Myocardial Protection During Cardiotoxic Chemotherapy.

O ver the last 20 years, the development of effective screening and treatment strategies has resulted in a 20% decline in cancer mortality, translating to an absolute increase of almost 1 400 000 cancer survivors in the United States. 1 Currently, it is estimated that 60% of adults newly diagnosed with cancer will be alive 5 years later. The price to be paid for such success has varied from overt treatment toxicities (eg, bone marrow suppression) to toxicities that became obvious only with the passage of time (eg, secondary malignancies). Although cardiac complications of chemotherapy first rose to the forefront with the recognition in the 1970s of overt clinical heart failure (HF) in patients receiving anthracycline-based chemotherapy, it took several decades for the full scope of toxicity to be truly appreciated. As cancer therapeutics have advanced, 3 points have become clear. First, cardiovascular toxicity is a widespread problem across many classes of cancer therapies. Second, it is critical to learn how to best monitor for, prevent, and treat cardiac complications of cancer therapy both to lower morbidity and mortality from the cardiac toxicity itself and to allow patients to receive their potentially life-saving/life-prolonging/palliative chemotherapy. This represents the concept of cardioprotection. Third, this is a field that at its very core is multidisciplinary, requiring the close collaboration of cardiologists and oncologists. The purpose of this article is to review the state-of-the-art evidence and to recommended practices to best protect patients against and treat patients with cardiac complications of chemotherapy with a focus on myo-cardial toxicity. A full review of the mechanisms of toxicity is beyond the scope of this article; however, a working understanding of the basic mechanisms yields important information about potential treatment strategies and the potential for myocardial recovery. Many antineoplastic drugs with broadly different mechanisms of action have cardiotoxic effects. These effects are often divided into 2 categories, depending on the revers-ibility of myocardial damage 2,3 : Type I agents (eg, anthracy-clines) cause direct cell death, leading to irreversible damage, and type II agents (eg, trastuzumab) cause ventricular dysfunc-tion, which is reversible once the drug is withdrawn. Although the mechanisms and outcomes of cardiac toxicity from these medication classes clearly differ, caution must be used with these terms, which carry the implication that type II toxicity is regularly reversible and without long-term sequelae, a finding not consistently supported by clinical trial evidence. 4 For many years, anthracycline cardiotoxicity …