oxide to form a platform bonded with N, Zn co-doped graphene quantum dots (N, Zn-GQDs). The N, Zn-GQDs was successfully prepared as the raw materials of graphite powder and characterized. Antibodies of cTnI were bonded to the surface of N, Zn-GQDs as the nanoprobe by amide bonds. The signals of electrochemiluminescence (ECL) and differential pulse voltammetry (DPV) were exposed to decrease in the presence of cTnI, which caused the signal substance to move farther away from the electrode. It was found that the immune complex layer attenuated the intensity of ECL and DPV which could be used as the good overall signal for determining concentration of cTnI. The ratiometric biosensor had a good response to cTnI with the detection limit is 4.59 pg L−1 in the concentration range of 10–106 pg L−1. The developed method was evaluated for the detection of cTnI in human serum, and the obtained results were consistent compared to the reference values obtained by hospital standard enzyme linked immunoassay (ELISA) with 9.09%–11.1% of RSD. Our findings suggested that this ratiometric biosensor could be used to the detection of cTnI in human serum with lower cost and higher sensitivity, it also might be better potential application prospect based on N, Zn-GQDs to detect other biomarkers.

Elevated troponin I levels on admission predict long-term mortality in patients with acute cerebral infarction following thrombolysis

Background/objectiveCardiac diseases are frequently accompanied by elevated levels of biomarkers, among which, troponin is commonly investigated. The levels of plasma cardiac troponin I (cTnI), which has been shown to predict short-term mortality, are elevated in patients with acute cerebral infarction (ACI). However, few studies have assessed the association between cTnI concentration and long-term mortality in patients with ACI following thrombolysis.MethodsPatients with ACI admitted between January 1, 2014, and December 31, 2016, were registered. Data on demographics and outcomes with elevated cTnI levels were also collected.ResultsA total of 145 patients with ACI were recruited; 97 (66%), 30 (20%), and 18 (12%) patients had cTnI concentrations < 0.030 (group 1), 0.030–0.10 (group 2), and > 0.10 μg/L (group 3), respectively. cTnI elevation was associated with older age, atrial fibrillation, congestive heart failure, renal insufficiency, coronary artery disease, stroke severity (National Institutes of Health Stroke Scale score), and prior smoking history at admission. After adjusting for comorbidities and severity at 3 months after ACI, cTnI elevation on admission was significantly associated with ascending 5-year mortality (hazard ratio, 1.80; 95% confidence interval, 1.22–2.65).ConclusionsEven after adjusting for several possible confounders, cTnI elevation in patients with ACI treated with rt-PA was associated with a 1.80-fold increased risk of 5-year mortality.

Cardiac troponins and growth-differentiation factor-15 (GDF-15) for prediction of angiographic coronary artery disease in chest pain patients without myocardial injury

Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Grieg Foundation and Western Norway Regional Health Authority. Background There is a growing evidence that patients with angiographic signs of coronary artery disease should receive preventive therapy to reduce the risk of future adverse cardiac events. Purpose Evaluate whether cardiac troponin T and I (cTnT and cTnI) concentrations within the range from the limit of detection of the assay to the 99th percentile or GDF-15 may help identify patients with angiographic evidence of coronary artery disease (CAD). Methods A subgroup of 550 patients from the WESTCOR study with both cTnT and cTnI concentrations ≤99th percentile was evaluated with coronary computed tomography angiography (CCTA). CAD was defined as ≥10% narrowing of lumen of any coronary artery on CT angiogram or too high calcium score for anatomy to be evaluated. Overall diagnostic accuracy of cTnT, cTnI and GDF-15 and their combination were evaluated calculating the area under the receiver-operating characteristics curve (ROC-AUC). cTn analysis were performed using high-sensitivity assays from Roche Diagnostics (cTnT, limit of detection of 5 ng/L and gender-neutral 99th percentile of 14 ng/L) and Abbott Diagnostics (cTnI, limit of detection 1.6 ng/L and 99th percentile 16 ng/L for women and 34 ng/L for men). GDF-15 analyses were performed using the GDF-15 assay on Cobas e801 (Roche Diagnostics). Results A total of 53.5 percent (294 of 550 patients) had angiographic coronary disease. The risk of having CAD was significantly higher in patients with cTnT between 5 ng/ml and the gender-neutral 99th percentile compared to very low levels of cTnT &amp;lt;5 ng/ml, 65.7% (95% CI: 60-71%) vs 38.1% (95% CI: 32-44%, p-value for difference &amp;lt;0.001). Similar numbers for cTnI between 2 ng/ml and the gender-specific 99th percentile compared to very low levels &amp;lt;2 ng/ml was 62.9% (95% CI: 57-69%) vs 43.2% (95% CI: 37-49%, p-value for difference &amp;lt;0.001). The odds ratio for CAD if cTnT was ≥5 ng/ml or cTnI ≥2 compared to very low levels was 3.1 (2.1-4.4) for cTnT and 2.2 (1.6-3.1) for cTnI. For GDF-15, the risk of having CAD was lower in patients with low values &amp;lt;1200 ng/L (49.7%, 95% CI: 45-54%) compared to patients with higher concentrations &amp;gt;1200 ng/L (75.9%, 95% CI: 66-86%, p-value for difference &amp;lt;0.001). The accuracy of cTnT was significantly higher than for cTnI for identifying CAD (AUC 0.67, 95% CI 0.63-0.71 vs. 0.61, 95% CI 0.58-0.66, p-value for difference &amp;lt;0.01), and borderline higher than for GDF-15 (AUC 0.62, p-value for difference 0.067). Adding GDF-15 to cTn did not increase diagnostic performance of cTnT (AUC 0.67 vs. 0.68, p-value for difference 0.56) or cTnI (AUC 0.61 vs. 0.63, p-value for difference 0.23). Conclusion Overall diagnostic performance of cTnT is superior to cTnI in identifying patients without angiographic evidence of CAD. Adding GDF-15 does not increase overall diagnostic performance. Legend: Figure 1. Receiver-operating characteristics curve of cTnT, cTnI and GDF-15 for the identification of CAD (≥10% lumen reduction).

The Preliminary Chronic Effects of Electromagnetic Radiation from Mobile Phones on Heart Rate Variability, Cardiac Function, Blood Profiles, and Semen Quality in Healthy Dogs.

The present study aims to determine the effects of long-term exposure to electromagnetic radiation from mobile phones (MPs) on heart rate variability (HRV), cardiac function, blood profiles, body surface temperature, and semen quality in healthy dogs. Eight male dogs were exposed to MPs (1962–1966 MHz; specific absorption rate 0.96 W/kg) for 2 h/day, 5 days/week, for 10 weeks. Holter monitoring for HRV analysis was performed at baseline (BL) and every 2 weeks, until the end of the study. Electrocardiograms (ECG), blood pressure (BP), echocardiography, cardiac troponin I (cTnI), hematology and biochemistry profiles, body surface temperature, and semen quality were evaluated at BL, week 5, and week 10 during exposure. The results showed that most of the HRV parameters did not significantly differ among timepoints, except for the mean of an interval between continuous normal R waves in week 6 that was higher than that at BL (p = 0.022). The RR and QT intervals from ECG in week 5 were prolonged, compared to the BL values (p = 0.001 and p = 0.003, respectively), but those parameters were within the normal limits. The echocardiography, BP, cTnI concentrations, body surface temperature, and semen quality results were not different from BL values. In conclusion, this study found no evidence suggesting an adverse effect of cell phone exposure on HRV, cardiac function, blood profiles, body surface temperature, or semen quality in healthy dogs, when exposed for 10 weeks.

Possible pathophysiological mechanisms of cardiac troponin level elevations in blood serum and urine in arterial hypertension

The review aimed to discuss and detail the main mechanisms of myocardial cell injury and increased concentrations of cardiac specific troponin isoforms (cTnI and cTnT) in blood serum and urine in hypertension. The search and analysis of foreign and domestic literature were carried out using the MedLine, EMBASE, Scopus and eLibrary databases to achieve this goal. According to recent experimental and clinical researches using high and ultra-sensitive methods for determining cTnI and cTnT, cardiomyocytes are extremely sensitive to many damaging factors in a number of physiological and pathological conditions. The serum concentrations of cTnI and cTnT can increase at the earliest stages of cardiovascular diseases (for example, in prehypertension, latent forms of coronary heart disease, arterial hypertension) and are important for predicting subsequent complications in the form of acute and life-threatening cardiovascular diseases (myocardial infarction, stroke, heart failure, and others). Moreover, troponin molecules can be detected not only in blood serum but also in non-invasively obtained biological fluids, including urine and oral fluid, which in the future can be used as new methods for the non-invasive diagnosis of many cardiovascular diseases. Although elevated levels of cTnI and cTnT in blood serum and urine in hypertension have a fairly high diagnostic and prognostic value, the pathophysiological mechanisms of cardiac troponins level elevations in human biological fluids in this pathological condition remain unclear.

Comparison of elevated cardiac troponin I with SAPS-II and APACHE-II score in predicting outcome of severe intoxications.

Background and Aims:To date, different methods have been invented to risk-stratify critically ill patients, however, there is a paucity of information regarding assessing the severity of poisonings. This study was designed to determine the comparative efficacy of Simplified Acute Physiology Score-II (SAPS-II) and Acute Physiology and Chronic Health Evaluation-II (APACHE-II)score with cardiac troponin I (cTnI) in predicting severe intoxication outcomes.Methods:This was a prospective study conducted on patients who fulfilled defined severe intoxication criteria necessitating intensive care unit (ICU) admission over a period of 6 months. SAPS-II and APACHE-II scores were calculated and cTnI concentrations were measured. These indicators were compared to determine which has the better ability to prognosticate mortality and complications.Results:A total of 55 cases (median age, 35 [24-49] years) were enroled. Eight patients (14.5%) died. Mean SAPS-II, median APACHE-II score and median cTnI concentrations were 32.05 ± 11.24, 13 [10-17] and 0.008 [0.002-0.300] ng/ml, respectively, which were significantly different between the survivors and non-survivors. Receiver operating characteristics curve results of SAPS-II, APACHE-II score and cTnI concentrations in predicting mortality were 0.945, 0.932 and 0.763 and in predicting complications were 0.779, 0.739 and 0.727, respectively. High cTnI concentration (>0.37 ng/ml) correlated with soft clinical outcomes, including length of ventilatory support, length of ICU stay and length of hospital stay (LOS) (r: 0.928, 0.881 and 0.735 respectively; all P < 0.001).Conclusion:SAPS-II scores were superior in predicting death and complications, while cTnI correlated more closely with soft clinical outcomes, such as the length of ventilator support, length of ICU stay or LOS.

Immunosensor for rapid detection of human cardiac troponin I, a biomarker for myocardial infarction

A rapid detection approach based on quench-release for cardiac troponin I (cTnI), a biomarker of myocardial infarction, was developed. To ensure detection accuracy, a rabbit monoclonal antibody, RabMG4C80A (G4), that binds specifically to cTnI was used. The antigen-binding fragment of G4 was prepared and labeled with fluorescent dyes to produce a fluorescent immunosensor G4 Q-body that can be used for cTnI detection. Using this method, an assay could be completed in as little as 5 min, enabling rapid diagnosis following myocardial infarction and providing a timely basis for patient treatment. A dose–response curve of the G4 Q-body for cTnI detection was obtained from the fluorescence spectra, from which the concentration of cTnI in the sample was determined. The limits of detection and concentration for 50% of maximal effect of the assay were found to be below 10 pM and 3.8 nM, respectively, of cTnI. The optimal detection range was 10 pM–1000 nM. After the occurrence of acute myocardial infarction, the cTnI concentration rose to 2 nM in 1 h and persisted for 6–8 days at around 20 nM; the detection range of the assay therefore covered the clinically relevant range of cTnI during myocardial infarction. This is the first Q-body based on rabbit monoclonal antibodies, and it is expected to contribute to the rapid diagnosis and precise treatment of myocardial infarction.

High-sensitivity troponin T and I in patients suspected of acute myocardial infarction

Measurement of cardiac troponin (cTn) is the cornerstone in the diagnosis of myocardial infarction (MI). Potential disparities in concentrations of cTn, trajectories and mortality, following initial measurement warrant further investigation. Such data may guide clinicians treating patients suspected of MI. Plasma concentrations of cTnT and cTnI were measured in 503 consecutive patients at Aarhus University Hospital between June 13th and June 27th, 2019. cTnT was measured with the Roche cobas® E602 hs-cTnT assay, while cTnI was measured with the Siemens ADVIA Centaur® XPT hs-cTnI assay. Analytical agreement was determined based on assay-specific 99th percentiles. Medical records were reviewed for adjudication of the MI diagnosis. MI was the final diagnosis in 65 patients (12.9%) and the analytical agreement between cTnT and cTnI assays was 95.2%. For patients diagnosed with MI, cTnI reached higher peak concentrations in shorter time, compared to cTnT. All-cause mortality risk increased with increasing levels of both biomarkers. In this study, the analytical agreement of two cTn assays was high. However, some disparities in troponin trajectories were observed.

Effects of dexmedetomidine and its reversal with atipamezole on echocardiographic measurements and circulating cardiac biomarker concentrations in normal cats.

To investigate the effects of dexmedetomidine (DXM) and its subsequent reversal with atipamezole (APM) on the echocardiogram and circulating concentrations of cardiac biomarkers in cats. 14 healthy cats. Cats underwent echocardiography and measurements of circulating cTn-I and NT-proBNP concentrations before (PRE) and during (INTRA) DXM sedation (40 µg/kg IM) and 2 to 4 (2H POST) and 24 (24H POST) hours after reversal with APM. Administering DXM significantly decreased heart rate, right ventricular and left ventricular (LV) outflow tract velocities, and M-mode-derived LV free-wall thickness; increased LV end systolic diameter and volume; and caused valvar regurgitation. While sedative effects resolved within 25 minutes of APM reversal, the evolution of echocardiographic changes was mixed: LV ejection fraction and mitral valvar regurgitation score were different at 2H POST than at both INTRA and PRE (partial return toward baseline), LV end-diastolic volume was different PRE to INTRA and INTRA to 2H POST but not different PRE to 2H POST (full return toward baseline), and M-mode-derived LV free-wall thickness was significantly different from PRE to INTRA and PRE to 2H POST (no return toward baseline). Serum cTn-I and plasma NT-proBNP concentrations increased significantly with DXM, which remained significant 2H POST. Administration of DXM and APM reversal produced changes in echocardiographic results and in circulating cTn-I and NT-proBNP concentrations. Understanding these changes could help veterinarians differentiate drug effects from cardiac disease.

Effect of smoking cessation on cardiac troponin I concentrations

Chronic elevation of cardiac troponin I (cTnI) is associated with heart failure and cardiovascular death. Paradoxically, observational studies have indicated that current smokers have lower cTnI concentrations than non-smokers. We examined determinants of cTnI in smokers and the effect of smoking cessation on cTnI. Overweight or obese smokers received motivational support and varenicline to aid cessation and dietary advice to limit weight gain. Quitters were defined according to the Russell standard (≤5 cigarettes after the quit date) and validated with expired breath CO <10 ppm. Of the total 122 participants, 108 completed assessments at 12 weeks and 78 were classified as quitters versus 30 who continued smoking. cTnI was measured with a high-sensitivity assay with a limit of detection of 1.2 ng/L (Abbott Diagnostics), and concentrations (log-transformed) were compared between quitters and continuing smokers. cTnI concentrations were significantly higher in men than women and correlated with age, but not with number of cigarettes/day. Quitters had median baseline and 12-week levels of 1.4 ng/L (interquartile range [IQR] 1.2–2.5) and 1.4 ng/L (IQR 1.2–2.4), respectively, while nonquitters had baseline and 12-week levels of 1.5 ng/L (IQR 1.2–2.9) and 1.8 ng/L (IQR 1.3–3.4), respectively. The change in cTnI concentrations from baseline to 12 weeks did not differ between quitters and continuous smokers (p = .7). The results suggest that smoking cessation does not affect levels of cTnI, a marker of chronic subclinical myocardial injury, in contrast to prior observational data suggesting that tobacco smoking is associated with lower cTn concentrations.

Troponin I measurement after acute myocardial infarction and its correlation with left ventricular ejection fraction

Background: After acute myocardial infarction (MI), a patient's prognosis is closely related to the extent of irreversibly damaged myocardium. The evaluation of infarct size after acute MI (AMD) is important for predicting the subsequent clinical course. Cardiac troponin I (cTnl) is accepted as a highly reliable biochemical marker for detecting myocardial damage, and its use in the diagnosis of acute MI (AMI) is increasing. Its concentration is unaffected by thrombolysis after the first12 hours, following which it shows a stable plateau for about 48 hours.Methods: This study investigated the value of a single cTnl concentration, estimated 12-48 hours after admission, to provide an integrated measurement of the degree of cardiac damage following first acute MI, and its correlation with left ventricular ejection fraction (LVEF). This study of troponin I measurement after acute MI and its correlation with LVEF was conducted during the period between October 2019 and October 2021 at SMIMER hospital, Surat.Results: This study shows a strong negative correlation between cTnI concentration measured between 12-48 hours post MI and echocardiographic LVEF. It was also found that cTnl concentration more than 3.8 ng/ml is a sensitive (100%) and specific (78.12%) indicator of LVEF &lt;40% after a first acute MI. It can be considered as a significant prognostic marker.Conclusions: In conclusion, cTnl shows excellent promise as a marker of infarct size, and for the assessment of LVEF; and may potentially replace the CPK-MB as the cardiac specific marker for AMI detection.

Rapid and label-free detection of the troponin in human serum by a TiN-based extended-gate field-effect transistor biosensor

In this article, the TiN sensitive film as a sensing membrane was deposited onto n+-type Si substrate by a DC sputtering technique for extended-gate field-effect transistor (EGFET) pH sensors and detection of cardiac troponin-I (cTn-I) in the patient sera for the first time. The crystal structure, Raman spectrum, element profile, surface roughness, and surface morphology of the TiN sensitive film were characterized by X-ray diffraction, Raman spectroscopy, secondary ion mass spectroscopy, atomic force microscopy, and scanning electron microscopy, respectively. The sensing performance of the TiN sensitive film is correlated with its relative structural feature. A high sensitivity of 57.49 mV/pH, a small hysteresis voltage of ∼1 mV, and a low drift rate of 0.31 mV/h were obtained in the TiN sensitive film. In addition, the pH sensitivity of this TiN EGFET sensor was preserved approximately 57 mV/pH after operation time of 180 days. Subsequently, the cTn-I antibodies with carboxyl groups activated by 1-ethyl-3-(3-dimethylaminopropyl)-carbodiimide (EDC) along with N-hydroxysuccinimide (NHS) were immobilized on the TiN sensitive film functionalizing with 3-aminopropyl triethoxysilane (APTES). After obtaining the successful immobilization of cTn-I antibodies on the TiN EGFET biosensor, the cTn-I antigen specifically binds with its relative antibody. The cTn-I EGFET biosensor showed a high sensitivity of 21.88 mV/pCcTn-I in a wide dynamic range of 0.01–100 ng/mL. Furthermore, the concentrations of cTn-I in patient sera measured by our TiN EGFET biosensors are comparable to those determined by commercial enzyme-linked immuno-sorbent assay kits.

Integrating potential-resolved electrochemiluminescence with molecularly imprinting immunoassay for simultaneous detection of dual acute myocardial infarction markers

A novel potential-resolved molecularly imprinted electrochemical luminescence (ECL) immunosensor has been developed for the first time for the dual sensitive detection of markers of acute myocardial infarction (AMI): cardiac troponin I (cTnI) and myoglobin (Mb). In this work, cost-effective and robust molecularly imprinted polymer (MIP) as biomimetic antibody was used to construct the immunosensors through electropolymerization and elution to form polydopamine (PDA)-MIP modified electrode. In the presence of AMI biomarkers, two ECL probes including Ru(bpy)32+@ MOCs and MoS2 QDs functionalized by cTnI antibody and Mb aptamer could be specifically captured respectively. And two potential distinct ECL signals will be generated in one potential scan. The intensity of ECL reflects the concentrations of cTnI and Mb. The two ECL probes were characterized with field emission scanning electron microscopy, X-ray diffraction, FT-IR spectrum and UV–Vis diffuse reflectance spectroscopy. The prepared sensor exhibited a wide linear range (0.05–104 ng/mL) and a low detection limit (0.0184 ng/mL for cTnI and 0.0492 ng/mL for Mb). Additionally, the MIP-ECL sensor displayed excellent anti-interference, sensitivity and stability to detect cTnI and Mb. Therefore, it will be conducive to accelerate more precise and credible early diagnosis for AMI.

Role of apolipoprotein O in autophagy via the p38 mitogen-activated protein kinase signaling pathway in myocardial infarction

ObjectiveTo explore the role and possible mechanisms of action of apolipoprotein O (APOO) in autophagy in Myocardial Infarction (MI) in vivo and in vitro. MethodsDifferential gene expression and single Gene Set Enrichment Analysis (GSEA) were used to evaluate MI-related candidate genes. Animal and cell MI models were established. Sh-APOO, si-APOO, and SB203580 were used to inhibit the expression of APOO or p38MAPK. Western blot and qRT-PCR were used to analyze the expression levels of the target protein or mRNA. Apoptosis was observed using the TUNEL assay. The plasma concentrations of CK-MB and cTn-I in humans and mice were determined. ResultsIn the GSE23294 dataset, APOO mRNA was highly expressed in the left ventricle of mice with MI; GSEA revealed that APOO was positively correlated with p38MAPK, autophagy, and apoptosis. The plasma concentration of APOO in patients with MI was significantly higher than that in healthy subjects. The expression of APOO, Beclin-1, LC3, and Bax in mouse and AC16 cell MI models increased, while the level of Bcl-2 decreased. After silencing the APOO gene, the expression of APOO was downregulated; meanwhile, changes in autophagy, apoptosis and myocardial cell injury were reversed in vivo and in vitro. Furthermore, autophagy was alleviated after AC16 cells were treated with SB203580. ConclusionsThe increased APOO expression in mouse and cell MI models may activate autophagy and apoptosis by regulating the p38MAPK signaling pathway, thus aggravating the myocardial injury.

Genetically Predicted Cardiac Troponin I Concentrations and Risk of Stroke and Atrial Fibrillation

ObjectivesObservational studies have shown that elevated circulating cardiac troponin I (cTnI) concentrations were linked to higher risk of stroke and atrial fibrillation, but the causality remains unclear. Therefore, we used mendelian randomization to assess the potential causal effects of cTnI concentrations on the risk of stroke, its subtypes and atrial fibrillation. Materials and methodsThe instrumental variables for circulating cTnI concentrations were selected from a genome-wide association study meta-analysis of 48,115 European individuals. We examined the associations of circulating cTnI concentrations with stroke, ischemic stroke, ischemic stroke subtypes (cardioembolic, large artery, small vessel stroke), intracerebral hemorrhage and atrial fibrillation. ResultsGenetically predicted elevated circulating cTnI concentrations were associated with higher risk of cardioembolic stroke (odds ratio [OR], 1.80; 95% confidence interval [CI], 1.20–2.68; P = 0.004), but not associated with large artery stroke, small vessel stroke, total stroke, ischemic stroke and intracerebral hemorrhage. Additionally, we also found that elevated cTnI concentrations were causally linked to higher risk of atrial fibrillation (OR, 1.30; 95% CI, 1.10–1.53; P = 0.003). ConclusionsThis study provides evidence that genetically predicted circulating cTnI concentrations are causally linked to higher risk of cardioembolic stroke and atrial fibrillation.

Real-time impedimetric detection of cardiac troponin I using ITO-coated vertically aligned silicon nanowires

This research focuses on developing a sensitive nanoelectronic device (NED) with impedimetric detection of human cardiac troponin I (cTnI) for the real-time diagnosis of acute myocardial infarction. The sensing area of NED was composed of indium tin oxide (ITO)-coated vertically aligned silicon nanowires (VASiNWs). ITO-coated-VASiNWs were examined by X-ray diffraction and scanning electron microscope for the identification of crystalline structure and morphological observation, respectively. After cTnI antibody (cTnIAb) modification, various concentrations of cTnI in the human blood sera were then impedimetrically detected by cTnIAb-modified-ITO-coated-VASiNWs via microfluidic systems. Our device exhibited a linear range from 1.76011 to 17601.1 ng/mL with good sensitivity for the detection of cTnI.

Evidence of myocardial injury in horses with colic

Development of endotoxemia associated with gastrointestinal injury is often observed in horses with colic. Such patients are likely to develop cardiovascular complications associated with endotoxemia, including myocardial injury. Few studies have investigated the prevalence of myocardial injury in horses with colic. Cardiac biomarkers such as cardiac troponin I (cTnI) have been extensively used in human and veterinary medicine for diagnosis of myocardial injury. The aim of the present study was to investigate the occurrence of myocardial injury in horses with colic by measuring serum cTnI concentrations. Myocardial tissue samples from non-surviving horses were also subjected to histopathological evaluation. Serum cTnI concentration was measured in 10 healthy horses and 39 horses with colic. Associations were determined of cTnI concentration, and variables such as health status (healthy and horses with colic), type of colic (inflammatory, impaction, and unknown), the severity of abdominal pain (mild, moderate and severe), and clinical outcome (survivor to discharge and non-survivor). As compared with healthy horses, cTnI concentrations were significantly elevated in horses with colic (P = 0.004). In horses with colic, an abnormal cTnI concentration was significantly associated with inflammatory colic (P&lt;0.05), severe abdominal pain (P&lt;0.01), and negative clinical outcome (P&lt;0.0001). Further, histopathological evaluation of the myocardial muscles revealed a varying degree of myocardial degeneration and necrosis. The present study suggested that horses with severe colic and increased cTnI levels are more likely to develop myocardial injury. Elevated levels of cTnI may also be indicative of poor prognosis in horses with severe colic.

Forensic significance of cTnI serum for the detection of terminal myocardial damage in rats (Rattus norvegicus) caused by hyperthermia

ObjectivesTo determine whether the biochemical marker cTnI with circulating value has forensic significance in the detection of myocardial damage in rats in experimental conditions of hyperthermia by exposure to water temperatures of 41 °C. Material and methodsThe study was conducted on 24 adult Wistar rats that were divided into two experimental groups, depending on water temperature exposure of 37 °C (KG, n = 8) and 41 °C (G41, n = 16). Depending on the length of time of exposure to water temperatures of 41 °C are further divided into G41-AM (20 min of exposure), G41-PM (exposure until death). Blood for analysis of the concentration of cardiac troponin I (cTnI) was taken before the experiment and after the expiration of the given duration of the experiment of 20 min or death. The concentration of cTnI was determined in serum by ELISA method. The level of statistical significance was, p < 0.05. ResultsEight rats of the G41 group achieved a core temperature that is the threshold for heat stroke. The median survival time for group G41 was 175.5 min. The median cTnI was 358.64 for group KG 37. The control group of rats had significantly lower serum cTnI values compared to G41. Examination of the length of exposure to appropriate temperatures led to significant increases in cTnI in the serum; A significant difference was found in the values of cTnI KG37 and G41-PM. CTnI values differed significantly in the G41-AM and G41-PM groups. In G 41 °C, a positive correlation was found between serum cTnI values and body temperature measured in fatal outcome. ConclusionsCTnI with their changes in serum concentration indicate exposure to high water temperature.