Determination Of cTnI Research Articles

Usefulness of Serial Assessment of B-Type Natriuretic Peptide, Troponin I, and C-Reactive Protein to Predict Left Ventricular Remodeling After Acute Myocardial Infarction (from the REVE-2 Study)

Left ventricular (LV) remodeling after myocardial infarction (MI) indicates a high risk of heart failure and death. However, LV remodeling is difficult to predict, and limited information is available on the association of cardiac biomarkers with LV remodeling. Our aim was to study the association of B-type natriuretic peptide (BNP), cardiac troponin I (cTnI), and C-reactive protein with LV remodeling after MI. We designed a prospective multicenter study including 246 patients with a first anterior Q-wave MI. Serial echocardiographic studies were performed at hospital discharge and 3 months and 1 year after MI; quantitative analysis was performed at a core echocardiographic laboratory. Blood samples for determination of BNP, cTnI, and C-reactive protein levels were obtained at hospital discharge and the 1-month, 3-month, and 1-year follow up visits. One-year echocardiographic follow-up was obtained in 226 patients. End-diastolic volume increased from 52.3 ± 13.8 ml/m(2) at baseline to 62.3 ± 18.4 ml/m(2) at 1 year (p <0.0001); LV remodeling (>20% increase in end-diastolic volume) was observed in 87 patients (38%). At baseline, we found significant univariate relations between LV remodeling and the 3 biomarkers. During follow-up, high BNP levels and persistently detectable levels of cTnI were associated with LV remodeling. In multivariate analysis, none of the 3 biomarkers at baseline was independently predictive of LV remodeling. In contrast, during follow-up, high BNP and positive cTnI were independently associated with LV remodeling. In conclusion, circulating cardiac biomarkers may reflect pathophysiologic processes implicated in LV remodeling after MI. Determination of BNP and cTnI during follow-up can help refine risk stratification.

Effect of myocardial protection during beating heart surgery with right sub-axiliary approach

Background Cardiac troponin-I (cTnI) is one of the three regulatory subunits of the cardiac troponin which has the high sensibility and specificity of responding to myocardial injury. Studies have demonstrated that cTnI is released into the blood stream within hours following acute myocardial reperfusion injury. The clinical utility of cTnI for the assessment of myocardial damage is that it is more specific than creatine kinase MB (CKMB). This study investigated cTnI as a sensitive marker of myocardial reperfusion injury and its clinical value on beating heart surgery with right sub-axiliary incision. Methods From December 2002 through December 2004, 100 patients with atrial septal defect (ASD), ventricular septal defect (VSD), atrial septal defect and ventricular septal defect (ASD+VSD), and tetralogy of Fallot were randomly divided into two groups: the treatment group (n=50) was operated on with a beating heart under extracorporeal circulation (ECC), and the control group (n=50) on an conventional arresting heart under ECC. The two groups both used a right sub-axillary incision. Blood samples from a central venous catheter (CVC) were collected before, at the end of aortic clamping, immediately after discontinue cardiopulmonary bypass (CPB), 3, 6, 24, and 48 hours after operation. The Abbott Axsym system with hol-automation fluorescent immunity analyzer was used for the quantitative determination of cTnI. cTnI was detected to investigate the effect of myocardial ischemia reperfusion injury and the clinical value of beating heart surgery with right sub-axillary incision. Results There were no significant differences between the two groups before operation. At the end of aortic clamping and thereafter, cTnI significantly increased in both groups, and reached the peak point at 6 hours after operation. At all the tested points, cTnI was significantly higher in the control group than the beating heart group (P &lt;0.05), especially at 6 hours post operation (P &lt;0.01). The operating time and ECC duration were shortened and the dosage of dopamine was decreased, when compared with the control group. Conclusions There was less cTnI measured in the beating heart group than in the control group after CPB, demonstrating that beating heart surgery may significantly reduce myocardial reperfusion injury.

Relationship of MRI-Determined Infarct Size and cTnI Measurements in Patients with ST-Elevation Myocardial Infarction

The extent of myocardial infarction (MI) is related to patient outcomes (1), and clinicians often wish to have a sense for this critical measure. Imaging methods, although accurate, have limited accessibility and high cost. Thus clinicians often use biomarkers to provide such an estimate. Measurement of cardiac troponin T (cTnT) at 96 h after onset of MI was observed to correlate with MRI-determined infarct size in both ST-elevation MI (STEMI) and non-STEMI (2). We tested the hypothesis that cardiac troponin I (cTnI), another myocardium-specific biomarker, would provide an equivalent estimation in the subset of STEMI patients previously described (2). The 28 patients with STEMI had sufficient sample remaining to allow for determination of cTnI (2). The characteristics of this group have previously been reported (2), but in brief the mean age (SD) was 56 (11) years, and 17.4% of patients were women. Mean (SD) body mass index was 26.46 (3.5) kg/m2, and 71.4% of patients were hypertensive, 64.3% were current smokers, 60.7% had hypercholesterolemia, and 14.3% had diabetes. Blood samples were available at admission and at 24, 48, …

Cardiac Troponins as Indicators of Acute Myocardial Damage in Dogs

Cardiac troponin I (cTnI) and T (cTnT) have a high sequence homology across phyla and are sensitive and specific markers of myocardial damage. The purpose of this study was to evaluate the Cardiac Reader, a human point‐of‐care system for the determination of cTnT and myoglobin, and the Abbott Axsym System for the determination of cTnI and creatine kinase isoenzyme MB (CK‐MB) in healthy dogs and in dogs at risk for acute myocardial damage because of gastric dilatationvolvulus (GDV) and blunt chest trauma (BCT). In healthy dogs (n = 56), cTnI was below detection limits (&lt; 0.1 μg/L) in 35 of 56 dogs (reference range 0‐0.7 μg/L), and cTnT was not measurable (&lt; 0.05 ng/mL) in all but 1 dog. At presentation, cTnI, CK‐MB, myoglobin, and lactic acid were all significantly higher in dogs with GDV (n = 28) and BCT (n = 8) than in control dogs (P &lt; .001), but cTnT was significantly higher only in dogs with BCT (P= .033). Increased cTnI or cTnT values were found in 26 of 28 (highest values 1.1–369 μg/L) and 16 of 28 dogs (0.1‐1.7 ng/mL) with GDV, and in 6 of 8 (2.3–82.4 μg/L) and 3 of 8 dogs (0.1‐0.29 ng/mL) with BCT, respectively. In dogs suffering from GDV, cTnI and cTnT increased further within the first 48 hours (P &lt; .001). Increased cardiac troponins suggestive of myocardial damage occurred in 93% of dogs with GDV and 75% with BCT. cTnI appeared more sensitive, but cTnT may be a negative prognostic indicator in GDV. Both systems tested seemed applicable for the measurement of canine cardiac troponins, with the Cardiac Reader particularly suitable for use in emergency settings.

Cardiac Troponins as Indicators of Acute Myocardial Damage in Dogs

Cardiac troponin I (cTnI) and T (cTnT) have a high sequence homology across phyla and are sensitive and specific markers of myocardial damage. The purpose of this study was to evaluate the Cardiac Reader, a human point-of-care system for the determination of cTnT and myoglobin, and the Abbott Axsym System for the determination of cTnI and creatine kinase isoenzyme MB (CK-MB) in healthy dogs and in dogs at risk for acute myocardial damage because of gastric dilatation-volvulus (GDV) and blunt chest trauma (BCT). In healthy dogs (n = 56), cTnI was below detection limits (<0.1 microg/L) in 35 of 56 dogs (reference range 0-0.7 microg/L), and cTnT was not measurable (<0.05 ng/mL) in all but 1 dog. At presentation, cTnI, CK-MB, myoglobin, and lactic acid were all significantly higher in dogs with GDV (n = 28) and BCT (n = 8) than in control dogs (P < .001), but cTnT was significantly higher only in dogs with BCT (P = .033). Increased cTnI or cTnT values were found in 26 of 28 (highest values 1.1-369 microg/L) and 16 of 28 dogs (0.1-1.7 ng/mL) with GDV, and in 6 of 8 (2.3-82.4 microg/L) and 3 of 8 dogs (0.1-0.29 ng/mL) with BCT, respectively. In dogs suffering from GDV, cTnI and cTnT increased further within the first 48 hours (P < .001). Increased cardiac troponins suggestive of myocardial damage occurred in 93% of dogs with GDV and 75% with BCT. cTnI appeared more sensitive, but cTnT may be a negative prognostic indicator in GDV. Both systems tested seemed applicable for the measurement of canine cardiac troponins, with the Cardiac Reader particularly suitable for use in emergency settings.

The prevalence of false-positive cardiac troponin I in ED patients with rhabdomyolysis

Objective Cardiac troponin I (cTnI) is considered the most specific marker of cardiac muscle injury. We encountered several patients with rhabdomyolysis and elevated cTnI, although they did not otherwise have evidence of cardiac injury. We determined the prevalence of false-positive cTnI in emergency department (ED) patients with rhabdomyolysis. Methods We conducted a retrospective cohort study of ED patients admitted with a diagnosis of rhabdomyolysis. Patients were included in the study if they had a serum creatine kinase (CK) of 1000 U/L or greater and at least one serum cTnI determination. Patients with positive cTnI were considered true positives if they had either electrocardiography (EKG) or echocardiography abnormalities; false positives if both the EKG and the echocardiography were considered normal; or indeterminate if they did not have both an EKG and an echocardiogram. The primary outcome of the study was the prevalence of false-positive cTnI. Secondary outcomes included risk stratification by cocaine use, myoglobinuria, and renal failure and correlation of peak CK and troponin levels. Results One hundred nine patients were included in the final analysis; 55 (50%) patients had a positive cTnI. Of the 55 patients with positive cTnI, 32 (58%) were true positives, 18 (33%) were false positives, and 5 (9%) were indeterminate. The prevalence of false-positive cTnI was 17% (18/109, 95% confidence interval 0.10-0.25). There was no association between false-positive cTnI and cocaine use, renal failure, or myoglobinuria. There was poor correlation between peak CK and peak cTnI levels ( r = −.08, 95% confidence interval −0.34 to 0.19). Conclusion The prevalence of false-positive cTnI in ED patients with rhabdomyolysis is 17%.

Prognostic Value of Preoperative Cardiac Troponin I in Patients With Non-ST-Segment Elevation Acute Coronary Syndromes Undergoing Coronary Artery Bypass Surgery

Study objectives: Elevated levels of cardiac troponin I (cTnI) have been associated with adverse short-term and long-term outcomes in acute coronary syndrome (ACS) patients and in patients who underwent coronary artery bypass grafting (CABG); however, the prognostic implications of preoperative cTnI determination have not been investigated so far. Design and setting: Retrospective study in a department of cardiothoracic surgery of a university hospital. Patients and methods: A possible correlation between preoperative cTnI levels and major adverse cardiac events (MACE) and in-hospital mortality in CABG patients with non–ST-segment elevation ACS (NSTE-ACS) was investigated. cTnI was determined in 1,978 of 3,124 consecutive CABG patients. Among these, 1,592 patients had preoperative cTnI levels 1.5 ng/mL (group 3). cTnI levels, clinical data, MACE, and in-hospital mortality were recorded prospectively. Logistic regression and receiver operating characteristic analyses were applied to determine prognostic cutoff values of cTnI. Results: Perioperative myocardial infarction was found in 5.8% of the patients in group 1, 8.3% of the patients in group 2 (odds ratio [OR], 1.5; 95% confidence interval [CI], 0.9 to 2.5), and 18.2% patients in group 3 (OR, 3.6; 95% CI, 2.1 to 6.2; p Conclusions: Preoperative cTnI measurement before CABG appears as a powerful and independent determinant of short-term surgical risk in patients with NSTE-ACS.

RESCUE PERCUTANEOUS CORONARY INTERVENTION, REOPERATION, OR CONSERVATIVE TREATMENT IN ACUTE PERIOPERATIVE GRAFT FAILURE AFTER CORONARY ARTERY BYPASS SURGERY

Elevated levels of cardiac troponin I (cTnI) have been associated with adverse short-term and long-term outcomes in acute coronary syndrome (ACS) patients and in patients who underwent coronary artery bypass grafting (CABG); however, the prognostic implications of preoperative cTnI determination have not been investigated so far. Retrospective study in a department of cardiothoracic surgery of a university hospital. A possible correlation between preoperative cTnI levels and major adverse cardiac events (MACE) and in-hospital mortality in CABG patients with non-ST-segment elevation ACS (NSTE-ACS) was investigated. cTnI was determined in 1,978 of 3,124 consecutive CABG patients. Among these, 1,592 patients had preoperative cTnI levels < 0.1 ng/mL and therefore served as control subjects (group 1), 265 patients had NSTE-ACS with cTnI levels from 0.11 to 1.5 ng/mL (group 2), and 121 patients had NSTE-ACS with cTnI levels > 1.5 ng/mL (group 3). cTnI levels, clinical data, MACE, and in-hospital mortality were recorded prospectively. Logistic regression and receiver operating characteristic analyses were applied to determine prognostic cutoff values of cTnI. Perioperative myocardial infarction was found in 5.8% of the patients in group 1, 8.3% of the patients in group 2 (odds ratio [OR], 1.5; 95% confidence interval [CI], 0.9 to 2.5), and 18.2% patients in group 3 (OR, 3.6; 95% CI, 2.1 to 6.2; p < 0.0001, Cochran-Armitage trend test). Low cardiac output syndrome occurred in 1.5% of patients in group 1, 4.2% of patients in group 2 (OR, 2.8; 95% CI, 1.3 to 6.1), and 10.9% patients in group 3 (OR, 6.5; 95% CI, 2.9 to 14.4; p < 0.0001). In-hospital mortality was 1.5% in group 1, 3.0% in group 2 (OR, 2.0; 95% CI, 0.8 to 4.8), but 6.6% in group 3 (OR, 4.6; 95% CI, 1.9 to 11.1; p < 0.0001). Univariate and multivariate logistic regression analyses identified cTnI as the strongest preoperative predictor for MACE and in-hospital mortality, respectively. Preoperative cTnI measurement before CABG appears as a powerful and independent determinant of short-term surgical risk in patients with NSTE-ACS.

Leakage of cardiac troponin I in aortic valve stenosis

Degeneration and death of cardiomyocytes contribute to the genesis of heart failure (HF) in aortic valve stenosis (AS). We studied whether the ongoing myocyte damage in AS can be detected from circulating cardiac troponin I (cTnI) concentrations. A cross-sectional cohort study in a university hospital. We examined 131 adult patients undergoing echocardiography and cardiac catheterization for isolated AS. Blood was sampled from the aortic root and, in a subset of 49 patients, also from the coronary sinus for the determination of cTnI using a sensitive immunoanalysis. Seventy-three patients (56%) had detectable aortic cTnI (> or =5 ng L(-1)) with 30 of them (23% of the total group) having cTnI above the reference limit in healthy subjects (>14 ng L(-1)). Patients with detectable cTnI had a higher prevalence of HF than those with undetectable cTnI (42% vs. 19%, P = 0.004). Plasma cTnI rose from the aorta to the coronary sinus by > or =5 ng L(-1) in 13 of 49 patients with AS (27%) versus in none of 12 control patients free of structural heart disease (P = 0.044). AS patients with transcardiac cTnI gradients > or =5 ng L(-1) had lower left ventricular (LV) ejection fractions than AS patients with gradients <5 ng L(-1) (mean +/- SD, 52 +/- 14% vs. 61 +/- 11%; P = 0.011). Detectable circulating cTnI is not uncommon in AS and shows a moderate association with the presence of HF. Leakage of cTnI into the coronary sinus associates with impairment of LV systolic function. Monitoring cTnI could provide a means to expose incipient clinical deterioration in AS.

Myocardial injury in meningococcus-induced purpura fulminans in children.

To assess the incidence of myocardial ischemia in meningococcus-induced purpura fulminans in pediatric patients, to compare troponin I (cTnI) levels with changes in electrocardiogram (ECG) and to evaluate whether cTnI is related to myocardial function and contractility, to severe acquired anticoagulant deficiency and to the severity of disease. Twenty-two patients with acute meningococcemia, supported with inotropes or vasoactive agents, were studied, Blood samples for the determination of serum cTnI and conventional myocardial ischemia and coagulopathy markers were drawn daily. Measurements of cardiac index (CI), ejection (EF) and shortening fractions (SF) and ECGs were performed daily. The Leclerc score, the Neisseria sepsis index (NESI) and the pediatric risk of mortality (PRISM) score predicted a mean mortality rate of 34%, 27% and 23%, respectively. Four patients died (18%). Five patients (23 %) presented with myocardial ischemia. Their ECG ischemic changes were associated with pathologically high cTnI levels (1.93 +/- 0.13 vs 0.18 +/- 0.08 ng/ml, p < 0.001 for patients with or without ischemic changes) and depressed myocardial contractility (mean difference +/- SE -14 +/- 5%, p = 0.01, for the EF and -7.4 +/- 3, p < 0.02, for the SF). High cTnI values were significantly correlated to low protein C (PC) (p < 0.0001), factor VIII (p < 0.04) and antithrombin III (AIII, p = 0.01) levels, but not to the PRISM, Leclerc or the NESI scores. Means of AIII, VII, and especially of VIII, and PC, were significantly lower in ischemic than in non-ischemic patients, although severity scoring systems and inotropic support did not differ between the two groups. Survivors tended to significantly higher PC (p < 0.01) and factor VIII levels (p = 0.001) than non-survivors and, also, to lower levels of cTnI (p = 0.05) and CPK-MB (p < 0.05), while in meningococcal shock. The incidence of myocardial ischemia is increased in acute meningococcemia in pediatric patients and correlates with myocardial dysfunction. High cTnI is associated with severe coagulopathy, but not with clinical prognostic scores or inotropic support. Early recognition of myocardial injury, myocardial support and early replacement therapy with PC, AIII, factor VIII or fibrinogen might improve outcome in acute meningococcemia in children.

Effect of elevated concentration of alkaline phosphatase on cardiac troponin I assays.

Troponin I is the regulatory subunit of troponin complex associated with the actin thin filament within muscle cells. Cardiac troponin I (cTnI) is a good marker for diagnosis of myocardial damage. Several immunoassays are available for determination of cTnI in serum. The Stratus cTnI fluorometric enzyme immunoassay (Dade International) uses alkaline phosphatase (ALP) substrate. The microparticle enzyme immunoassay (MEIA) for cTnI (Abbott Laboratories) also uses ALP conjugate. On the other hand, the chemiluminescent assay (CLIA) for cTnI (Bayer Diagnostics) does not use ALP. ALP activity may frequently be elevated in serum of patients being evaluated for suspected myocardial infarction. Therefore, we studied the potential interference of ALP in cTnI assays. Serum pools were prepared from patients, and various concentrations of ALP solution were added to different aliquots. The cTnI concentrations were measured by the Stratus, MEIA, and CLIA assays. We observed no interference of ALP in the MEIA and CLIA assay for cTnI. On the other hand, we observed significant positive interference of ALP when cTnI concentrations were measured using the Stratus.

Comparison of diagnostic performance of cardiac troponin I on the IMMULITE system with other automated troponin I assays in minor myocardial damage

An analytical and clinical evaluation of cardiac troponin I (cTnI) on the IMMULITE system is presented. The assay results were compared with those of the Stratus II and the Dimension RxL-HM.A between-run imprecision CV<20% was found at a cTnI concentration of 0.23 µ g/L (functional limit of detection). On the basis of a reference study including 215 patients without ischemic heart disease (97.5th percentile: 0.294 µ g/L) and 36 patients clinically classified as having stable angina pectoris (<0.22 µ g/L) a preliminary cutoff level of 0.3 µ g/L was defined. Assay linearity, sample stability, influence of sample material and method comparison studies were performed. In patients with Duchenne's disease, chronic hemodialysis treatment, pulmonary embolism, coronary artery bypass surgery and minimally cardiacsurgery thecTnI results ofthe IMMULITE agreed better with the Dimension RxL-HM than with theStratus II data.Of142 samples from patients with unstable angina 67 samples were classified as cTnI positive with the IMMULITE, 76 with the Dimension RxL-HM, and 62 with the Stratus II. In conclusion, the new assay is sensitive for the determination of cTnI and easy to perform within 45min.

Evaluation of the new ImmuliteTurbo cTnI assay and the original Immulite cTnI assay

Objectives : An analytical and clinical evaluation of cTnI on the ImmuliteTurbo system with 15 min assay time compared to 45 min with the original Immulite assay is presented. Methods and Design : Detection limit, functional sensitivity, AMI decision limit, assay linearity, influence of sample material (serum, heparin, citrate and EDTA plasma), interference, analytical and clinical method comparison studies were performed. Results : Functional sensitivity (at CV 20%) was 0.35 compared to 0.23 mug/L for the original assay. AMI decision limit (99th percentile of a reference control group) was 0.48 mug/L for both assays. In patients with acute coronary syndromes, chronic renal failure or pulmonary embolism the assays showed concordant results in 87.2-96.5%. Differing results were only found around the cut-off level and were attributed to assay imprecision. Conclusion : The new assay is sensitive for the determination of cTnI, shows comparable results to the original assay version and is easy to perform within 15 min.

Cardiac troponin T and I, electrocardiographic wall motion analyses, and ejection fractions in athletes participating in the Hawaii Ironman Triathlon

Cardiac troponin T (cTnT) and troponin I (cTnI) are highly sensitive and specific for detecting myocardial damage even in the presence of skeletal muscle injury. In this study, we assessed whether ultraendurance exercise induced cardiomyocyte injury using plasma cTnT and cTnI measurements, quantitative echocardiographic wall-motion analysis, and ejection fraction measurement in athletes who participated in the Hawaii Ironman Triathlon. Twenty-three athletes (11 men) who completed the triathlon (3.9 km swim, 180.2 km bike, and 42.2 km run) participated in this study. Blood samples were obtained 2 days before and immediately after the triathlon for the determination of cTnT (Enzymun, Roche Diagnostics) and cTnI (Dade Behring) concentrations. Quantitative echocardiographic wall motion analysis and ejection fraction were obtained on 12 of the 23 participants before and immediately after the race. No subject had detectable cTnT or cTnI or abnormal echo score before the race. Following the race, 2 subjects (9%) had marked increases in both cTnT (0.15 and 0.33 μg/L) and cTnI (2.09 and 4.44 μg/L). Four additional subjects (17%) had moderate increases in cTnT (0.04 to 0.05 μg/L) but no detectable cTnI. Race time correlated inversely with cTnT (r = −0.65, p <0.01). Mean change in the number of abnormal echo segments after the race was 6.5 in those with a marked increase in cTnT and cTnI, 2.3 in those with a moderate increase in cTnT, and 1.7 in those with no increase. Ejection fraction decreased by an average of 24% after the race (p <0.002). Thus, ultraendurance exercise may cause myocardial damage as indicated by biochemical cardiac-specific markers and echocardiography. The cellular nature of this damage and whether it is transient or permanent is unclear at present.

Release kinetics of serum cardiac troponin i in ischemic myocardial injury

Objectives: The study was undertaken to evaluate the release kinetics of cardiac troponin I (c-cTn-I) in ischemic myocardial injury. Design and Methods: The reference range for cTn-I was established by determination of cTn-I in sera and plasma obtained from 622 healthy volunteers (Group 1). cTn-I was compared to: (a) Creatine kinase (CK) MB mass and myoglobin in 12 patients with severe skeletal muscle damage (Group 2); (b) CK-MB activity in 48 patients with myocardial infarction (MI) receiving intravenous thrombolysis (Group 3) (in this group, an additional 43 patients with MI were analyzed separately to characterize cTn-I patterns in thrombolyzed and nonthrombolyzed populations); and in 44 patients with unstable angina (Group 4). Results: In Groups 1 and 2, no positive results (⩾0.1 μg/L) were obtained. In Group 3, the time-courses of cTn-I were mostly monophasic in form. A pathologic increase occurred earlier in cTn-I than in CK-MB activity ( p = 0.0002); the period with increased cTn-I was longer ( p = 0.001), the overall sensitivity of cTn-I (93.9%) was higher than that of CK-MB activity ( p = 0.00001). cTn-I was more sensitive at admission ( p = 0.0004). In additional patients, the cTn-I peak occurred and cTn-I disappeared significantly later in nonthrombolyzed than in the thrombolyzed group. In Group 4, positive tests results were detected in 45% of patients for cTn-I, 16% for CK-MB activity, and 32% for CK-MB mass. Conclusions: The cTn-I assay appears to be ideally suited for the detection of ischemic myocardial injury in complex clinical situations because of its high specificity; cTn-I indicates myocardial tissue damage in patients with unstable angina and is superior to CK-MB activity and mass in this respect.