Abstract
In the era of improved cancer outcomes, increased therapeutic options, and growing population of cancer survivors, the acute and long-term adverse effects of cancer therapies are becoming increasingly relevant. Improved tools for cardiovascular (CV) risk prediction may allow physicians to better tailor cancer therapy, identify patients who would benefit from close CV monitoring and consider CV protective approaches prior, during and after cancer treatment. Ongoing major advances in oncology therapeutics, with vast repertoire of new molecules targeting key tumor pathways, have brought unprecedented opportunities to combat cancer and occasionally manifested unexpected CV side effects pointing to important, unexplored interactions between new therapeutics and CV homeostasis. Probably most widely known example is the one of trastuzumab, HER2targeted monoclonal antibody used in the treatment of HER2-positive breast cancer, that can cause left ventricular (LV) dysfunction and heart failure in susceptible individuals [1,2]. Major strides have been made to limit CV toxicity of trastuzumab and related new HER2-targeted agents, pertuzumab and ado-trastuzumab emtansine, including mandatory assessment of cardiac function prior and during treatment with HER2-targeted agents, and holding or stopping therapy in patients with abnormal LV systolic function [3–5]. These clinical practice recommendations evolved from clinical trial experiences and represent an important step forward in recognizing and limiting cardiotoxicity or HER2-targeted therapies, nevertheless a number of questions continue to challenge daily clinical practice. They include the concerns that stopping and holding HER2-therapy in patients whose cardiac function is only mildly reduced may compromise their cancer outcomes (to improve what may be a low cardiac risk). On the other side of the coin are the patients with normal cardiac function at baseline who continue to experience cardiotoxicity and OpiniOn Special Focus Issue: Cardio-oncology
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