Mechanisms and biomarkers to detect chemotherapy-induced cardiotoxicity

A cardiotoxicity is a considerable event for cardiologists and oncologists during and after chemotherapy. The use of certain chemotherapy agents such as trastuzumab, programmed death-1 inhibitors, and Doxorubicin increased in cancer therapy; however, these agents associate with an increase in mortality and cardiotoxicity. Detecting cardiotoxicity is based on patient's medical history and physical examination since there is no exact biomarker or polymorphism for its early diagnosis. Therefore, we still need potential biomarkers for cardiotoxicity risk. Treatment of several cancers is manageable while preventing cardiotoxicity, as chemotherapy side effect, is essential since it might be a greater risk than the malignancy if not detected at early stages. Early detection of cardiotoxicity, during and after chemotherapy, is crucial to decrease permanent and devastating cardiac damages. Recently, troponin but also atrial-type and brain-type natriuretic peptides were reported as good diagnostic biomarkers for cardiotoxicity. Micro-RNAs and inflammatory mediators are candidates as prognostic biomarkers. Genetic biomarkers such as C282Y allele of hemochromatosis gene makes the patients more susceptible to cardiotoxicity; therefore, genome studies are valuable in predicting chemotherapy results. In this review, we present the mechanisms of developing chemotherapy-induced cardiotoxicity and biomarkers for its detection in patients. Echocardiographic techniques are very strong techniques which could be used along with biomarkers for more reliable and quicker diagnosis.