How Target Therapy can Induce Cardiotoxicity: The Onco-Cardiologist Point of View
The life expectancy of an oncological patient has been increased significantly decades due to the evolution of cancer therapies. The aim of this paper is to review how these new target molecules, which have a direct impact on the cancer cell as opposed to the classical chemotherapy, known to all of us for a long time. How do they act specifically? What are their cardiotoxic effects at a short and long time period? How can they be monitored?
How can they be prevented and treated? And above all, how can we prevent an oncological patient to become a cardiovascular one later on, due to induced cardiotoxicity caused by oncological therapies. We have to treat our patients as a whole and not only, target therapy to one of the pieces of the puzzle.
Cardiotoxicity can be defined as all damage caused directly or indirectly to the cardiomyocyte.
This is a broad term which affects the cardiovascular system in many ways. The classical definition refers a reduction in left ventricular ejection fraction and the development of heart failure.1
However, they can be divided in ten categories: myocardial dysfunction, heart failure,
coronary artery disease, arrhythmias, arterial hypertension, thromboembolic disease, peripheral vascular disease, stroke, pulmonary hypertension and pericardial complications.
First of all, when a patient presents himself with a certain lifestyle risk factors (smoking, alcohol, obesity), demographic and other cardiovascular risk factors (age, arterial hypertension or diabetes mellitus) then it is needed to be checked whether the factors are known or unknown, treated and controlled or not. Depending on past history, he may also have cardiovascular disease such as heart failure or myocardial infarct.
Cancer Stud Mol Med Open J. 2017; 3(2): 23- 26. doi: 10.17140/CSMMOJ-3-119
