Role of advanced cardiovascular imaging in chemotherapy-induced cardiotoxicity

The development of cardiotoxicity induced by cancer treatments has emerged as a significant clinical problem, both in the short run, as it may influence drug administration in chemotherapeutic protocols, and in the long run, because it may determine adverse cardiovascular outcomes in survivors of various malignant diseases. Therefore, early detection of anticancer drug-related cardiotoxicity is an important clinical target to improve prevention of adverse effects and patient care. Today, echocardiography is the first-line cardiac imaging techniques used for identifying cardiotoxicity. Cardiac dysfunction, clinical and subclinical, is generally diagnosed by the reduction of left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS). However, myocardial injury detected by echocardiography is preceded by other alterations, such as myocardial perfusion and mitochondrial and metabolic dysfunction, that can only be recognized by second-level imaging techniques, like cardiac magnetic resonance (CMR) and nuclear imaging, which, using targeted radiotracers, may help to provide information on the specific mechanisms of cardiotoxicity. In this review, we focus on the current and emerging role of CMR, as a critical diagnostic tool of cardiotoxicity in the very early phase, due to its availability and because it allows the contemporary detection of functional alterations, tissue alterations (mainly performed using T1, T2 mapping with the evaluation of extracellular volume-ECV) and perfusional alteration (evaluated with rest-stress perfusion) and, in the next future, even metabolic changes. Moreover, in the subsequent future, the use of Artificial Intelligence and big data on imaging parameters (CT, CMR) and oncoming molecular imaging datasets, including differences for gender and countries, may help predict cardiovascular toxicity at its earliest stages, avoiding its progression, with precise tailoring of patients’ diagnostic and therapeutic pathways.