Diagnosis of cardiotoxicity
Cardiotoxicity is a common complication of chemotherapy (CT). The clinical manifestation of cardiotoxicity can range from transient asymptomatic left ventricular dysfunction to
cardiac death.This is a growing problem in the setting of clinical oncology due to the tendency in using progressively higher doses of anthracyclines, as well as newer compounds, as thyroxin kinesis inhibitors, antiangiogenic drug, and monoclonal antibodies potentially deserve cardiotoxic implications. The clinical implications of cardiotoxicity are particularly relevant in those cancer patients in which onset of cardiac dysfunction, even asymptomatic, seriously limits their therapeutic opportunities and negatively impacts on clinical outcome. At present, oncologic guidelines recommend regular cardiac function assessment (generally by echocardiography or MUGA scan) to detect CT- induced cardiac damage in an early phase. The weak point of such an approach is that these techniques have low sensitivity and poor predictive value. Indeed, cardiotoxicity is usually detected when cardiac damage has already occurred. In our clinical practice we utilize different tools for the early identification of patients at increased risk if cardiotoxicity: biomarkers of myocardial damage, like Troponin I, and hemodynamic markers like NT-proBNP. For all of them, an accurate predictive value has been demonstrated by our investigations.
Cardiotoxicity prevention
The possibility to identify patients at higher risk of developing late myocardial dysfunction by cardiac biomarkers (Troponin I, NT-proBNP) provides
a rationale for the development of prophylactic strategies directed against CT-induced cardiotoxicity. Considering the results of our published studies, a possible clinical application of these markers is the evaluation of pharmacological strategies in selected high-risk patients, with the aim to prevent acute cardiac damage, left ventricular dysfunction, and cardiac events. Two different therapeutic strategies could be implemented in order to reduce the clinical impact of cardiotoxicity: 1) use of specific cardiologic treatments given to cancer patients during CT in the attempt of preventing or blunting the rise of these markers; 2) use of cardiologic treatments given only to those selected cancer patients showing an increase in these markers after CT. This with the aim to interfere with the natural evolution of cardiac toxicity, and prevent the occurrence of left ventricular dysfunction and cardiac adverse events. In particular, the increase of Troponin I soon after CT is a strong predictor of left ventricular dysfunction and poor cardiologic outcome.
Cardiotoxicity treatment
CT-induced cardiotoxicity can result in a cardiomyopathy generally considered to be irreversible, and leading to congestive heart failure and cardiac death.
Clinical manifestations of cardiotoxicity may appear months or even years after the end of CT, and are preceded, in most cases, by asymptomatic left ventricular dysfunction. In no monitored patients, symptoms of congestive heart failure usually represent the first manifestation of cardiotoxicity. In our recently published experience, most patients receiving early adequate treatment that included ACE-inhibitors and beta-blockers, showed a complete recovery of cardiac function in most cases, associated with relevant improvement in clinical status and a better cardiologic prognosis.