Cardiotoxicity of anticancer chemotherapy and possible therapeutic approaches

Nowadays great advances have been achieved in the treatment of cancer patients. New medical technology, new treatment methods are constantly being developed. Increase in 5 year survival rate is being witnessed for most types of cancer. However along with this success, in parallel to it, another problem is observed, which is induced by the cardiotoxicity of chemotherapeutic drugs. Currently the exact mechanisms behind the cardiovascular toxicity associated with the use of the chemotherapeutic drugs are unknown. There are quite a few hypotheses trying to explain this pathological phenomenon. Fundamentally two mechanisms for the development of cardiotoxicity can be distinguished. The first mechanism is due to disruption and modification of the DNA replication and transcription processes. The second mechanism is caused by excessive formation of reactive oxygen species, depletion of the antioxidant system, induction of lipid peroxidation, leading to damage of the sarcolemma and the development of mitochondrial dysfunction, which in turn causes disruption of the oxidative phosphorylation processes. There are a large number of drugs available to prevent cardiotoxicity, but their effects vary and depend on many factors. This article attempts to summarize the pathophysiological mechanisms of cardiotoxicity associated with the use of chemotherapeutic drugs. The mechanisms of anthracycline-induced cardiotoxicity, as well as potential therapeutic strategies for its prevention and treatment, are reviewed in detail. There is a clear connection between the development of theoretical foundations and their practical application. Nowadays the diagnostic methods are being improved, which make it possible to detect cardiotoxicity in the early stages. However, despite the advances in the field of diagnostics, prevention and treatment of cardiotoxicity remain as the “dark matter” of cardio-oncology.