Results of plasma N-terminal pro B-type natriuretic peptide and cardiac troponin monitoring in GIST patients do not support the existence of imatinib-induced cardiotoxicity

Background: Recently, case reports of patients treated withimatinib (imatinib mesylate; Gleevec®; Glivec®) indicatedthat this tyrosine kinase inhibitor may induce cardiomyopathy.Consequently, careful cardiac monitoring was advocated for clinicalstudies. The purpose of this study was to prospectively evaluatewhether imatinib (Gleevec) induces early, subclinical, cardiactoxicity. Patients and methods: History and physical examination werecarried out with special attention for symptoms of heart failure.Additionally, assessments of serial plasma N-terminal pro B-typenatriuretic peptide (NT-proBNP) and serum cardiac troponin T(cTnT) measurement before and 1 and 3 months after the startof imatinib treatment (400–800 mg daily) were done inpatients with advanced and/or metastatic gastrointestinal stromaltumours (GIST). Results: A total of 55 GIST patients were enrolled. Only onepatient, with a normal pretreatment NT-proBNP, showed an increasein NT-proBNP to above age-specific normal values during imatinibtreatment and developed symptomatic heart failure due to pre-existentcardiac valvular disease. cTnT levels remained stable. Conclusions: In our study population, imatinib treatment forGIST was not associated with an increase in plasma NT-proBNPlevels, indicating that the risk of subclinical cardiac toxicityis limited with the use of this agent. These results do notsupport the current strategy to standard cardiac monitoringin all patients. This may be restricted to GIST patients witha history of cardiac disease. Key words: cardiotoxicity, GIST, imatinib mesylate, NT-proBNP, troponin TReceived for publication August 15, 2007. Revision received August 24, 2007. Accepted for publication August 29, 2007.