Determination Of Cardiac Troponin Research Articles

Sandwich-type electrochemical aptasensor based on polydopamine-Au-metal ions as signal label and coralloid Au-conductive carbon architecture-modified electrode for the simultaneous detection of cardiac troponin I and myoglobin

The determination of cardiac troponin I (cTnI) and myoglobin (Myo) is increasingly significant considering their potential in acute myocardial infarction (AMI) diagnosis. Here, we constructed a sandwich-type electrochemical aptasensor for the simultaneous detection of cTnI and Myo. The polydopamine-Au-metal ions (PDA-Au-Pb2+/Cu2+) were synthesized and used as the labels of second aptamers (TrO6 and S232). The labels displayed different peaks at different potential sites, thus making the simultaneous detection method available. Meanwhile, the synthesized zirconium-based carbon architecture (CC) was well-conductive originating from the annealing process. After the modification of CC on the bare electrode (screen-printed carbon electrode, SPCE), the coralloid Au (CAu) was further decorated on the electrode by electro-deposition, thus forming CAu/CC/SPCE with high conductivity. Hence, the aptasensor proposed here showed admirable simultaneous quantitative analysis performance towards cTnI and Myo with wide linear ranges (1 μg/mL-0.01 pg/mL, 1 μg/mL-0.1 pg/mL) and low detection limits (3.8 fg/mL, 35 fg/mL). These results demonstrated that the aptasensor held the potential application in clinical diagnosis.

Electro-immunosensor for ultra-sensitive determination of cardiac troponin I based on reduced graphene oxide and polytyramine.

This work reports the construction of a novel nanostructured immunosensor for detection of the troponin I biomarker (cTnI). Anti-troponin I antibody was anchored on the modified graphite electrode with reduced graphene oxide and polytyramine for detection of troponin I in serum samples. The performance of the electro-immunosensor was evaluated by differential pulse voltammetry. The immunosensor presented a wide work range, from 4ng mL-1 to 4pg mL-1 , whose detection limit (4pg mL-1 ) is significantly lower than the basal level in human serum, and maintained 100% of response after 30 days of storage. Moreover, the immunosensor showed good selectivity for detection of cTnI in real sample containing interfering substances and specificity of response to cTnI in the serum of healthy and sick patients, and demonstrated the possibility of reuse for two consecutive analyses, in addition to using a simplified and inexpensive platform when compared to other devices, demonstrating them excellent potential for application in diagnosis in the early stages of acute myocardial infarction.

An impedimetric aptamer-based sensor for sensitive and selective determination of cardiac troponin I

An impedimetric aptamer-based sensor for sensitive and selective determination of cardiac troponin I

Diagnostic value of high-sensitivity troponin T in postmortem diagnosis of sudden cardiac death

IntroductionIschemic heart disease is the most common cause of sudden cardiac death. By autopsy, there may be no histologic evidence of acute myocardial damage few hours after death. The use of cardiac troponins in the postmortem diagnosis of sudden cardiac death is well known in the forensic setting. However, high-sensitivity cardiac troponin T (Hs-TnT) assay in cadaver fluids was tested in few studies. The aim of this study is to assess the diagnostic value of postmortem dosage of Hs-TnT in the diagnosis of sudden cardiac death. Material and methodsOur study is prospective, dealing with cadavers autopsied at the Department of Forensic Medicine of the University Hospital Habib Bourguiba of Sfax-Tunisia from December 2016 to April 2018. Were excluded from the study resuscitated cases, severely traumatized victims and cadavers that were examined more than 36 h after death. Levels of Hs-TnT were measured in pericardial fluid, cardiac blood and peripheral blood. ResultsA total of 80 cases were identified with an average age of 44.5 ± 19 years. Hs-TnT levels in pericardial fluid and heart blood were correlated significantly between cardiac and non-cardiac groups with a p-value respectively at 0.14 and 0.04. Receiver-operator characteristic curves analysis showed that the pericardial fluid had the best sensibility (75%) and specificity (64%) with a cut-off level at 17.72 ng/ml and an area under the curve at 0.747. We found also a significant correlation between postmortem interval and Hs-TnT levels in pericardial fluid, cardiac and peripheral blood. ConclusionOur data indicate that determination of cardiac troponin T by a highly sensitive assay in pericardial fluid may be a powerful aid in the postmortem diagnosis of sudden cardiac death.

Cardiac Troponin I Microfluidic Chip Driven by Adaptive Pressure

To develop and design an adaptive microfluidic chip for accurate determination of cardiac troponin I (cTnI) in whole blood sample and explore the operating parameters of the chip in detecting cTnI, in order to provide a novel strategy for the detection of cTnI, cTnI microfluidic chip was prepared by injection moulding, and the improved polystyrene polymer was used as the chip substrate to construct a three-layer composite structure, namely the upper, middle, and lower layers. The antihuman troponin I antibody I/II was grafted onto the chip surface to construct the detection reaction zone using UV-induced production of surface-active free radicals. The stability of the chip preparation process, the running performance of the chip, and the analytical performance of the whole blood samples were investigated. It was shown that I adaptive pressure-driven microfluidic chip has the advantages of easy bonding, integration, and a simple and stable production process. In the actual detection and analysis, the chip has high selectivity for cTnI in whole blood, lower detection limit (0.054 ng/mL), and small difference between batches (RSD% 2.50%). Therefore, the chip is assumed to provide novel strategy for the assessment of myocardial infarction by detecting cTnI.

Sensitive and Quantitative Determination of Cardiac Troponin I Based on Silica-Encapsulated CdSe/ZnS Quantum Dots and a Fluorescence Lateral Flow Immunoassay

Cardiac troponin I is generally used as a biomarker of myocardial infarction or acute myocardial infarction. A timely and rapid diagnosis method for cardiac troponin I is of great importance. In this paper, a novel CdSe/ZnS quantum dot (QD) based fluorescence lateral flow immunoassay (QD-LFIA) is reported for the rapid and quantitative detection of cardiac troponin I in human serum. The water-soluble silica-encapsulated QDs (QDs@SiO2) serve as a new fluorescent probe and an economical, portable, quantitative instrument was used for the first time to detect cardiac troponin I antigen. By using the optimized immunoassay procedure with clinical samples, cardiac troponin I was determined in 10 min with high sensitivity (as low as 5.6 × 10−3 ng/mL), broad linear range (0.8–200 ng/mL), and good precision (the coefficient of variation was less than 10%). The comparison of this new QD-LFIA and a standard direct chemiluminescence assay demonstrated that the former platform was rapid, low-cost, and sensitive. It may be further applied to the quantitative determination and monitoring of cardiac troponin I levels in clinical use.

Label-Free Electrochemiluminescence Immunosensor for the Determination of Cardiac Troponin I Using a Cadmium Sulfide–Molybdenum (IV) Sulfide Nanocomposite Modified Glassy Carbon Electrode

A label free electrochemiluminescence (ECL) immunosensor for the determination of cardiac troponin I was developed using CdS-MoS2 composites as the electrochemiluminescence emitters. The CdS-MoS2 composites were synthesized by a hydrothermal method and used for the construction of the electrochemiluminescence biosensing platform. For the fabrication of the immunosensor, CdS-MoS2 composites, chitosan, cardiac troponin I antibodies, and bovine serum albumin were consecutively assembled on the glass carbon electrode. Under the optimum conditions, the label free electrochemiluminescence determination of cardiac troponin I was obtained. Due to the excellent electrochemiluminescence performance of CdS-MoS2 composites and high specificity of the immunoreactions, the sensor shows satisfactory selectivity and high sensitivity for cardiac troponin I determination. The detection limit was 1.0 pg mL−1 and the linear range was from 5.0 pg mL−1 to 100.0 ng mL−1. Moreover, the method was successfully used to determine cardiac troponin I in human serum samples with recoveries between 85.4 and 111.0%. This label-free immunosensor possesses many merits, including a simple sensing process, good electrochemiluminescence performance of the CdS-MoS2 composites, and high flexibility for extending the strategy for the determination of other biomarkers.

Role of TRPV1/CGRP signaling pathway in lidocaine postconditioning-induced reduction of myocardial ischemia-reperfusion injury in rats

Objective To evaluate the role of transient receptor potential vanillic acid subtype 1(TRPV1)/calcitonin gene-related peptide(CGRP) signaling pathway in lidocaine postconditioning-induced reduction of myocardial ischemia-reperfusion(I/R) injury in rats. Methods Forty healthy male Sprague-Dawley rats, aged 3 months, weighing 250-300 g, were divided into 5 groups(n=8 each) using a random number table method: sham operation group(group Sham), group I/R, lidocaine postconditioning group(group LP), lidocaine postconditioning plus CGRP8-37 group(group LP+ CGRP8-37), and lidocaine postconditioning plus capsazepine group(group LP+ Capz). Myocardial ischemia was induced by ligating the anterior descending branch of left coronary artery for 30 min, followed by 120-min reperfusion in anesthetized rats. Lidocaine 2 mg/kg was injected via the tail vein at 5 min before reperfusion in group LP. In group LP + CGRP8-37, lidocaine was intravenously injected, and CGRP receptor selective antagonist CGRP8-37 2 mg/kg was intravenously injected at the same time. In group LP+ Capz, lidocaine was injected intravenously, and TRPV1 blocker capsazepine 3 mg/kg was injected intravenously at the same time. A catheter was retrogradely implanted to the left ventricle, and heart rate(HR), left ventricular systolic pressure(LVSP), left ventricular end-diastolic pressure(LVEDP), and the maximum rate of increase or decrease in left ventricular pressure(±dp/dtmax) were continuously monitored and recorded. Blood samples were collected from the carotid artery at 120 min of reperfusion for determination of cardiac troponin I(cTnI), myoglobin(Myo) and creatine kinase-MB(CK-MB) concentrations in serum. Rats were then sacrificed for determination of myocardial infarct size. Results Compared with Sham group, the serum concentrations of cTnI, Myo and CK-MB were significantly increased, LVSP, + dP/dtmax and HR were decreased, and LVEDP and -dP/dtmax were increased in I/R group and LP group(P 0.05). Compared with group LP, the serum concentrations of cTnI and Myo, myocardial infarct size and LVEDP were significantly increased, and + dP/dtmax was decreased in group LP+ CGRP8-37, and the serum concentrations of cTnI and Myo and myocardial infarct size were significantly increased, LVSP and + dP/dtmax were decreased, and LVEDP was increased in group I/R+ Lido+ Capz(P<0.05). Conclusion The mechanism by which lidocaine postconditioning mitigates myocardial I/R injury is related to activating TRPV1/CGRP signaling pathway in rats. Key words: Lidocaine; Ischemia postconditioning; Myocardial reperfusion injury; Calcitonin gene-related peptide; TRPV cation channels

Cardiac troponin for predicting all-cause mortality in patients with acute ischemic stroke: a meta-analysis.

Cardiac troponins are specific biomarkers of cardiac injury. However, the prognostic usefulness of cardiac troponin in patients with acute ischemic stroke is still controversial. The objective of this meta-analysis was to investigate the association of cardiac troponin elevation with all-cause mortality in patients with acute ischemic stroke. PubMed and Embase databases were searched for relevant studies up to April 31, 2017. All observational studies reporting an association of baseline cardiac troponin-T (cTnT) or troponin-I (cTnI) elevation with all-cause mortality risk in patients with acute ischemic stroke were included. Pooled adjusted risk ratio (RR) and corresponding 95% confidence interval (CI) were obtained using a random effect model. Twelve studies involving 7905 acute ischemic stroke patients met our inclusion criteria. From the overall pooled analysis, patients with elevated cardiac troponin were significantly associated with increased risk of all-cause mortality (RR: 2.53; 95% CI: 1.83–3.50). The prognostic value of cardiac troponin elevation on all-cause mortality risk was stronger (RR: 3.54; 95% CI: 2.09–5.98) during in-hospital stay. Further stratified analysis showed elevated cTnT (RR: 2.36; 95% CI: 1.47–3.77) and cTnI (RR: 2.79; 95% CI: 1.68–4.64) level conferred the similar prognostic value of all-cause mortality. Acute ischemic stroke patients with elevated cTnT or cTnI at baseline independently predicted an increased risk of all-cause mortality. Determination of cardiac troponin on admission may aid in the early death risk stratification in these patients.

Impact of physical activity of individuals and creatine kinase on 99th percentiles of troponin I assays

Determination of cardiac troponin I (cTnI) is one central means for diagnosis of myocardial infarction. Assay performance of three troponin I assays was compared previously in a large reference population detecting sex-differences in the 99th percentile only for the Dimension Vista cTnI assay. The present study examined the underlying effects.Values for cTnI were reused. Creatine kinase (CK) activity was determined in 2358 samples from blood donors. Information on physical activity was evaluated from health questionnaires. Using quantile regression data were analysed to investigate the impact of sex, physical activity, and CK on the 99th percentile of the cTnI assay.We report significant sex-differences for the 99th percentile of cTnI. Physical activity was significantly associated with cTnI values. Strong association of CK activity with cTnI values was detected only in men. Adjustment for CK in quantile regression abolished sex-differences in the 99th percentile. Two other contemporary sensitive cTnI assays were not relevantly affected by physical activity or CK.Sex-differences in the 99th percentile for the Dimension Vista cTnI assay arise from a positive association between cTnI and physical activity and were abrogated when data were adjusted for CK activity. These findings should be taken into account when using this assay.

Gender-specific diagnostic performance of a new high-sensitivity cardiac troponin I assay for detection of acute myocardial infarction.

The determination of cardiac troponin is essential for diagnosing myocardial infarction. A troponin I assay has recently been developed that provides the highest analytical sensitivity to date. The analysis included 1560 patients with chest pain, of whom 1098 were diagnosed with non-coronary chest pain, 189 with unstable angina pectoris and 273 with non-ST-segment elevation myocardial infarction. The troponin I concentration was determined on admission (0 hours) and 3 hours later. The diagnostic algorithm incorporated troponin I elevation above the gender-specific 99th percentile as well as predefined relative or absolute 3-hour changes in the troponin I concentration (delta). The diagnostic criterion of troponin I above the 99th percentile resulted in a negative predictive value of 98.0% and 98.2% in men and women, respectively. For rule-in of non-ST-segment elevation myocardial infarction, the use of absolute deltas yielded higher positive predictive values and sensitivities compared to relative deltas. With detection rates of about 85% and 82% in men and women, respectively, non-ST-segment elevation myocardial infarction was diagnosed with a positive predictive value close to 84% in men and 80% in women. The investigational troponin I assay provides an excellent non-ST-segment elevation myocardial infarction rule out. With gender-specific differences, the application of absolute changes in troponin concentration was superior to relative changes to rule in patients with non-ST-segment elevation myocardial infarction.

Significance and Determinants of Cardiac Troponin I in Patients With Obstructive Hypertrophic Cardiomyopathy

Serum cardiac troponins have been demonstrated to have important clinical implications in patients with hypertrophic cardiomyopathy (HC). However, little is known about their roles in patients with obstructive HC. The aim of this study was to explore the clinical significance and determinants of serum cardiac troponin I (cTnI) in patients with obstructive HC using cardiovascular magnetic resonance imaging. We investigated the relations between serum cTnI levels and clinical, echocardiographic, and cardiovascular magnetic resonance parameters and assessed the determinants of serum cTnI in 149 consecutive patients with obstructive HC. The median level of serum cTnI was 0.019 ng/ml (interquartile range 0.009 to 0.044). CTnI was elevated (≥0.04 ng/ml) in 42 (28%) of the overall cohort. Patients with elevated cTnI had greater maximum wall thickness (p <0.001), larger left ventricular mass index (LVMI, p <0.001), more frequency of left atrium diameter ≥50 mm (p = 0.020), higher plasma values of N-terminal pro-B-type natriuretic peptide (p <0.001), and less hypertension (p = 0.014). Serum cTnI levels were positively correlated with maximum wall thickness (r = 0.444, p <0.001), LVMI (r = 0.556, p <0.001), N-terminal pro-B-type natriuretic peptide (r = 0.305, p <0.001), left ventricular end-diastolic volume index (r = 0.246, p = 0.002), and left ventricular end-systolic volume index (r = 0.272, p = 0.001) but negatively with left ventricular ejection fraction (r = -0.180, p = 0.028). On multivariate analysis, LVMI was independently associated with both elevated cTnI (odds ratio 1.032, p = 0.001) and increasing serum cTnI levels (β = 0.556, p <0.001). In addition, the presence of hypertension was independently related to less likely elevated cTnI (odds ratio 0.307, p = 0.029) and decreasing levels of serum cTnI (β = -0.165, p = 0.015). In conclusion, levels of serum cTnI are elevated in a significant proportion of our patients. Serum cTnI is associated with multiple parameters of disease severity, suggesting its great significance in assessing cardiac remodeling in patients with obstructive HC. Left ventricular hypertrophy, as indicated by LVMI, is the major determinant of serum cTnI levels.

Determination of Cardiac Troponin I in the Blood and Heart of Calves with Foot-and-Mouth Disease

The current study was designed to determine the changes of the cardiac troponin I (cTnI) expression in blood and tissue during the myocardial degeneration in calves with foot-and-mouth disease (FMD). Seventeen crossbred calves presenting pathological signs for FMD confirmed by viral analysis were studied. A biochemistry panel and immunohistochemistry were performed on 17 diseased calves and 7 calves used as controls. Creatine kinase (CK), CK-myocardial band (CK-MB), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities were analyzed for both groups. Cardiac troponin I levels were measured by a commercially available enzyme-linked immunosorbent assay kit. Mean cTnI (14.8 +/- 1.9 ng/ml) concentration and CK (573 +/- 407 U/l), CK-MB (238 +/- 37 U/l), AST (84 +/- 7), and LDH (298 +/- 29 U/l) activities were higher in FMD cases compared with controls. Immunohistochemistry revealed loss or depletion of cTnI expression in myocardium of all cases. None of the 7 controls showed loss of cTnI expression. Increased serum cTnI concentration correlated with myocardial injury and loss of cTnI immunolabeling in cardiomyocytes of calves with FMD.

Prevalence and Determinants of Troponin T Elevation in the General Population

The prevalence and determinants of cardiac troponin T (cTnT) elevation in the general population are unknown, and the significance of minimally increased cTnT remains controversial. Our objective was to determine the prevalence and determinants of cTnT elevation in a large, representative sample of the general population. cTnT was measured from stored plasma samples in 3557 subjects of the Dallas Heart Study, a population-based sample. cTnT elevation (> or =0.01 microg/L) was correlated with clinical variables and cardiac MRI findings. The sample weight-adjusted prevalence of cTnT elevation in the general population was 0.7%. In univariable analyses, cTnT elevation was associated with older age, black race, male sex, coronary artery calcium by electron beam CT, a composite marker of congestive heart failure (CHF), left ventricular hypertrophy (LVH), diabetes mellitus (DM), and chronic kidney disease (CKD) (P<0.001 for each). Subjects with minimally increased (0.01 to 0.029 microg/L) and increased (> or =0.03 microg/L) cTnT had a similar prevalence of these characteristics. In multivariable logistic regression analysis, LVH, CHF, DM, and CKD were independently associated with cTnT elevation. In the general population, cTnT elevation is rare in subjects without CHF, LVH, CKD, or DM, suggesting that the upper limit of normal for the immunoassay should be <0.01 microg/L. Even minimally increased cTnT may represent subclinical cardiac injury and have important clinical implications, a hypothesis that should be tested in longitudinal outcome studies.

Markers for Perioperative Myocardial Ischemia: What Both Interventional Cardiologists and Cardiac Surgeons Need to Know

All novel markers of myocardial ischemia (ischemia-modified albumin, choline, unbound free fatty acids) lack cardiac specificity. Therefore, for the specific detection of myocardial ischemia selective blood sampling from an inserted coronary sinus catheter is needed, which limits the applicability of these markers in most clinical routine settings. In addition, the superiority of these novel markers over the calculation of myocardial lactate production, the current criterion standard for the laboratory diagnosis of myocardial ischemia, has not been demonstrated so far, and even comparative data is frequently lacking. Further the superiority of these new candidate markers over lactate determination for the diagnosis of myocardial ischemia in peripherally drawn blood samples has not been demonstrated either, and these novel parameters appear not to be a breakthrough for laboratory diagnosis of myocardial ischemia during or after percutaneous coronary interventions or coronary artery bypass grafting. The determination of cardiac troponin I or troponin T is the current criterion standard for the laboratory diagnosis of myocardial damage due to their higher sensitivities and specificities compared to creatine kinase isoenzyme MB. According to current knowledge, troponin increases in peripherally drawn blood samples must be regarded as an indicator of myocardial necrosis which, however, may be limited, only detectable by troponin and may be missed by creatine kinase isoenzyme MB determination. After on-pump coronary artery bypass grafting the generally applied troponin discriminator limits are not valid as there is limited, inevitable cardiac tissue damage occurring during the surgical procedure. Therefore, troponins are significantly increased after reperfusion of the arrested heart over values seen before bypass and also in patients without complications. Perioperative myocardial infarctions can be reliably identified by their characteristic troponin time courses, and both peak concentrations and time of peak values are diagnostic criteria. Troponin release is lower in off-pump compared to on-pump bypass surgery. Despite the controversy over the significance of troponin elevations after clinically uncomplicated and successful procedures, it is tempting to postulate that less myocardial damage as detected by troponin release is beneficial for the patient. After elective percutaneous coronary interventions, only troponin increases >8-fold the upper reference limit were associated with increased mortality in long-term follow-up.

Determination of Cardiac Troponin I for the Auxiliary Diagnosis of Acute Myocardial Infarction by Anodic Stripping Voltammetry at a Carbon Paste Electrode

An electrochemical immunoassay for cardiac troponin I (cTnI) combining the concepts of the dual monoclonal antibody "sandwich" principle, the silver enhancement on the nano-gold particle, and the anodic stripping voltammetry is described. Four main steps were carried out to obtain the analytical signal, i.e., electrode preparation, immunoreaction, silver enhancement, and anodic stripping voltammetric detection. A linear relationship between the anodic stripping peak current and concentration of cTnl from 1 to 20 ng/ml and a limit of detection of 0.8 ng/ml were obtained. The established method was tested by determining cTnI in acute myocardial infarction (AMI) samples using enzyme-linked immunoadsorbent assay (ELISA) for comparison analysis, and good results were obtained.

Sevoflurane but Not Propofol Preserves Myocardial Function During Minimally Invasive Direct Coronary Artery Bypass Surgery

Volatile anesthetics exert cardioprotective properties in experimental and clinical studies. We designed this study to investigate the effects of sevoflurane on left ventricular (LV) performance during minimally invasive direct coronary artery bypass grafting (MIDCAB) without cardiopulmonary bypass. Fifty-two patients scheduled for MIDCAB surgery were randomly assigned to a propofol or a sevoflurane group. Apart from the anesthetics used, there was no difference in surgical and anesthetic management. After determination of cardiac troponin T, creatine kinase, and creatine kinase MB, electrocardiographic (ECG) data and echocardiography variables (myocardial performance index and early to atrial filling velocity ratio) the left anterior descending coronary artery (LAD) was clamped until anastomosis with the left internal mammary artery was completed. During LAD occlusion and during reperfusion, echocardiography measurements were repeated. Blood samples were obtained repeatedly for up to 72 h. After LAD occlusion, myocardial performance index and early to atrial filling velocity ratio in the propofol group deteriorated significantly from 0.40 +/- 0.12 and 1.29 +/- 0.35 to 0.49 +/- 0.10 and 1.13 +/- 0.22, respectively, whereas there was no change in the sevoflurane group. In the propofol group myocardial performance index remained increased (0.47 +/- 0.11) compared with baseline during reperfusion. There were no significant differences in ECG and laboratory values between groups. In conclusion, during a brief period of ischemia in patients undergoing MIDCAB surgery, sevoflurane preserved myocardial function better than propofol.

Myocardial Stress after Competitive Exercise in Professional Road Cyclists

Based on the determination of cardiac troponin (cTnT), brain natriuretic peptide (BNP), and echocardiographic measurements, recent investigations have reported myocardial damage and reversible cardiac dysfunction after prolonged endurance exercise in apparently healthy subjects. In the present study, we investigated the myocardial stress reaction in professional endurance athletes after strenuous competitive physical exercise. Eleven highly trained male professional road cyclists (age 27 +/- 4 yr; .VO2peak 67 +/- 5 mL.kg-1.min-1; training workload 34,000 +/- 2,500 km.yr-1) were examined. The following parameters were determined before and after one stage of a 5-d professional cycling race: BNP, cTnT (third-generation assay that shows no cross reactivity with skeletal TnT), creatine kinase (CK), creatine kinase MB (CKMB), myoglobin (Myo), and urea. All participants were submitted to a careful cardiac examination including echocardiography and stress ECG. None of the athletes showed pathological findings in the cardiac examination. CK (P < 0.01), CKMB (P < 0.05), and Myo (P < 0.01) were increased after the race. Normal postexercise cTnT levels indicate that the increase in CK, CKMB, and Myo was of noncardiac origin. In contrast, BNP rose significantly from 47.5 +/- 37.5 to 75.3 +/- 55.3 pg.mL-1 (P < 0.01). Pre- and postexercise values of BNP as well as the individual exercise-induced increase in BNP were significantly correlated with age (R2 = 0.68, R2 = 0.66, and R2 = 0.58, respectively; P < 0.05). Strenuous endurance exercise in professional road cyclists does not result in structural myocardial damage. The rise in BNP in older athletes may reflect a reversible, mainly diastolic left ventricular dysfunction. This needs to be confirmed by larger trials including different intensities, sports, and age groups.

Results of exercise testing at a mean age of 10 years after neonatal arterial switch operation.

This prospective follow-up study investigated long-term exercise capacity at a mean age of 10 y after neonatal arterial switch operation for transposition of the great arteries in a large group of homogeneous unselected children. 56 asymptomatic children, aged 7.9-14.3 y (10.5 +/- 1.6, mean +/- SD), were examined with respect to exercise tolerance, electrocardiographic (ECG) response and activity of biochemical markers for myocardial injury. The protocol included standard electrocardiography, M-mode and two-dimensional echocardiography at rest, a Bruce walking treadmill test to voluntary exhaustion, and determination of cardiac troponin I and T, creatine kinase and myoglobin from venous blood samples at rest and 4 h after exercise. Heart rate, blood-pressure response to exercise stress and endurance time were compared with published results of age-matched normal children. 54 patients (96.4%) had normal exercise capacity; a reduction in 2 patients was not due to cardiac disease. Heart rate and systolic blood pressure rose significantly between rest and peak exercise and did not differ from normal controls, whereas diastolic blood pressure was lower. ECG remained normal at rest and on exercise in 54 children (96.4%). Serum values of cardiac troponin I and T, creatine kinase and myoglobin were normal at rest and after exercise in all patients. The study demonstrates excellent long-term exercise capacity after neonatal arterial switch operation. Exercise testing is a useful and non-invasive screening method to detect patients with clinically relevant exercise-induced myocardial ischaemia and should be routinely performed in growing patients.

Determination of cardiac troponin I forms in the blood of patients with unstable angina pectoris

Objective: To determine the predominant form in which cardiac troponin I circulates in the bloodstream of unstable angina patients. Design and methods: The cardiac troponin I forms released in the bloodstream of 25 patients suffering from unstable angina were examined by using three immunoenzymatic assays: the total cTnI assay for detection of free and complexed cTnI, the IC-TIC assay for detection of the IC and TIC troponin complexes, and the IT-TIC assay for detection of the IT and TIC troponin complexes. Results: Approximately 60% of patients with unstable angina had at least one positive value in the total cTnI assay or in the IC-TIC assay. Our results demonstrated that the predominant cardiac troponin I form circulating in the bloodstream of patients with unstable angina was the IC complex. Free cTnI, IT, and/or TIC forms were seldomly found, the frequency of IT and/or TIC complexes being higher than that observed previously in patients with acute myocardial infarction. Conclusions: The release pattern of cTnI in patients suffering from unstable angina is similar to that previously observed in patients with acute myocardial infarction, i.e., a predominance of the IC complex.