Cancer therapy related cardiac dysfunction (CTRCD) in the setting of Anthracycline chemotherapy (AC): Analysis of breast cancer patients utilizing multi-layer two-dimensional speckle tracking echocardiography

Abstract

Objectives To evaluate subclinical dysfunction in breast cancer patients treated with AC and determine the echocardiographic and patient factors associated with such changes. Background Anthracycline chemotherapy (AC) though central to breast cancer therapy, can be limited by chemotherapy related cardiac dysfunction (CTRCD), defined as a reduction in left ventricular (LV) ejection fraction on transthoracic echocardiography (TTE). More recently, TTE derived LV global longitudinal systolic strain (GLS) can identify subclinical cardiac dysfunction prior to development of overt CTRCD. LV GLS changes are used ubiquitously to identify patients at risk for developing potentially irreversible changes in LV ejection fraction. Methods 114 HER2 negative breast cancer patients treated with AC were prospectively recruited. and underwent serial echocardiograms prior to AC, at 3 months and at one year. Clinical parameters, LVEF and LVGLS were evaluated at the 3 time points. CTRCD was defined as an asymptomatic reduction in LVEF of 10% or symptomatic drop of 5% to LVEF <53%, while subclinical LV dysfunction was defined as a reduction of ≥10% in GLS compared to baseline. Results No participant demonstrated CTRCD, by reduction in LVEF. 43 patients (38%) demonstrated a ≥10% greater reduction in GLS at 12 months. In this group 20/43 (47%) had a reduced absolute GLS to <17%. This ‘at risk group’ were older, had hypertension, increased LV mass, lower e’ velocity and baseline GLS. Patients with baseline LV GLS of ≥20.5% had a sensitivity of 75% and specificity of 87% to maintain an absolute LV GLS ≥16%, despite a ≥10% reduction from baseline GLS. Conclusions This cohort of HER2 negative breast cancer patients, followed with serial echocardiography for one year following AC therapy. These findings may help to re-stratify patients with a high baseline GLS into a lower risk group, which may in turn enable fidelity to cardioprotective treatment and allay patient and clinician concerns despite transient GLS decrements during therapies.