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Annals of Oncology Advance Access originally published online on October 24, 2007
Annals of Oncology 2008 19(2):359-361; doi:10.1093/annonc/mdm468
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© 2007 European Society for Medical Oncology. For Permissions, please email: journals.permissions@oxfordjournals.org

gastrointestinal tumors

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

P. J. Perik1,2, B. Rikhof1, F. A. de Jong3, J. Verweij3, J. A. Gietema1 and W. T. A. van der Graaf4,*

1 Department of Medical Oncology
2 Department of Cardiology, University of Groningen and University Medical Centre, Groningen
3 Department of Medical Oncology, Erasmus University Medical Centre Rotterdam, Rotterdam
4 Department of Medical Oncology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

* Correspondence to: Prof. W. T. A. van der Graaf, Department of Medical Oncology, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands. Tel: +31-24-3610353; Fax: +31-24-3540788; E-mail: w.vandergraaf{at}onco.umcn.nl

Background: Recently, case reports of patients treated with imatinib (imatinib mesylate; Gleevec®; Glivec®) indicated that this tyrosine kinase inhibitor may induce cardiomyopathy. Consequently, careful cardiac monitoring was advocated for clinical studies. The purpose of this study was to prospectively evaluate whether imatinib (Gleevec) induces early, subclinical, cardiac toxicity.

Patients and methods: History and physical examination were carried out with special attention for symptoms of heart failure. Additionally, assessments of serial plasma N-terminal pro B-type natriuretic peptide (NT-proBNP) and serum cardiac troponin T (cTnT) measurement before and 1 and 3 months after the start of imatinib treatment (400–800 mg daily) were done in patients with advanced and/or metastatic gastrointestinal stromal tumours (GIST).

Results: A total of 55 GIST patients were enrolled. Only one patient, with a normal pretreatment NT-proBNP, showed an increase in NT-proBNP to above age-specific normal values during imatinib treatment and developed symptomatic heart failure due to pre-existent cardiac valvular disease. cTnT levels remained stable.

Conclusions: In our study population, imatinib treatment for GIST was not associated with an increase in plasma NT-proBNP levels, indicating that the risk of subclinical cardiac toxicity is limited with the use of this agent. These results do not support the current strategy to standard cardiac monitoring in all patients. This may be restricted to GIST patients with a history of cardiac disease.

Key words: cardiotoxicity, GIST, imatinib mesylate, NT-proBNP, troponin T

Received for publication August 15, 2007. Revision received August 24, 2007. Accepted for publication August 29, 2007.


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