The Cardiovascular Event Risk Associated with Tyrosine Kinase Inhibitors and the Lipid Profile in Patients with Chronic Myeloid Leukemia

Author:

Saez Perdomo María Nieves1,Stuckey Ruth1ORCID,González-Pérez Elena1,Sánchez-Sosa Santiago12,Estupiñan-Cabrera Paula1,Lakhwani Lakhwani Sunil3,González San Miguel José David4,Hernanz Soler Nuria5,Gordillo Marina6,González Brito Gloria3,Tapia-Torres María7,Ruano Ana1,Segura-Díaz Adrián1,Luzardo Hugo1,Bilbao-Sieyro Cristina18,Gómez-Casares María Teresa19

Affiliation:

1. Hospital Universitario de Gran Canaria Dr. Negrín, 35019 Las Palmas de Gran Canaria, Spain

2. Universidad de Las Palmas de Gran Canaria, 35001 Las Palmas de Gran Canaria, Spain

3. Hospital Universitario de Canarias, 38320 La Laguna, Spain

4. Hospital Universitario Insular de Gran Canaria, 35016 Las Palmas de Gran Canaria, Spain

5. Hospital Universitario Nuestra Señora de Candelaria, 38010 Santa Cruz de Tenerife, Spain

6. Hospital José Molina Orosa, 35500 Las Palmas de Gran Canarias, Spain

7. Hospital General de La Palma, 38713 Santa Cruz de Tenerife, Spain

8. Morphology Department, Universidad de Las Palmas de Gran Canaria, 35001 Las Palmas de Gran Canaria, Spain

9. Department of Medical Sciences, Universidad de Las Palmas de Gran Canaria, 35001 Las Palmas de Gran Canaria, Spain

Abstract

Background: Second- and third-generation tyrosine kinase inhibitors (TKIs) are now available to treat chronic-phase chronic myeloid leukemia (CP-CML) in the first and second line. However, vascular adverse events (VAEs) have been reported for patients with CML treated with some TKIs. Methods: We retrospectively evaluated the cumulative incidence (CI) and cardiovascular risk for 210 patients included in the Canarian Registry of CML. Result: With a mean follow up of 6 years, 19/210 (9.1%) patients developed VAEs, all of whom presented at least one cardiovascular risk factor at diagnosis. The mean time to VAE presentation was 54 months from the start of TKI treatment. We found a statistically significant difference between the CI for nilotinib-naïve vs. nilotinib-treated patients (p = 0.005), between dasatinib-naïve and dasatinib-treated patients (p = 0.039), and for patients who received three lines of treatment with first-line imatinib vs. first-line imatinib (p < 0.001). From the multivariable logistic regression analyses, the Framingham risk score (FRS) and patients with three lines of TKI with first-line imatinib were the only variables with statistically significant hazard ratios for VAE development. Significant increases in HDL-C and total cholesterol may also be predictive for VAE. Conclusions: In conclusion, it is important to estimate the cardiovascular risk at the diagnosis of CML as it can help determine whether a patient is likely to develop a VAE during TKI treatment.

Funder

Fundación DISA

Incyte

Publisher

MDPI AG

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