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.
Highlights
The number of cancer survivors has increased dramatically over the past few decades with the advancement of new cancer treatment regimes
Any patient who was in a critical state or end stage of cancer and who were unable to give informed consent; patients who received chemotherapy that does not belong to the anthracycline family; patients who were diagnosed with any structural heart disease, hypertension, or cardiomyopathy; and patients who developed any acute noncardiac complications before the recruitment to the study were excluded from the study
Cardiotoxicity evident in anthracycline chemotherapy is observed as acute cardiotoxicity which usually occurs during or immediately after infusion of anthracyclines, early-onset chronic progressive cardiotoxicity which occurs within one year of discontinuation of chemotherapy, and late-onset chronic progressive cardiotoxicity which occurs after one year of exposure [12]
Summary
The number of cancer survivors has increased dramatically over the past few decades with the advancement of new cancer treatment regimes. In the USA, 16.9 million cancer survivors were expected by Jan 2019, and it is projected to be increased to 21.7 million by the year 2029 [1]. They are vulnerable to a plethora of conditions resulting primarily from the effects of chemotherapy, and anthracycline-induced cardiac dysfunction has been recognized as a serious side effect since its introduction in the 1960s [2]. The mechanism of doxorubicin-induced cardiotoxicity is multifactorial, free radical-induced oxidative stress, mitochondrial dysfunction, and calcium overload are considered as major contributory factors [3]
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