The use of trastuzumab, a humanized monoclonal antibody against the extracellular domain of human epidermal growth factor receptor 2 (ERBB2; formerly HER2), is complicated by its association with an increased risk of cardiotoxic effects.1 These toxic effects may be explained by the functional presence of ERBB2 in cardiomyocytes.2 ERBB2 signaling is important to cardiomyocyte survival because its binding with neuregulin-1 initiates cell survival pathways maintaining cardiac function.3 Trastuzumab causes congestive heart failure by increasing systemic vascular resistance and myocardial workload while reducing microvascular coronary blood flow.4 A recently published population-based study of more than 2000 patients receiving adjuvant-based chemotherapy revealed that a large proportion of patients were receiving suboptimal cardiac monitoring.5 Thus, efforts to improve the efficiency of cardiac monitoring are needed, especially in the context of trastuzumab delivery.