Patients taking tyrosine kinase inhibitors (TKIs) for chronic myeloid leukemia (CML) face an increased risk for arterial and venous vascular events. The findings are published in Annals of Internal Medicine.

CML is a type of cancer that starts in certain blood-forming cells of the bone marrow and is triggered by the BCR-ABL1 fusion gene. It is a slow growing form of leukemia that usually targets older adults. However, without treatment, CML generally progresses to a fatal form of acute leukemia in only a few years. TKIs, which target the BCR-ABL1 fusion gene, have increased survival dramatically for patients with CML, but continuous administration of these drugs may elicit long-term toxicity.

Researchers sought to determine the incidence of vascular events in patients with CML treated with first-generation TKIs (imatinib) and second-generation TKIs (nilotinib or dasatinib). The researchers used a Swedish registry of patients diagnosed with CML between January 2002 and December 2012 and matched each patient by birth year and sex to 5 control individuals randomly selected from Sweden's Total Population Register. The data showed that patients taking TKIs for CML had a greater risk for arterial and venous thrombotic events compared to the general population. The researchers observed a greater risk for myocardial infarction among patients treated with a second-generation TKI compared with those on a first-generation therapy, but the number of events was too small to allow statistical comparison. Further study is needed to determine whether the risk for myocardial infarction increases with second-generation drugs. The authors suggest that clinicians consider this risk for vascular events when initiating TKI therapy in patients with CML.

Article: Cardiovascular Events Associated With Use of Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia: A Population-Based Cohort Study, Torsten Dahlén, MD; Gustaf Edgren, MD, PhD; Mats Lambe, MD, PhD; Martin Höglund, MD, PhD; Magnus Björkholm, MD, PhD; Fredrik Sandin, MSc; Anders Själander, MD, PhD; Johan Richter, MD, PhD; Ulla Olsson-Strömberg, MD, PhD; Lotta Ohm, MD, PhD; Magnus Bäck, MD, PhD; Leif Stenke, MD, PhD, on behalf of the Swedish CML Group and the Swedish CML Register Group, Annals of Internal Medicine, doi:10.7326/M15-2306, published online 14 June 2016.