Anthracycline-Induced Cardiotoxicity in Breast Cancer Patients from Southern Sri Lanka: An Echocardiographic Analysis

Abstract

Anthracycline-induced cardiotoxicity has never been investigated in Sri Lanka. Therefore, this study was conducted to determine the prevalence of anthracycline-induced cardiotoxicity in breast cancer patients using echocardiographic findings. A prospective cohort study was performed. All newly diagnosed breast cancer patients who were administered with anthracycline and cyclophosphamide (AC schedule) for the first time were enrolled in the study. In the hospital setting, anthracycline is administered only as a combination therapy, and only this combination was selected to limit the effect of other cardiotoxic chemotherapy agents. Records of echocardiography were obtained: one day before anthracycline chemotherapy (baseline), one day after the first chemotherapy dose, one day after the last chemotherapy dose, and six months after the completion of anthracycline chemotherapy. Following parameters were recorded from the echocardiography results: ejection fraction (EF, %), fractioning shortening (FS, %), posterior wall thickness, left ventricle (PWT, mm), the thickness of interventricular septum (IVS, mm), left ventricular end-diastolic diameter (LVEDD, mm), and left ventricular end-systolic diameter (LVESD, mm). Statistical analysis of the echocardiography results was performed using ANOVA at four stages. A p value <0.05 was considered significant. Subclinical cardiac dysfunction was defined as a fall of EF >10% during the follow-up echocardiography. There was no significant change ( p > 0.05 ) between the baseline echocardiographic parameters and one day after the 1st anthracycline dose. However, significant differences ( p < 0.05 ) were observed between the baseline echocardiographic parameters and one day after the last anthracycline dose and six months after the completion of anthracycline therapy with a gradual and progressive deterioration in functional parameters including EF, FS, PWT, and IVS over time. There were 65 patients out of 196 (33.16%) who developed subclinical cardiac dysfunction six months after the completion of anthracycline chemotherapy. The prevalence of subclinical anthracycline-induced cardiotoxicity was relatively higher in these patients. An equation was also developed based on left ventricular ejection fraction (LVEF) to predict the anthracycline-induced cardiotoxicity of a patient six months after the completion of anthracycline chemotherapy. We believe that this will help in the monitoring of patients who undergo anthracycline therapy for cardiotoxicity. It is recommended to carry out a long-term follow-up to detect early-onset chronic progressive cardiotoxicity in all patients who were treated with anthracycline therapy.

Prevalence of cancer therapy cardiotoxicity as assessed by imaging procedures: A scoping review

“…Table 1 showed the demographic data and clinical characteristics of patients 16–59 . Cancer type, treatment, and imaging technique for each study are reported in Table 2 16–59 . Patient population ranged from 28 to 2625 subjects.…”

Anthracycline-Induced Cardiotoxicity in Breast Cancer Patients: A Five-Year Retrospective Study in 10 Centers

“…This is lower compared to the results from other studies done in Asia where the incidence ranged from 25% to 33%. This may in part be due to the use of varying definitions of AIC [ 13 , 15 , 16 ]. In this study, the investigators strictly followed the definition of the American and European Society of Echocardiography Expert Consensus of Anthracycline-induced cardiotoxicity, which is a reduction of LVEF by more than 10%, to a value below 53% [ 10 ].…”

“…A minimum of 340 breast cancer patients were required for this study based on a level of significance of 5%, assuming that 33.16% [ 13 ] of patients will develop cardiotoxicity, with the desired width of CI (precision) of 10% [ 14 ] as noted from the reference article by Sandamali et al, 2020 [ 13 ].…”

Anticancer Drug-Induced Cardiotoxicity: Insights and Pharmacogenetics

“…CP exposure in the myocardial cell is responsible for an increase in the formation of NO due to the activity of eNOS and iNOS. On myocardial cells, eNOS and iNOS have been shown to have both protective and toxic effects [ 31 , 32 ]. The protective effect is due to the formation of NO, but generated NO when reacting with oxygen free radicals generates peroxynitrite (ONOO − ), which is responsible for the toxic effects on the myocardial cell.…”