Imatinib or nilotinib treatment for 1 year may be safe and effective for patients with chronic myeloid leukemia (CML) without a history of cardiovascular disease, according to a study published in Cardiovascular Toxicity.

While the cardiotoxic effects of certain tyrosine kinase inhibitors (TKI) such as pazopanib, sunitinib, and sorafenib are well documented, the negative cardiac effects of imatinib and nilotinib — 2 TKIs used as standard therapy for Philadelphia-positive CML — are not fully understood. 

For this single-center prospective study, researchers assessed the outcomes of 11 patients with CML who were treated with imatinib or nilotinib. Eligible patients were TKI-therapy naïve, and were excluded from the study if they had a history of treatment- or nontreatment-related cardiovascular disease. Patients underwent laboratory, clinical, and quality-of-life assessments at baseline.

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After 1 year of follow up, all patients retained a similar quality of life and showed no signs of reduced cardiovascular function.

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Laboratory results showed that there were no elevations of cystatin-C and NT-proBNP, biomarkers predictive of cardiovascular mortality, and no changes in systolic or diastolic function were observed in echocardiogram readings. Other measures of cardiovascular function, such as global longitudinal strain, global circumferential strain, and global radial strain, remained consistent with baseline assessments after 1 year of treatment.

Results showed that 1-year treatment with imatinib or nilotinib did not have any negative effects on cardiovascular health and may be safe in the treatment of CML. The authors were, however, cautiously optimistic and concluded that “because of the low global incidence of CML, these promising findings need to be confirmed with a larger multicenter study.”


Francisco ARG, Alves DA, David C, Guerra L, Pinto FJ, Almeida AG. Cardiotoxicity in hematological diseases: are the tyrosine kinase inhibitors imatinib and nilotinib safe? [published online April 3, 2018]. Cardiovasc Toxicol. doi: 10.1007/s12012-018-9453-3