Silvio Henrique Barberato et al. Ludhmila Abrão Hajjar
In recent decades, advances in cancer treatment have led to a significantly increased survival rate for several types of cancer. On the other hand, cancer survival increases patients’ vulnerability to cardiovascular complications induced by potentially cardiotoxic cancer therapy., Cardiovascular diseases are currently recognized as a main cause of morbidity and mortality in cancer survivors depending on the type of therapeutic approach used, patient age, and the presence of preexisting cardiovascular risk factors. Due to the high incidence of breast cancer in women, anthracyclines and monoclonal antibodies against human epidermal growth factor receptor type 2 (HER2) are the drugs most well-known as potential cardiotoxicity (CTX) inducers. However, other medications such as vascular endothelial growth factor inhibitors, tyrosine kinase inhibitors, proteasome inhibitors, and immunological checkpoint inhibitors, in addition to mediastinal radiotherapy, are also recognized for having a possible deleterious effect on the cardiovascular system. It is worth mentioning that CTX can express not only as myocardial dysfunction but also as acute coronary syndrome, arrhythmia, valve disease, pericardial disease, systemic arterial hypertension, and pulmonary hypertension. Thus, although left ventricular (LV) systolic dysfunction secondary to anticancer therapy is not the only CTX presentation, its development is among the most worrisome in clinical cardio-oncology practice, and the terms are often used interchangeably.
The diagnosis of LV dysfunction in a CTX setting is traditionally based on the serial evaluation of the LV ejection fraction (LVEF) using the Simpson method on two-dimensional echocardiography. Despite variation between international guidelines and cancer trials, the most commonly used CTX definition is a decrease of at least ten absolute points for a LVEF below the lower limit of normal after cancer treatment (considered below 53% by the cardiovascular imaging consensus of the European Association of Cardiovascular Imaging/American Society of Echocardiography [EACVI/ASE], or below 50% by the European Society of Cardiology [ESC]). However, LVEF measurements have important limitations, which include significant inter- and intra-observer variability, dependence on loading conditions, and low sensitivity to small LV function changes. Therefore, it was postulated that LVEF changes would occur later, when myocardial damage is severe enough to determine an irreversible cardiomyopathy.
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