Over the past decades, chemotherapy has significantly increased the overall prognosis and survival of several patients diagnosed with cancer. However, the usefulness of some chemotherapeutic agents has been hindered by a collateral dose-dependent cardiotoxicity. To date, although extensive efforts have been directed to the early detection of subclinical toxicity in patients treated with these drugs, it remains unclear which approach would be best in order to prevent chemotherapy-induced cardiotoxicity (CIC). For many years, conventional echocardiography has been among preferred noninvasive imaging modality to monitor left ventricular ejection fraction (LVEF) in patients undergoing chemotherapy. Unfortunately, a significant reduction in LVEF is not recognized early on after chemotherapy-induced myocardial damage. Moreover, delayed recognition has been associated with poor recovery potential and poor clinical outcome. Thus, there is a critical need to identify early, reliable parameters of subclinical injury. Myocardial deformation imaging, also known as strain imaging echocardiography (SIE), is becoming readily available for advanced routine echocardiography and has shown value in detecting subclinical ventricular dysfunction in several clinical scenarios. Abnormalities in systolic deformation parameters have been identified as early manifestation but left ventricular diastolic properties remain less well defined. We hypothesize that onset as well as progression of cardiotoxicity not only should disturb deformation curves of myocardial contraction, but also relaxation. Hence, SIE may detect subtle myocardial changes in diastole that could be of potential benefit in the early prediction of CIC. If this premise is proven correct, the use of a standardized advanced echocardiographic imaging protocol using both, systolic and diastolic strain imaging, will prove to be a powerful noninvasive tool as baseline and follow-up of these patients. Furthermore, it will foster the developing of more effective screening strategies in at risk cancer survivor populations, or identify the best time to start cardioprotective therapy to prevent CIC. Also, this experience might be extrapolated to other non-oncologic patient population in need of a surveillance tool to early recognize cardiac injury secondary to the use of cardiotoxic medications.