Anti-Cancer Drug-Induced Cardiotoxicity

Cardiovascular disease (CVD) remains the leading cause of death worldwide. An emerging contributory factor to the global burden of CVD is the impact that certain chronic medications may have on cardiovascular function. Indeed, the possibility of non-specific or off-target effects of non-cardiac drugs on the heart is an ongoing concern for safety pharmacology in the pharmaceutical industry with enormous long term impact both socially and economically. Anti-cancer drugs in particular have received widespread attention due to reports of off-target detrimental effects on cardiovascular function. Although many new anti-cancer drugs have significantly improved survival rates from cancer, there is evidence for a growing number of patients presenting with cardiovascular complications as a consequence of their therapeutic intervention. Depending on the anti-cancer agent in question, these effects can range from pericardial complication, thromboembolic disease and hypertension to arrhythmias and left ventricular failure and can occur in patients who have no prior history of CVD. The situation is made even more complex by the fact that the anti-cancer drug effect can be influenced by patient age, underlying co-morbidities as well as whether the patient has also received radiotherapy. This phenomenon of 'anti-cancer drug cardiotoxicity' has given birth to a new clinical discipline called cardio-oncology. This interdisciplinary approach to patient care combines cardiology and oncology and has resulted in more effective patient management going forward. That said, anti-cancer drug cardiotoxicity is a growing global challenge. The number of new anti-cancer drugs continues to increase and we still do not fully understand why or how many of these drugs will be cardiotoxic. The true extent of the overall risk to cancer patients is unknown and the underlying mechanism(s) responsible for the cardiotoxic effects remain to be fully identified. Strategies to prevent or mitigate cardiotoxicity resulting from cancer treatment are urgently needed to ensure the best cancer care possible. Future management of anticancer drug-related cardiotoxicity will rely on improved understanding of the cellular effects of these agents in the heart and vasculature. This, combined with improved biomarker identification and cardiac imaging for monitoring purposes, will be crucial in an overarching strategy to design effective cardioprotective agents that can reduce or reverse the cardiotoxic effects