: Arterial stiffness, measured by pulse wave velocity (PWV), is a validated surrogate of vascular damage and CV risk, but evidence on TKI-specific patterns of arterial stiffness and their prognostic relevance in chronic myeloid leukemia (CML) is limited. We primarily evaluated the longitudinal association between TKI type and arterial stiffness, and secondarily explored the association between arterial stiffness and CV adverse events (CVAEs). In this prospective cohort study, 69 patients with CML receiving imatinib (n = 30), dasatinib (n = 18), or nilotinib (n = 21) underwent non-invasive assessment of carotid-femoral PWV. Longitudinal PWV trajectories were analyzed with prespecified adjustment sets including key clinical and hematologic-inflammatory covariates. Associations between PWV and CVAEs were explored. No significant interaction between time and TKI type was observed in unadjusted (χ²=1.81, p = 0.41), clinically adjusted (χ²=1.60, p = 0.45), or hematologic-inflammatory adjusted LME models (χ²=1.68, p = 0.43). During a median follow-up of 19 months, 21 CVAEs occurred. Higher PWV was associated with CVAEs after multivariable adjustment (OR = 1.40, p = 0.037), together with ≥ 2 TKI treatment lines (OR = 2.70, p = 0.042). In this real-world cohort, no evidence of differential longitudinal progression of arterial stiffness according to TKI type was detected. Arterial stiffness and treatment-related variables were associated with CVAEs, whereas no differential PWV trajectory according to TKI type was detected. These findings are exploratory and require validation in larger prospective cohorts with longer follow-up before definitive clinical recommendations can be made.
Arterial stiffness in patients with chronic myeloid leukemia receiving tyrosine kinase inhibitors: An exploratory prospective observational study
Olga MulasPrimo
;Alessandro Sestu;Alessandro Costa
;Eleonora Atzeni;Giovanni CaocciPenultimo
;Angelo ScuteriUltimo
2026-01-01
Abstract
: Arterial stiffness, measured by pulse wave velocity (PWV), is a validated surrogate of vascular damage and CV risk, but evidence on TKI-specific patterns of arterial stiffness and their prognostic relevance in chronic myeloid leukemia (CML) is limited. We primarily evaluated the longitudinal association between TKI type and arterial stiffness, and secondarily explored the association between arterial stiffness and CV adverse events (CVAEs). In this prospective cohort study, 69 patients with CML receiving imatinib (n = 30), dasatinib (n = 18), or nilotinib (n = 21) underwent non-invasive assessment of carotid-femoral PWV. Longitudinal PWV trajectories were analyzed with prespecified adjustment sets including key clinical and hematologic-inflammatory covariates. Associations between PWV and CVAEs were explored. No significant interaction between time and TKI type was observed in unadjusted (χ²=1.81, p = 0.41), clinically adjusted (χ²=1.60, p = 0.45), or hematologic-inflammatory adjusted LME models (χ²=1.68, p = 0.43). During a median follow-up of 19 months, 21 CVAEs occurred. Higher PWV was associated with CVAEs after multivariable adjustment (OR = 1.40, p = 0.037), together with ≥ 2 TKI treatment lines (OR = 2.70, p = 0.042). In this real-world cohort, no evidence of differential longitudinal progression of arterial stiffness according to TKI type was detected. Arterial stiffness and treatment-related variables were associated with CVAEs, whereas no differential PWV trajectory according to TKI type was detected. These findings are exploratory and require validation in larger prospective cohorts with longer follow-up before definitive clinical recommendations can be made.
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