Purpose. To detect LV mechanical dispersion(MD) and to test it as marker of early damage and arrhythmogenic risk in patients with breast cancer who underwent chemotherapy.Methods. 58 female patients (age 56±11 years) before the beginning of chemotherapy were enrolled. The study protocol included clinical examination, ECG with QTc calculation, lab test (BNP and troponin I) and echocardiography with TDI and speckle tracking analysis (STI), that were performed before the beginning of the chemotherapy (basal) and after 3, 6 and 12 months. LV MD was assessed as the standard deviation of the time (in msec) between aortic valve opening (AVO) and systolic strain peak (time to peak), around aortic valve closure (AVC), for each of the 17 LV myocardial segments. Results: Statistically significant data are summarized in the Table. There were not significant differences about: diastolic blood pressure, troponin I, QTc, LV end­diastolic volume, E/A ratio, deceleration time, sPAP and TAPSE. Nobody experienced major events whereas 10 reported minor events (dispnoea, chest pain, palpitations, syncope). Only one patient had ventricular arrhythmias (ventricular extrasystoles and one episode of not sustained ventricular tachycardia). In this patient, MD was increased at 3 months FU (from 39 to 44 msec) and decreased after 12 months (28 msec). Conclusions: MD increases during chemotherapy with anthracyclines and could be a marker of arrhythmogenic risk, as already reported in other patients groups. MD increase could be due to the cardiomyocites necrosis induced by anthracyclines, repair processes and collagen fiber deposition. Further studies are needed with bigger sample size to confirm our data.

Mechanical dispersion and cardiotoxicity in patients who underwent chemotherapy for breast cancer: an echocardiographic study

C Zito;L Longobardo;R Manganaro;C Casile;A Bava;R Costantino;A Bracco;MC Todaro;F Ranieri;C D'angelo;G Altavilla;S Carerj
2019-01-01

Abstract

Purpose. To detect LV mechanical dispersion(MD) and to test it as marker of early damage and arrhythmogenic risk in patients with breast cancer who underwent chemotherapy.Methods. 58 female patients (age 56±11 years) before the beginning of chemotherapy were enrolled. The study protocol included clinical examination, ECG with QTc calculation, lab test (BNP and troponin I) and echocardiography with TDI and speckle tracking analysis (STI), that were performed before the beginning of the chemotherapy (basal) and after 3, 6 and 12 months. LV MD was assessed as the standard deviation of the time (in msec) between aortic valve opening (AVO) and systolic strain peak (time to peak), around aortic valve closure (AVC), for each of the 17 LV myocardial segments. Results: Statistically significant data are summarized in the Table. There were not significant differences about: diastolic blood pressure, troponin I, QTc, LV end­diastolic volume, E/A ratio, deceleration time, sPAP and TAPSE. Nobody experienced major events whereas 10 reported minor events (dispnoea, chest pain, palpitations, syncope). Only one patient had ventricular arrhythmias (ventricular extrasystoles and one episode of not sustained ventricular tachycardia). In this patient, MD was increased at 3 months FU (from 39 to 44 msec) and decreased after 12 months (28 msec). Conclusions: MD increases during chemotherapy with anthracyclines and could be a marker of arrhythmogenic risk, as already reported in other patients groups. MD increase could be due to the cardiomyocites necrosis induced by anthracyclines, repair processes and collagen fiber deposition. Further studies are needed with bigger sample size to confirm our data.
2019
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3178497
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