In breast cancer patients undergoing treatment, 19% experienced therapy-induced left ventricular systolic dysfunction, associated with older age and higher levels of hs-cTnT.
Can a prediction model using hs-cTnT and echocardiographic parameters predict early therapy-induced left ventricular systolic dysfunction in breast cancer patients receiving anthracyclines and trastuzumab?
In breast cancer patients receiving anthracyclines and trastuzumab, older age, pre-existing diastolic dysfunction, and elevated hs-cTnT are significant predictors of early therapy-induced left ventricular systolic dysfunction.
Absolute Event Rate: 0% vs 0%
Abstract Background Subclinical left ventricular dysfunction can be detected early during breast cancer therapy by global longitudinal strain (GLS). The aim of this study was to establish a prediction model to evaluate the risk for early therapy-induced left ventricular systolic dysfunction (LVSD) in patients with breast cancer when the GLS is not available. Methods A total of 75 patients who received anthracyclines and trastuzumab therapy were included in the study and underwent echocardiography baseline and at least 3 time points during the course of therapy. Blood tests were performed too, before and after therapy, including high-sensitive cardiac troponin T (hs-cTnT) and metabolic indicators such as low-density lipoprotein cholesterol, fasting glucose, triglycerides and uric acid. All patients were evaluated for nonmodifiable and modifiable risc factors and concomitant diseases. Left atrial volume index (LAVI), left ventricular mass index (LVMI), left ventricular dimensions and volume inexes (LVEDV/BSA and LVESV/BSA) and LVEF were estimated by echocardiography. Tissue Doppler velocities were measured from medial and lateral annulus, including E/e index. Unidimensional longitudinal strain (ULS) was used as a simple echocardiographic parameter for the assessment of myocardial structural deformation. Results The prevalence of LVSD, defined as asymptomatic or symptomatic reduction in left ventriculae ejection fraction, was of 19%. LVSD patients were older (65 ± 6.0 vs 55 ± 7.7, p= 0.0001), with greater frequency of left ventricular diatolic dysfunction in initial echocardiographic examination: LAVI (36.4 ±16.7 vs 25.8 ± 8.8, p=0.002) and E/e (14.0± 4.0 vs 10.1 ± 3.2, p=0.001) and with poorer left ventriular longitudinal function compared with patients who did not experience LVSD, ULS was significantly lower in LVSD patients (-14.9 ± 2.2 vs -17.7 ± 1.8, p=0.0001). Values of hs-cTnT (5.8±1.27vs4.2±1.48, p=0.001) and uric acid (399±118.8.9 vs 294±20.0, p=0.041) were significantly higher in LVSD group. LVSD associated with older age (1.470 (1.100-1.965), p = 0.009) and with higher hs-cTnT (2.247 (1.115-4.384, p=0.018). Cut-off value of hs-cTnT to predict od LVSD was 5.1, determined at a sensitivity of 83% and specificity of 71% (AUC 0.787, p=0.002). Risk for LVSD was higher in women over 60 (AUC 0.841, p=0.0002), determined at a sensitivity and specificity of 75%. Conclusion Unfortunately, the prevalence of LVSD in breast cancer patients during treatment was high, 19%. Cancer treatment related LVSD has been associated with older age, pre-existing lef ventricular diastolic dysfuncion and also with pre-existing myocardial structural deformation. hs-cTnT can be useful in detection of patients at risk for LVSD in order to prevent eventual future adverse cardiovascular events, especially those over 60.
Stevanovic et al. (Thu,) reported a other. In breast cancer patients undergoing treatment, 19% experienced therapy-induced left ventricular systolic dysfunction, associated with older age and higher levels of hs-cTnT.