Cardio-oncology: Understanding the different mechanisms of cardiovascular toxicity

Due to the success of finding treatments for various types of cancer, overall cancer survival has increased substantially in recent decades. Ironically, the clinical success of antineoplastic therapy is attenuated by the comorbidity of cardiovascular diseases, which appear to be the main complications of intense cancer treatment and are the second main cause of long-term morbidity and mortality among cancer survivors. Cardio-oncology is the new area of cardiology that aims to treat the specific cardiologic status of cancer patients. Most antineoplastic therapies are associated with some degree of cardiovascular toxicity, ranging from asymptomatic and transient cardiac events to clinically significant and long-lasting events. Antineoplastic agents are responsible for different cardiovascular injuries, which can be reversible or permanent. All anatomical structures of the heart can, however, be affected by transthoracic radiotherapy. Cardiotoxicity mechanisms are recognized according to the presence or absence of structural anomalies and their reversibility, being classified into Type I and Type II, aiming to distinguish the drugs that induce irreversible damage (Type I) from the drugs that predominantly induce reversible left ventricular dysfunction (Type II). While anthracyclines and anti-HER2 agents form the two major groups of cardiotoxic drugs, other antineoplastic agents, such as other monoclonal antibodies, certain tyrosine kinase inhibitors and antiangiogenic drugs can also be cardiotoxic via different mechanisms. This article presents the different pathophysiological mechanisms of cardiovascular toxicity according to the treatment regimen used.