Serial Measurements Of Cardiac Troponin Research Articles

The importance of serial cardiac troponin measurement for evaluating the response to immunosuppressive therapy for myocarditis

A 71-year-old woman was admitted to our department because of acute myocarditis. She was ameliorated with conventional heart failure treatment, however she developed left ventricular dilatation and cardiac troponin T (cTnT) was elevated again to >1.0 ng/ml 6 month after the first admission. She was re-admitted because of recurrent decompensated heart failure in spite of conventional treatment. Right ventricular endomyocardial biopsy revealed active myocarditis. Immunosuppressive therapy with prednisolone and azathioprine improved her symptoms and left ventricular function accompanied by a striking decrease of cTnT levels. The decreased cTnT level indicated an effective response to immunosuppression early after the beginning of treatment. These findings suggested that it is possible to evaluate the response to immunosuppressive therapy by serial measurement of cardiac troponin.

Whole-Blood Hypercholinemia and Coronary Instability and Thrombosis

Whole-blood choline (WBCHO) and plasma choline (PLCHO) have been reported to be predictive for cardiac events in patients with suspected acute coronary syndromes (1)(2). The differential information of whole-blood vs plasma choline offers insights into the biochemistry and pathophysiology of acute coronary syndromes. A previous study has shown that mean (SD) WBCHO concentrations are significantly increased in patients with non-ST-elevation myocardial infarction \[31.1 (18.8) μmol/L] and high-risk unstable angina [47.4 (22.8) μmol/L] compared with patients with noncardiac chest pain [19.4 (6.8) μmol/L\] (1) or healthy volunteers [15.8 (9.5) μmol/L]. For interpretation of WBCHO, a cutoff of 28.2 μmol/L has been proposed (1), which also represents the 90th percentile of a reference population. For PLCHO, the optimum cutoff has not been determined, and 25 μmol/L (99th percentile of a reference population) and lower cutoffs (18.5 μmol/L) have been used for risk stratification. We have selected 3 cases with the constellation of increased WBCHO in combination with low PLCHO to discuss potential pathophysiologic implications. All choline analyses were performed with HPLC–mass spectrometry (1), and choline concentrations were not available for clinical decision-making. ### Case 1. A 68-year-old man presented to the emergency department with acute chest pain for 1.5 h. He had a history of stable angina pectoris, arterial hypertension, and type II diabetes mellitus treated with glibenclamide. The patient had no history of bleeding or thrombosis, and results of routine blood cell analyses, including platelet count, mean platelet volume, coagulation indices, and renal function, as well as the physical examination were normal. Serial electrocardiographic (ECG) recordings demonstrated dynamic anterior ST changes and T-wave inversions, a left anterior hemiblock, and frequent ventricular premature beats. Serial measurements of cardiac troponin I (cTnI; Stratus CS) and T (cTnT; Elecsys 2010) were positive (0.99, 1.28, and 2.65 μg/L for cTnI and 0.23, 0.30 and 0.69 μg/L …

Single and serial measurements of cardiac troponin I in asymptomatic patients on chronic hemodialysis.

Coronary artery disease is the major cause of death in patients with end-stage renal failure on dialysis. This study aimed to assess the predictive value of a single cardiac troponin I (cTnI), and also the kinetics of serial values. Since cTnI is a potential biomarker of cardiac outcome, the present study examined single cTnI measurements (n = 88 patients) and its predictive value for future cardiac events, and a kinetic substudy of serial weekly cTnI measured for 8 weeks (n = 57) in a group of patients on hemodialysis. Single cTnI measurements: 9 patients (10.2%) had a detectable cTnI at baseline and 79 patients (89.8%) had a negative baseline cTnI. There were no significant differences in age, sex, history of ischemic heart disease, diabetes, smoking or dyslipidemia between patients with detectable and negative cTnI. At the end of 9 months, the rate of combined primary endpoints, which included myocardial infarction, cardiac death and cardiac revascularization, was significantly higher in the patients with a detectable baseline cTnI (55.6%), compared to patients with a negative cTnI (6.3%) (p = 0.0007). Serial weekly cTnI measurements: significant fluctuations in cTnI were noted over time; 27% of patients with an undetectable cTnI measured at baseline had subsequent detectable levels in the serial follow-up. A single detectable cTnI in asymptomatic patients on hemodialysis defines patients at high risk of future cardiac events. However, the incidence of detectable cTnI levels is markedly increased when serial weekly measurements are performed. The clinical significance of detectable serial measurements of cTnI is the focus of ongoing studies.

A randomized trial of aprotinin (Trasylol) on blood loss, blood product requirement, and myocardial injury in total arterial grafting

Background Total arterial grafting is increasingly preferred in coronary artery bypass grafting, but it increases blood loss. Aprotinin (Trasylol; Bayer Corp, Leverkusen, Germany) reduces blood loss in cardiac surgery but has not been subjected to a randomized trial in total arterial grafting. Methods A single-center, randomized, double blind, placebo-controlled trial of aprotinin administration in total arterial grafting was performed. The primary outcome variable was postoperative blood loss, and the secondary outcome variable was the number of units of donor blood or coagulant products transfused. The incidence of myocardial injury was determined from serial measurements of cardiac troponin T and creatine kinase-MB and renal injury from serum creatinine. Results The placebo group (n = 34) and aprotinin group (n = 36) were similar with respect to all preoperative and intraoperative comparisons. One patient in each group underwent reexploration for bleeding. Open-label aprotinin was administered to 9 patients in the placebo group (26%) and to 2 patients in the aprotinin group (6%). There was a highly significant reduction in the median (interquartile range) blood loss in the aprotinin group compared with the placebo group (785 mL [590-1025 mL] vs 1525 mL [1175-1920 mL], respectively). Similarly, the aprotinin group demonstrated a marked reduction in the need for blood transfusion (77% vs 39%; P = .0001), the mean number of transfused blood units (2.6 vs 0.8, P < .001), and the number of patients requiring coagulant products (24% vs 3%; P < .001). There was no difference in myocardial injury in the 2 groups. Four patients in the aprotinin group had persistently elevated creatinine levels in the postoperative period (3 of whom had elevated preoperative creatinine levels and perioperative complications). Conclusions Aprotinin significantly reduces blood loss and the need for blood component transfusion in patients undergoing total arterial grafting without increasing the risk of myocardial injury. Aprotinin should be considered routinely in patients undergoing total arterial grafting but cautiously in patients with an elevated preoperative creatinine level.

Clinically Recognized Cardiac Dysfunction: An Independent Determinant of Mortality Among Critically III Patients: Is There a Role for Serial Measurement of Cardiac Troponin I?

To determine the relative importance of clinically recognized cardiac dysfunction and unrecognized cardiac injury to hospital mortality. Prospective, blinded, single-center study. Medical ICU of Barnes-Jewish Hospital, St. Louis, a university-affiliated teaching hospital. Two hundred sixty adult patients requiring admission to the medical ICU. Daily blood collection. The presence of cardiac dysfunction (myocardial infarction, unstable angina, cardiac arrest, or congestive heart failure) as determined by the physicians responsible for the care of the patient. Daily measurement of levels of cardiac troponin I, a sensitive, highly specific, and long-lived marker of myocardial injury. Fifty-five (21.2%) patients had clinical evidence of cardiac dysfunction, among whom 22 (40%) had an elevated level of cardiac troponin I. A total of 41 (15.8%) patients had evidence of acute myocardial injury based on elevated levels of cardiac troponin I. Patients with clinically recognized cardiac dysfunction had a significantly greater hospital mortality rate compared to patients without clinically recognized cardiac dysfunction (45.5% vs 10.2%; p < 0.001). Similarly, patients with elevated blood levels of cardiac troponin I had a greater hospital mortality rate compared to patients without elevated blood levels of cardiac troponin I (26.8% vs 16.0%; p = 0.095). Multiple logistic-regression analysis controlling for potential confounding variables demonstrated that the presence of clinically recognized cardiac dysfunction was independently associated with hospital mortality (adjusted odds ratio = 3.0; 95% confidence interval = 1.9 to 4.8; p = 0.016). However, having an elevated blood level of cardiac troponin I was not found to be an independent determinant of hospital mortality. Among critically ill medical patients, clinically recognized cardiac dysfunction is an independent determinant of hospital mortality. The identification of unrecognized cardiac injury, using serial measurements of cardiac troponin I, did not independently contribute to the prediction of hospital mortality.

Early assessment of reperfusion therapy using cardiac troponin T

Objectives. The purpose of this study was to investigate the utility of cardiac troponin T for early assessment of reperfusion therapy.Background. Several biochemical markers are used for early poninvasive detection of reperfusion during intravenous thrombolytic therapy. However, cardiac troponin T, a new myocardialspecific marker, has not been used previously for this purpose.Methods. We measured troponin T and creatine kinase, MB isoenzyme (CK-MB) levels in 38 patients with acute myocardial infarction whose infant-related artery was totally occluded before reperfusion therapy. Subjects comprised 14 patients with successful angioplasty (group 1), 12 patients with successful thrombolytic therapy (group 2) and 12 patients with unsuccessful attempted reperfusion (group 3). Blood samples were taken every 15 min, and coronary angiography was performed every 5 to 8 rain until 60 min after reperfusion (groups land 2) or after the initiation of treatment (group 3). We calculated the increase in troponin T (Δtroponin T) and CK-MB (ΔCK-MB) 60 min after treatment was initiated and 60 min after reperfusion in groups 1 and 2.Results. Mean (±SD) Δtroponin T and ΔCK-MB levels were 9.35 ± 7.83 ng/ml and 125 ± 83 mU/ml in group 1 and 3.23 ± 3.08 ng/ml and 130 ± 137 mU/ml in group 2, respectively, 60 min after treatment and were 10.1 ± 8.35 ng/ml and 131 ± 84 mU/ml in group 1 and 6.84 ±8.30 ng/ml and 158 ± 146 mU/ml in group 2, respectively, 69 min after reperfusion. These values were significantly higher than those 60 min after treatment in group 3: 0.16 ± 0.19 ng/ml and 10 ± 9 mU/ml, respectively. The predictive accuracy for detecting reperfusion using a threshold value of 0.50 ng/ml of Δtropoata T and 25 mU/ml of ΔCK-MB was 100% in group 1 and 92% in (group 2 60 min after treatment, respectively. There was significant correlation between Δtroponin T and ΔCK-MB.Conclusions. Serial measurements of cardiac troponin T as wen as of CK-MB are useful for early assessment of reperfusion therapy.