Biomarkers as Predictors of Cardiac Toxicity From Targeted Cancer Therapies

• Targeted cancer therapies have substantial rates of cardiac toxicity.
• Cardiac biomarker screening may allow for the early detection of cardiac toxicity.
• Troponin I has potential as a biomarker for trastuzumab toxicity.
• NT-proBNP has potential as a biomarker for tyrosine kinase inhibitor toxicity.

BackgroundCardiac biomarkers have been extensively investigated as early detectors of cardiac toxicity from cancer therapies. Whereas the role of biomarkers in monitoring anthracycline toxicity is generally well understood, substantial uncertainty remains regarding their role in monitoring newer targeted cancer therapies.Methods and ResultsThis review article examines all major published studies using cardiac troponins and/or N-terminal pro–B-type natriuretic peptide (NT-proBNP) in monitoring for cardiac toxicity with trastuzumab, tyrosine kinase inhibitors, and mammalian target of rapamycin (mTOR) inhibitors. There is substantial variability among studies regarding biomarker assays used, sensitivity of the assays, and definitions of abnormal results. In general, troponin I predicts early but not late cardiac events when trastuzumab is administered after anthracyclines, but troponin increases likely reflect anthracycline injury rather than trastuzumab injury. NT-proBNP detects cardiac toxicity with tyrosine kinase inhibitors and mTOR inhibitors, but not independently from echocardiography.ConclusionsTroponin I can serve as a marker for susceptibility to cardiac toxicity during early trastuzumab treatment in patients who have received recent anthracyclines. NT-proBNP can serve as a useful marker of cardiac toxicity in patients treated with tyrosine kinase inhibitors or mTOR inhibitors if echocardiographic screening is not being used.