Myocardial dysfunction and the subsequent development of symptoms and signs of heart failure, which has been usually referred as cardiotoxicity, is one of the problems in cancer treatment therapies, that has raised highest concerns. Despite the different ways in which different drugs may cause myocardial damage, anthracyclines are drugs applied to most solid tumors and to patients with oncohematological pathologies, where the risk of developing heart failure can be as high as 48%.
Most of the already used therapies are combined and/or sequential, implying the risk of exposure to many drugs that can induce the development of heart failure during the evolution of the treatment. As an example, this applies to patients treated with monoclonal antibodies, mainly trastuzumab (widely used in approximately 25% of breast cancer cases), or in the case of alkylating agents used in patients with non-Hodgkin lymphoma or in the pre-transplant of bonemarrow(especiallycyclophosphamide)[1-3]. The development of adverse cardiovascular effects may, in some cases, have an impact at the psychological level (depression), leading to another negative effect: the interruption of cancer treatment [4-7]. The importance of research on variables that can predict or detect subclinical cases of heart failure has led to the rise of troponin I as predictor of cardiotoxicity in treatments using anthracyclines, trastuzumab and a combination of these two [8-10]. Additionally, echocardiograms (a widely available method of diagnostics), also allows the early detection of ventricular function deterioration. In turn, this leads to the use of cardioprotective drugs, of easy and frequent use, having the possibility to reduce the adverse effects, helping to avoid the interruption of cancer treatment. These drugs are the betablockers and inhibitors of angiotensin converting enzyme [11-13].
 

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