Diagnosis and risk stratification of patients with anginal pain and non-diagnostic electrocardiograms

Patients with acute chest pain suggestive of myocardial ischaemia, and normal or non-diagnostic electrocardiograms, form a difficult subgroup for diagnosis and early risk stratification. We prospectively evaluated the role of troponin T (cTnT), troponin I (cTnI), CKMB mass and myoglobin, in the diagnosis and risk stratification of 214 patients with acute chest pain of < or = 24 h and non-diagnostic or normal ECGs admitted directly to the Cardiac Unit of the Royal Victoria Hospital Belfast from the Mobile Coronary Care Unit or the Accident/Emergency Department. This was a single-centre prospective study, and follow-up (3 months) was complete for all patients. Blood was assessed for quantitative cTnT, cTnI, CKMB mass and myoglobin, and qualitative cTnT on admission and at 12 h. Diagnosis of index event and incidence of new cardiac events (death, non-fatal myocardial infarction, revascularization, or readmission for unstable angina) over 3 months were assessed. Based on standard criteria, myocardial infarction occurred in 37/214 (17%), and unstable angina in 72/214 (34%). At 12 h from admission, cardiac troponins had higher sensitivity for the diagnosis of acute coronary syndromes (myocardial infarction and unstable angina) than conventional markers (cTnI 48%, cTnT 38%, CKMB mass 30% or myoglobin 27%). At 3 months, a new cardiac event had occurred in 42/214 (20%). Significantly higher event rates occurred when any of the biochemical markers was elevated, but the statistical significance was highest for patients with elevated cTnI (p < 0.0001). Whilst gender, history of ischaemic heart disease (IHD), stress test response, cTnT, cTnI, CKMB mass and myoglobin were univariate predictors, cTnI at 12 h and stress test response were the only two independent significant predictors for a subsequent cardiac event at 3 months. Raised cTnI at 12 h after admission had the highest sensitivity for the diagnosis of acute coronary syndromes, and was independently associated with a 2-3 times increased risk of future cardiac events within 3 months among patients with acute chest pain suggestive of myocardial ischaemia but with normal or non-diagnostic ECGs.     

Cardiac troponins and left ventricular hypertrophy in hemodialysis patients

BACKGROUND: Cardiovascular diseases are the leading cause of death in hemodialysis patients. Left ventricular (LV) hypertrophy is an important predictor of cardiovascular morbidity and mortality in these patients. Cardiac troponins (cTnT and cTnI) are indicators of myocardial cell damage. AIM: The aim of this study was to determine prevalence of LV hypertrophy, prevalence of elevated serum cTnT and cTnI in hemodialysis patients, and identify the correlation between cardiac troponins and LV hypertrophy. METHODS: The study included 115 hemodialysis patients (71 men and 44 women), mean age 53.30 +/- 12.17 years, mean time on dialysis 4.51 +/- 4.01 years and average Kt/Vsp 1.17 +/- 0.23. Mean serum cTnT was 0.14 +/- 0.23 ng/ml, mean serum troponin I 0.20 +/- 0.48 ng/ml. Mean LV posterior wall thickness in diastole (LVPWd) was 11.44 +/- 2.09 mm, mean LV interventricular septal wall thickness in diastole (IVSd) 11.21 +/- 2.12 mm, mean LV end diastolic volume index (iLVEDV) 100.80 +/- 34.62 mL/m2 and mean LV mass index (LVMi) 143.85 +/- 41.21 g/m2. RESULTS: We found statistically significant positive correlations (p <0.05) between serum troponin T concentration, IVSd, LVPWd and iLVEDV. A highly significant positive correlation (p < 0.01) was found between serum troponin T and LVMi. One-year follow-up showed that patients with cardiac troponin T > 0.10 ng/ml and cardiac troponin I > 0.15 ng/ml had significantly lower (p < 0.01) survival rate than patients with troponin T < or = 0.10 ng/ml and troponin I < or = 0.15 ng/ml. CONCLUSION: A significant positive correlation exists between serum troponin T concentration and echocardiographic indicators of LV hypertrophy in hemodialysis patients. Patients with higher serum levels of cardiac troponins have lower survival rates during one year follow up.     

Prognostic implications of myocardial necrosis triad markers' concentration measured at admission in patients with suspected acute coronary syndrome

The aim of the study was to analyze the prognostic implications of 3 myocardial necrosis markers measured at admission in short-term observation of patients with suspected acute coronary syndrome. The study group consisted of 336 consecutive patients whose concentration of cardiac troponin I, creatine kinase-MB fraction, and myoglobin were measured at admission. All patients referred due to chest pain and suspected acute coronary syndrome and were followed up for 30 days. The patients who died had statistically higher concentration of cardiac troponin I (8.7 +/- 17.2 vs 0.9 +/- 3.2 ng/mL; P = .0006), myoglobin (215.2 +/- 181.5 vs 109.7 +/- 151.5 ng/mL; P = .003), and creatine kinase-MB (21.9 +/- 30.7 vs 8.8 +/- 25.9 ng/mL; P = .005), compared to patients who stayed alive. There was statistically significant increase in 30-day all-cause mortality with increasing numbers of positive markers-0.6% for patients with nonpositive marker, 3.4% for patients with 1 positive marker, and 11.5% for patients with at least 2 positive markers (P = .001 for trend).     

Serum cardiac troponin T in patients hospitalized with heart failure is associated with left ventricular hypertrophy and systolic dysfunction

BACKGROUND: Cardiac troponin T (cTnT) is a highly sensitive and specific marker of acute myocardial infarction. Serum cTnT is also slightly elevated in patients with severe heart failure and is associated with left ventricular hypertrophy (LVH) in patients treated with haemodialysis. In this study serum cTnT concentrations and echocardiographic findings were investigated in heart failure patients without acute coronary syndrome. cTnT was also compared with other cardiac markers and plasma levels of brain natriuretic peptide (BNP). METHODS: Twenty-six patients hospitalized with heart failure were included in the study. Echocardiographic measurements and blood sampling were carried out 12-36 h after admission. Serum cTnT (3rd generation assay), cardiac troponin I (cTnI), creatine kinase MB (CKMB) and CK were measured. Plasma BNP was analysed using the Shionoria assay. LVH was defined as left ventricular mass index (LVMI) > 125 g/m for males and > 110 g/m for females. Left ventricular systolic function was estimated from the mitral annulus motion (AV-mean LV). RESULTS: Median cTnT was 0.012 (< 0.010-0.032) microg/L. Sixty-two percent of the patients (16 of 26) had elevated serum cTnT >or= 0.010 micro/L. cTnT was positively correlated with CKMB (rho = 0.40, p = 0.04) and BNP (rho = 0.43, p = 0.03), but not with cTnI and CK. A negative correlation was found between cTnT and AV-mean LV (rho = -0.58, p = 0.007), and there was a positive correlation between cTnT and LVMI (rho = 0.44, p = 0.03). No other analyte was correlated to LVMI. CONCLUSIONS: Serum cTnT but not cTnI was associated with left ventricular dysfunction and LVH in patients hospitalized with heart failure. This explains why cTnT tends to be slightly elevated in patients with heart failure without symptoms of acute myocardial ischaemia.     

Cardiac troponin and beta-type myosin heavy chain concentrations in patients with polymyositis or dermatomyositis

Cardiac troponin T (cTnT), cardiac troponin I (cTnI), myosin heavy chains (MHC), myoglobin, creatine kinase (CK), and creatine kinase isoenzyme MB (CKMB), were measured in blood samples from 39 polymyositis (PM) or dermatomyositis (DM) patients without clinical evidence for cardiac involvement to evaluate their clinical usefulness in this patient population. MHC, myoglobin, and CKMB were frequently elevated and correlated with each other and with disease severity. Undetectable cTnI in all but one patient indicated that MHC was released from skeletal muscle, thereby providing the first laboratory evidence of frequent slow-twitch muscle fibre-necrosis in patients with PM or DM. CKMB was elevated in 51%, cTnT in 41%, and cTnI in only 2.5% of patients. cTnI did not correlate with other markers or with disease severity scores. The close correlations found between cTnT and skeletal muscle damage markers and the relationship between cTnT with disease severity without clinical evidence for myocardial damage suggest a release of cTnT from skeletal muscle. The relationship of cTnT with disease severity indicates a possible role of the marker for risk stratification. However, the prognostic values of cardiac troponins and other muscle damage markers in PM/DM patients remain to be compared in prospective outcome trials.     

Myocardial Injury During Radiofrequency Catheter Ablation: Comparison of Focal and Linear Lesions

The aim of study was to investigate the extent of myocardial injury incurred by creation of continuous RF current induced linear ablation lesions (LL; ablation of atrial fibrillation, right atrial procedure) in comparison to focal RF lesions (FL; AV node reentry tachycardia, WPW tachycardia). In 23 patients with LL (age 51.3 +/- 11.2 years, 18 men, 5 women) and in 16 patients with FL (age 53.9 +/- 5.1 years, 8 men and 8 women), levels of creatine kinase (CK), myoglobin (MG), CKMB mass (CKMB M), CKMB activity (CKMB A), and cardiac troponin T (cTnT) were determined before and 2, 4, 8, 24, and 48 hours after ablation. CKMB A was normal in 87% in LL and 100% in FL (< 6% of CK) with median maximum CK values of 214 (45-1583) U/L in LL and 36 (29-212) U/L in FL. Peak values of all parameters were significantly higher in LL than in FL. The sensitivity of cTnT was 50% in FL and 100% in LL. In FL MG, total CK, and CKMB M were abnormal in only 12.5% of cases while in LL MG and CKMB M were pathological in 100% and total CK was abnormal in 91.3% of patients. The amount of energy and number of RF applications correlated with cTnT, MG, and CKMB M (P = 0.01). In conclusion, (1) long linear RF current lesions for ablation of atrial fibrillation are associated with significantly greater myocardial injury than focal ablations. (2) In focal lesions only cTnT provided a sensitivity of 50% in the detection of myocardial injury while in linear lesions cTnT, CKMBM, and CKMB M seemed suitable for detection of RF current induced myocardial damage with 100% sensitivity. All biochemical parameters do not differentiate patients with coronary ischemia up to 48 hours after an ablation. (3) Further investigations are necessary to determine if RF current linear lesions lead to impaired atrial contractility in cases of extensive tissue damage.     

Myoglobin stratifies short-term risk in acute major pulmonary embolism

BACKGROUND: Concentrations of cardiac troponins can be elevated in acute pulmonary embolism (APE) indicating myocardial injury. Although concentration of myoglobin (MYO) increases after myocardial damage, even before detectable rise of cardiac troponin levels occurs, MYO was not evaluated in APE. Therefore, we assessed prevalence and prognostic significance of myoglobin in major APE. METHODS: We studied 46 patients (30 women, aged 61.9+/-17.8 years) with major APE defined with right ventricular dilatation. On admission serum myoglobin, and cardiac troponin T (cTnT) were measured. Serum MYO concentrations >58 ng/ml for women, and >72 ng/ml for men were considered abnormal. CTnT>0.01 ng/ml was regarded to indicate myocardial injury. RESULTS: MYO levels exceeding sex specific norms were found in 21/46 (45.7%) of patients, while detectable cTnT was found in 24/46 (52.1%) of patients. Seven patients died during hospitalization. Elevated MYO significantly predicted in-hospital mortality (OR 25, 95% CI 1.3-474.2), while increased cTnT concentration did not affect the survival. Among clinical and echocardiographic variables only older age indicated worse prognosis (OR 1.6, 95% CI 1.06-2.41). CONCLUSIONS: Myoglobin levels are elevated in serum on admission in almost half of patients with major APE. Elevated myoglobin level, marker of myocardial injury, is a powerful predictor of increased risk of fatal outcome in major pulmonary embolism.     

Serum cardiac troponin T in patients hospitalized with heart failure is associated with left ventricular hypertrophy and systolic dysfunction

Background: Cardiac troponin T (cTnT) is a highly sensitive and specific marker of acute myocardial infarction. Serum cTnT is also slightly elevated in patients with severe heart failure and is associated with left ventricular hypertrophy (LVH) in patients treated with haemodialysis. In this study serum cTnT concentrations and echocardiographic findings were investigated in heart failure patients without acute coronary syndrome. cTnT was also compared with other cardiac markers and plasma levels of brain natriuretic peptide (BNP). Methods: Twenty-six patients hospitalized with heart failure were included in the study. Echocardiographic measurements and blood sampling were carried out 12-36?h after admission. Serum cTnT (3rd generation assay), cardiac troponin I (cTnI), creatine kinase MB (CKMB) and CK were measured. Plasma BNP was analysed using the Shionoria assay. LVH was defined as left ventricular mass index (LVMI)&;gt;125?g/m&;lt;formula&;gt;²&;lt;/formula&;gt; for males and&;gt;110?g/m&;lt;formula&;gt;²&;lt;/formula&;gt; for females. Left ventricular systolic function was estimated from the mitral annulus motion (AV-mean LV). Results: Median cTnT was 0.012 (&;lt;0.010-0.032)?μg/L. Sixty-two percent of the patients (16 of 26) had elevated serum cTnT≥0.010?μg/L. cTnT was positively correlated with CKMB (ρ=0.40, p=0.04) and BNP (ρ=0.43, p=0.03), but not with cTnI and CK. A negative correlation was found between cTnT and AV-mean LV (ρ=?0.58, p=0.007), and there was a positive correlation between cTnT and LVMI (ρ=0.44, p=0.03). No other analyte was correlated to LVMI. Conclusions: Serum cTnT but not cTnI was associated with left ventricular dysfunction and LVH in patients hospitalized with heart failure. This explains why cTnT tends to be slightly elevated in patients with heart failure without symptoms of acute myocardial ischaemia.     

Clinical and experimental results on cardiac troponin expression in Duchenne muscular dystrophy

BACKGROUND: Because of controversial earlier studies, the purpose of this study was to provide novel experimental and additional clinical data regarding the possible reexpression of cardiac troponin T (cTnT) in regenerating skeletal muscle in Duchenne muscular dystrophy (DMD). METHODS: Plasma from 14 patients (mean age, 7.5 years; range, 5.7-19.4 years) with DMD was investigated for creatine kinase (CK), the CK MB isoenzyme (CKMB), cTnT and cardiac troponin I (cTnI), and myoglobin. cTnT concentrations were measured by an ELISA (second-generation assay; Roche) using the ES 300 Analyzer. cTnI, myoglobin, and CKMB were measured by an ELISA using the ACCESS System (Beckman Diagnostics). Troponin isoform expression was studied by Western blot analysis in remnants of skeletal muscle biopsies of three patients with DMD and in an animal model of DMD (mdx mice; n = 6). RESULTS: There was no relation of cTnT and cTnI to clinical evidence for cardiac failure. cTnI concentrations remained below the upper reference limit in all patients. cTnT was increased (median, 0.11 microg/L; range, 0.06-0.16 microg/L) in 50% of patients. The only significant correlation was found for CK (median, 3938 U/L; range, 2763-5030 U/L) with age (median, 7.5 years; range, 6.8-10.9 years; r = -0.762; P = 0.042). Western blot analysis of human or mouse homogenized muscle specimens showed no evidence for cardiac TnT and cTnI expression, despite strong signals for skeletal muscle troponin isoforms. CONCLUSIONS: We found no evidence for cTnT reexpression in human early-stage DMD and in mdx mouse skeletal muscle biopsies. Discrepancies of cTnT and cTnI in plasma samples of DMD patients were found, but neither cTnT nor cTnI plasma concentrations were related with other clinical evidence for cardiac involvement.     

Troponin T levels in detection of perioperative myocardial infarction after coronary artery bypass surgery

OBJECTIVES: The present study was designed to evaluate the clinical relevance of serum cardiac troponinT (cTnT) assay in detection of perioperative myocardial infarction (PMI) after coronary artery bypass grafting (CABG). MATERIALS AND METHODS: The clinical utility of cTnT was compared to that of total CK, CKMB mass, CKMB activity and myoglobin. Serial venous blood samples were obtained before surgery and 4, 8, 16, 24, 48 and 72 hours after aortic unclamping (AU) in 42 patients who underwent CABG. We had 6 PMI patients, 24 patients with minor myocardial damage (MMD) and 12 without ischemic myocardial changes (no IMC). RESULTS: In discriminating no IMC from PMI the diagnostic sensitivity, specificity and the predictive values of cTnT were superior to that of CKMB mass, CKMB activity, myoglobin and total CK during 72 hours after AU. In discriminating MMD from PMI the diagnostic performance for CKMB mass and CKMB activity was superior to that of cTnT during the first 24 hours. After 24 hours the diagnostic performance for cTnT was improved but began to decline for CKMB isoenzymes. The discriminatory power of myoglobin measurements was lower than that of cTnT and CKMB mass. CONCLUSION: Our results indicate that troponin T is an accurate marker for the detection and monitoring of perioperative myocardial damage, especially 24 hours after AU.     

Clinical evaluation of the first medical whole blood, point-of-care testing device for detection of myocardial infarction

BACKGROUND: Validation of whole blood, point-of-care testing devices for monitoring cardiac markers to aid clinicians in ruling in and ruling out myocardial infarction (MI) is necessary for both laboratory and clinical acceptance. METHODS: This study evaluated the clinical diagnostic sensitivity and specificity of the First Medical Cardiac Test device operated by nursing and laboratory personnel that simultaneously measures cardiac troponin I (cTnI), creatine kinase (CK) MB, myoglobin, and total CK on the Alpha Dx analyzer in whole blood for detection of MI. Over a 6-month period, 369 patients initially presenting to the emergency department with chest pain were evaluated for MI using modified WHO criteria. Eighty-nine patients (24%) were diagnosed with MI. RESULTS: In whole blood samples collected at admission and at 3- to 6-h intervals over 24 h, ROC curve-determined MI decision limits were as follows: cTnI, 0.4 microgram/L; CKMB, 7.0 microgram/L; myoglobin, 180 microgram/L; total CK, 190 microgram/L. Based on peak concentrations within 24 h after presentation, the following sensitivities (+/- 95% confidence intervals) were found: cTnI, 93% +/- 5.5%; myoglobin, 81% +/- 9.7%; CKMB, 90% +/- 6.3%; total CK, 86% +/- 7.5%. Sensitivities were maximal at >90% for both cTnI and CKMB at >12 h in MI patients, without differences between ST-segment elevation and non-ST-segment elevation MI patients. CONCLUSIONS: The First Medical point-of-care device provides cardiac marker assays that can be used by laboratories and clinicians in a variety of hospital settings for ruling in and ruling out MI.     

Pharmacokinetics of rosiglitazone in patients with end-stage renal disease

The pharmacokinetics and tolerability of a single 8-mg oral dose of rosiglitazone, an anti-diabetic agent, were compared in 10 long-term haemodialysis patients and 10 healthy volunteers. Haemodialysis patients received rosiglitazone 4 h after haemodialysis (non-dialysis day) and 3 h before haemodialysis (dialysis day). Haemodialysis did not influence rosiglitazone pharmacokinetics, and dialytic clearance was low (0.10 1/h). The mean area under the concentration-time curve (AUC(0-infinity)), the maximum observed plasma concentration (Cmax) and the half-life for rosiglitazone were similar in haemodialysis patients (non-dialysis day) and healthy individuals (2192 +/- 598 ng.h/ml versus 2388 +/- 494 ng.h/ml, 338 +/- 114 ng/ml versus 373 +/- 95 ng/ml, and 3.70 +/- 0.75 h versus 3.81 +/- 0.86 h, respectively). AUC(0-infinity) and Cmax were not markedly influenced by haemodialysis. Rosiglitazone dose adjustments are not warranted in patients with type 2 diabetes with end-stage renal failure on haemodialysis.     

Comparison of the diagnostic value of cardiac troponin I and T determinations for detecting early myocardial damage and the relationship with histological findings after isoprenaline-induced cardiac injury in rats

Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. The purpose of this study was to investigate the diagnostic value of cTnI and cTnT with regard to creatine kinase (CK) and lactate dehydrogenase (LD) and to determine whether they can be used for early diagnosis of myocardial damage in rats, and to examine the relationship between cTnl and cTnT release with histological examinations, using isoprenaline-induced cardiac muscle damage as an experimental model in the rat. Eighteen Wistar rats per group were treated with a single dose of either isoprenaline (iso) or with normal saline as a control group. The anti-cTnI and cTnT monoclonal antibodies (mAbs) employed in the cTnI (Access) and cTnT (Elecsys) assays cross-react with cTnI and cTnT of the rat. A highly significant rise of cTnl or cTnT was found already 2 h after iso. The time-courses of cTnI and cTnT were monophasic in form. The highest cTnI (mean+/-S.D., 1.1+/-2.3 ng/ml) and cTnT (mean+/-S.D. 3.6+/-30 ng/ml) were found 4 h after iso. cTnI and cTnT significantly increased in iso-treated rats in comparison with controls whether the differences between 2-, 4- and 6-h levels and basal levels were considered or not. The areas under cTnl and cTnT curves (AUC) (0-6 h) and the maximal cTnI and cTnT (0-6 h) after iso were significantly different from the controls. For CK and LD, no elevation in comparison with controls could be detected (except a trend for LD whether or not the difference between 6-h levels and basal levels were considered (P=0.08) and for LD AUC (0-6 h) (P=0. 059)). Correlations between maximal cTnI and cTnT and AUC were 0.69 (P=0.0001) and 0.60 (P=0.0066), respectively. Histological examinations of iso-treated rats revealed acute focal or multifocal myofibrillar degeneration of the myocardial tissue in ten out of 14 rats and showed the earliest alterations 4 h after iso in one treated rat. Only four of the controls exhibited evidence of mild changes and slight mononuclear cell infiltration. cTnl and cTnT peak values to at least 0.35 and 1.3 ng/ml, respectively, were necessary to detect histological myocardial cell injury after iso. cTnI and cTnT were found to be early markers for diagnosing iso-induced myocardial damage in comparison with CK and LD. Elevations of cTnI and cTnT appeared to relate to the severity of histologic changes after myocardial injury. Although there was a difference in the absolute concentration of results between cTnI and cTnT assays, due to a lack of standardization and heterogeneity in the cross-reactivities of mAbs to various troponin I and T forms, cTnI and cTnT can be used as easily measurable target parameters for detection of cardiotoxic and/or cardiodegenerative effects in rats.     

Plasma 99th percentile reference limits for cardiac troponin and creatine kinase MB mass for use with European Society of Cardiology/American College of Cardiology consensus recommendations

BACKGROUND: The European Society of Cardiology/American College of Cardiology (ESC/ACC) consensus document for definition of myocardial infarction (MI) is predicated on increased cardiac troponin or creatine kinase (CK) MB mass above the 99th percentile reference limit. The purpose of this study was to determine the plasma (heparin) 99th percentile reference limits for the leading in vitro diagnostic cardiac troponin and CKMB mass assays. METHODS: Blood (heparin plasma) was obtained from healthy adults (n = 696; age range, 18-84 years) stratified by gender and ethnicity. Cardiac troponin I (cTnI) and T (cTnT) and CKMB mass concentrations were measured by eight assays. Reference limits were determined by nonparametric statistical analysis. RESULTS: Two cTnI assays demonstrated at least a 1.2- to 2.5-fold higher 99th percentile for males vs females, with the mean concentrations significantly higher for males (P <0.05). Two cTnI assays also demonstrated a 1.1- to 2.8-fold higher 99th percentile for blacks vs Caucasians, with the mean concentrations significantly higher for blacks (P = 0.05). There was a 13-fold variance between the lowest measured 99th percentile (0.06 microg/L) and the highest (0.8 microg/L). All CKMB assays demonstrated a 1.2- to 2.6-fold higher 99th percentile for males vs females, with mean concentrations significantly higher for males (P <0.0001). Four CKMB assays also showed significantly higher (1.2- to 2.7-fold) mean concentrations for blacks (P <0.02) vs Caucasians. CONCLUSIONS: The heparin-plasma 99th percentile reference limits for cardiac troponin and CKMB mass provide an evidence base in support of the ESC, ACC, and American Heart Association guidelines for detection of myocardial injury. Selective gender and ethnic differences were demonstrated. These data allow clinicians, trialists, and epidemiologists a common point for operational use.     

Diagnostic utility of new immunoassays for the cardiac markers cTnI, myoglobin and CK-MB mass

OBJECTIVES: We investigated the diagnostic value of a new system, the Innotrac Aio! immunoassays for troponin, myoglobin and CK-MB, in 270 samples from patients with ACS, after bypass surgery (CABG) or with stable heart failure in comparison to the respective Roche assays. RESULTS: The values of the cardiac markers assessed by the respective assays correlated (cTnT/cTnI Rho = 0.94, myoglobin Rho = 0.87, CK-MB Rho = 0.84). If values were dichotomised, we found a high concordance of test positive and negative classified patients by troponins with the respective assays. CONCLUSION: There is strong evidence that the Innotrac Aio! system for cTnI measurement can be used reliably.     

Myoglobin,creatine kinase MB isoforms and creatine kinase MB mass in early diagnosis of myocardial infarction in patients with acute chest pain

OBJECTIVES: Measurements of myoglobin and creatine kinase (CK)-MB isoforms have been suggested to be sensitive tests for the early diagnosis of myocardial infarction (MI). We have investigated the utility of myoglobin, creatine kinase (CK)-MB isoforms and creatine kinase MB mass (CK-MBm) in early diagnosis of MI using cardiac troponin T (cTnT) positivity as a reference. DESIGN AND METHODS: The study population comprised 440 patients who had had chest pain for less than 12 h. Patients were divided into cTnT negative (cTnT-) or cTnT positive (cTnT+) patients (concentration of cTnT >0.1 microg/L at two different time points during 72 h). RESULTS: At the time of admission to the emergency department receiver operating characteristics (ROC) curves of CK-MB isoforms and CK-MBm were not better than that of myoglobin. Six hours after admission CK-MB isoforms and CK-MBm provided statistically significantly larger areas under the curve (AUC) than myoglobin (p < 0.01). When ROC curves were related to the onset of chest pain (< 3 h, 3-6 h, and > 6 h) there were no significant differences between the cardiac markers studied. CONCLUSIONS: According to the present findings, CK-MB isoforms or myoglobin offer no advantage over CK-MBm as early markers of myocardial infarction.     

Evaluation of a Bedside Whole-blood Rapid Troponin T Assay in the Emergency Department

Objective : To evaluate the performance of a new bedside whole-blood rapid assay for cardiac troponin T (cTnT) in patients presenting to the ED with symptoms consistent with acute coronary ischemia. Methods : A prospective, observational trial was performed in 8 participating medical centers. Serial blood samples were obtained on presentation to the ED and 3 and 6 hours later. The cTnT whole-blood rapid assays were performed immediately at the site. Treating physicians and patients were blinded to the results of the rapid assays. Serum samples were analyzed at the core laboratory for serum cTnT, creatine kinase (CK)-MB, and myoglobin. The sensitivity of the rapid assay for detecting acute myocardial infarction (AMI) was compared with the sensitivities of serum cTnT, CK-MB, and myoglobin assays. Results : Of 721 patients, 102 were diagnosed as having AMI. The median elapsed time from symptom onset to ED arrival was 3 hours. The sensitivities of the rapid assay for detecting AMI were 19.6%, 59.0%, and 69.7% at 0, 3, and 6 hours, respectively. The sensitivities of the serum cTnT assay (p-values for comparison with the rapid assay for cTnT) were 25.0% (p = 0.18), 69.6% (p = 0.04), and 79.8% (p = 0.02) at 0, 3, and 6 hours, respectively. The CK-MB and myoglobin sensitivities were 21.9%, 64.5%, and 81.0%; and 43.8%, 77.4%, and 71.4%, respectively. There were 7 patients with AMI who had negative rapid assay readings and positive serum cTnT levels; 4 of these patients were enrolled at the same site. Twenty patients not diagnosed as having AMI had at least one positive rapid assay. Fourteen of these 20 patients had a diagnosis of clinically relevant cardiac disease. Conclusions : The sensitivity of this whole-blood rapid cTnT assay for detecting AMI is comparable to that of current serum assays and offers the advantage of providing rapid bedside results. Discrepancies between serum and whole-blood assays for cTnT noted in this study may indicate the need for further education for the test reader prior to patient use.     

Cardiac markers (BNP, NT-pro-BNP, Troponin I, Troponin T, in female amateur runners before and up until three days after a marathon

PURPOSE: Transient cardiac ventricular dysfunction or sudden cardiac deaths have been reported for male athletes participating in marathon racing. Less is known about the myocardial response in females. We examined natriuretic peptides and cardiac troponins in female athletes after a marathon. METHODS: At the 31st real,- Berlin Marathon plasma levels of NT-pro-BNP, BNP, cTnI and cTnT were measured in 15 women (age 35+/-6 years; finishing times between 3:22 h and 5:21 h) at four different time points (before, immediately after, day one and day three). RESULTS: An increase in [NT-pro-BNP] was observed immediately after the marathon (median [NT-pro-BNP] before: 39.6 pg ml(-1), after: 138.6 pg ml(-1), p=0.003) with a further increase on day one. [BNP] did not increase immediately after the marathon but increased on day one (median [BNP] before: 15 pg ml(-1), day one: 27.35 pg ml(-1), p=0.006). On day three, [NT-pro-BNP] and [BNP] returned to initial values. [cTnI] was under the detection limit prior to the marathon in all runners. [cTnT] was under the detection limit before the marathon except in one runner who presented a concentration of 0.03 ng ml(-1). Cardiac troponins (median [cTnl] after: 0.098 ng ml(-1), p=0.028; median [cTnT] after: 0.032 ng ml(-1), p=0.012) increased immediately after the marathon and returned to initial values on day one [cTnT] and three [cTnI]. DISCUSSION: Parameters representing cardiac stress increased in females after a marathon. Different kinetics of natriuretic peptides BNP and NT-pro-BNP post-marathon could be due to their different half-lives and dependence on renal function. The increase of cTnI and cTnT may result from minor myocardial lesions.     

Analytical and diagnostic performance of troponin assays in patients suspicious for acute coronary syndromes

BACKGROUND: The controversy whether there is a clinically significant difference between troponin T (cTnT) and troponin I (cTnI) in regard to predictive value and cardiac specificity is still ongoing. METHODS: We evaluated enzyme-linked immunosorbent assay systems for cTnI and cTnT in patients with acute coronary syndromes and multiple control groups to define threshold values for risk stratification and compare their predictive value. RESULTS: In 312 patients with noncardiac chest pain, cTnI levels were below the detection limit of 0.2 microg/L and cTnT levels were 0.011 [0.010-0. 013] microg/L. In patients with end-stage renal failure (n = 26) and acute (n = 38) or chronic (n = 16) skeletal muscle damage, median concentrations were 0.20 [0.20-0.35], below the detection limit, and 0.20 [0.20-0.25] for cTnI, and 0.04 [0.01-0.10], 0.011 [0.005-0.025], and 0.032 [0.009-0.054] microg/L for cTnT. In patients with acute coronary syndromes (n = 1130), maximized prognostic value for 30-day outcome (death, infarction) was observed at a threshold level of 1.0 microg/L for cTnI (29.0% positive) and at 0.06 microg/L for cTnT (35. 0% positive). Significant differences in the area-under-the-curve values were observed between cTnI and cTnT (0.685 vs. 0.802; p = 0. 005). For both markers, the area-under-the-curve values did not increase with the second (within 24 h after enrollment) or third (48 h) blood draw. CTnI showed a less strong association with 30-day outcome than cTnT. When cTnI was put in a logistic multiple-regression model first, cTnT did add significant information. CONCLUSION: By using the defined threshold values and the employed test systems, single testing for cTnI and cTnT within 12 h after symptom onset was appropriate for risk stratification. Despite the lower cardiac specificity for cTnT, it appears to have a stronger association with the patients' outcome, whereas, as previously shown, the ability to identify patients who benefit from treatment with a GP IIb/IIIa receptor antagonist is similar.     

Measurement of serum myoglobin by a turbidimetric latex agglutination method.

We evaluated an immunoturbidimetric quantitation for serum myoglobin by the latex agglutination method using an automated biochemical analyzer. This method is rapid, specific, accurate, precise, and has wide dynamic range. The total assay time is 10 min and is performed at 37 degrees C with continuous monitoring at 570 nm. The assay results were compared with radioisotopic immunoassay results and showed a good correlation coefficient, r = 0.99; Y = 0.98 x + 9.3; N = 79. Sera from healthy adults has a myoglobin concentration in the range of 15-80 ng/ml(N = 362). Sex- and age-related differences were observed. The serum myoglobin levels in males and elderly people showed higher concentration than in females and younger people. The peak elevation of serum myoglobin compared with other cardiac markers was observed within 6 hours after onset of chest pain as well as the CK-isoform ratio (MM3/MM1). All of the serum from 21 patients with definite acute myocardial infarction showed increased serum myoglobin levels (100-1200 ng/ml) upon admission and within 6 hours. The results suggest that assays for serum myoglobin levels are helpful in the early diagnosis of acute myocardial necrosis.