Treatment Of Cardiovascular Toxicity Research Articles

Advances in immune checkpoint inhibitors induced-cardiotoxicity.

Immune checkpoint inhibitors (ICIs) are approved as the first-line drug for treating many cancers and has shown significant survival benefits; however, it also causes immune-related adverse events (irAEs) while activating the immune system, involving multiple organs. Among them, cardiovascular immune-related adverse events (CV-irAE) are rare, but common causes of death in ICIs treated cancer patients, which manifest as myocardial, pericardial, vascular and other cardiovascular toxicities. Therefore, it is important that irAEs, especially CV-irAE should be carefully recognized and monitored during the whole ICIs treatment because early detection and treatment of CV-irAE can significantly reduce the mortality of such patients. Consequently, it is urgent to fully understand the mechanism and management strategies of CV-irAE. The effects of ICIs are multifaceted and the exact mechanism of CV-irAE is still elusive. Generally, T cells identify tumor cell antigens as well as antigen in cardiomyocytes that are the same as or homologous to those on tumor cells, thus causing myocardial damage. In addition, ICIs promote formation of cardiac troponin I (cTnI) that induces cardiac dysfunction and myocardial dilatation; moreover, ICIs also increase the production of cytokines, which promote infiltration of inflammation-linked molecules into off-target tissues. Currently, the management and treatment of cardiovascular toxicity are largely dependent on glucocorticoids, more strategies for prevention and treatment of CV-irAE, such as predictive markers are being explored. This review discusses risk factors, potential pathophysiological mechanisms, clinical manifestations, and management and treatment of CV-irAE, guiding the development of more effective prevention, treatment and management strategies in the future.

Arterial hypertension and anticancer drug therapy: pathophysiological relationships and clinical significance

Arterial hypertension (AH) is one of the most common cardiovascular complications of anticancer drug therapy. In this review article, we consider the main groups of anticancer drugs that may cause the development of iatrogenic AH, the pathophysiological mechanisms of increased blood pressure, as well as the clinical significance of AH developed during treatment with cytostatics and targeted drugs in the practice of an oncologist and a cardiologist. It was found that AH is frequently associated with the use of angiogenesis inhibitors, as well as alkylating cytostatics, antimetabolites, taxanes, and proteasome inhibitors. In addition, erythropoietins, glucocorticosteroids, and non-steroidal anti-inflammatory drugs used as part of supportive therapy may contribute to an increase in blood pressure. Management of hypertension in cancer patients is an important part of antitumor treatment therapy whose implementation contributes to improving their quality of life. Research into various clinical and pathophysiological aspects of cardiovascular disorders in cancer patients is becoming increasingly relevant, which is indicated by the rapid development of cardio-oncology, a new interdisciplinary field of knowledge aimed at developing practical recommendations for the prevention, diagnosis, and treatment of cardiovascular toxicity caused by anticancer therapy.