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Accessible online at: www.karger.com/onk Fax +49 761 4 52 07 14 Information@Karger.de www.karger.com liver and renal function during the study. Cardiac evaluation was performed at baseline (before CT), the day after the first CT with anthracyclines (mean cumulative dose 135.8 ± 28.5 mg/m2, median 150), the day after the last CT with anthracyclines (mean cumulative dose 472.1 ± 115.0 mg/m2, median 423), and approximately 6 months after completion of CT. Concentrations of cardiac troponins diagnostic for cardiotoxicity of oncology treatment have not yet been established. In our study, values above the reference range recommended by the manufacturer were considered elevated. The cut-off value for cTnT was 0.01 μg/l (Roche Diagnostics), and for cTnI 0.40 μg/l (Randox Laboratories Ltd.). Echocardiographic evaluation was performed on a Hewlett Packard Image Point machine by an experienced echocardiographer who was blinded to the cardiac troponin data. Parameters of systolic and diastolic left ventricular (LV) function were assessed. Systolic LV dysfunction was defined as LV ejection fraction (LVEF) ≤ 55%. Diastolic LV dysfunction was defined as E/A inversion and a E wave deceleration time above 220 ms on the transmitral Doppler curve (impaired relaxation). Statistical analysis was performed with Statistica for Windows, version 5.0 (StatSoft, Tulsa, OK, USA). Analysis of variance test was used. Correlations were evaluated with normal and Spearman correlation tests. The values are expressed as mean ± standard deviation (SD). Probability values (p) of < 0.01 were considered statistically significant. The results are summarized in table 1. Of the cardiac troponins, only cTnI became positive on the days after the first and last CT with anthracyclines, which was observed in a total of 4 (17.4%) patients. Positivity of cTnI correlated with systolic and diastolic LV dysfunction on echocardiography: r = 0.712; p < 0.00001 and r = 0.591; p < 0.0001, Cardiac toxicity is among the undesirable side effects of oncology treatment. Of the cytostatics, anthracyclines represent the greatest risk for development of cardiotoxicity [1]. Various methods have been recommended for monitoring cardiotoxicity in oncology [2, 3]. Echocardiography and electrocardiography are routinely used, and recently, the applicability of cardiac troponins in the detection of cancer therapy-induced cardiotoxicity has been investigated [4]. In some studies, administration of anthracyclines did not cause any elevation of cardiac troponins [5–7]. In other studies, cardiac troponins became positive after anthracycline treatment, correlated with disease severity, and were suggested as predictors of subsequent major cardiac events during follow-up [8–10]. The results of clinical studies are inconsistent, and cardiac troponins have not been established in clinical practice for monitoring cardiotoxicity in oncology. The aim of our study was to evaluate acute and chronic cardiotoxicity of anthracyclines with cardiac troponins. We used current immunoassays for cardiac troponin T (cTnT; Roche Diagnostics, Mannheim, Germany) and cardiac troponin I (cTnI; Randox Laboratories Ltd., Crumlin, Co. Antrim, UK), and correlated the results with echocardiography findings. A total of 23 patients (mean age 47.0 ± 11.1 years; 14 males, 9 females) with acute leukemia were studied. The patients were treated with 3–6 cycles of conventional chemotherapy (CT) containing anthracyclines at a total cumulative dose of 472.1 ± 115.0 mg/m2; to calculate the total cumulative anthracycline dose, we applied conversion factors derived from the maximum recommended cumulative doses for the individual agents used (idarubicin, daunorubicin, mitoxantrone). Six patients were treated for arterial hypertension; other patients had no history of cardiovascular disease. All patients had normal Cardiac Troponin I Seems to Be Superior to Cardiac Troponin T in the Early Detection of Cardiac Injury Associated with Anthracycline Treatment