Chronic myeloid leukaemia in the contemporary era (from 2001) was associated with a similar adjusted risk of MACE compared to matched controls without CML (HR 1.27; 95% CI 0.96-1.43).
Cohort (n=46,618)
Does the use of tyrosine kinase inhibitors alter the risk of major adverse cardiovascular events in patients with chronic myeloid leukaemia compared to matched controls?
In the contemporary TKI era, CML patients face an increased risk of cerebrovascular and peripheral arterial events compared to matched controls, though overall MACE risk is similar across different TKIs.
Hazard Ratio: 1.27 (95% CI 0.96–1.43)
Absolute Event Rate: 20.3% vs 12.6%
OBJECTIVES: (1) Describe how the risk of major adverse cardiovascular events (MACE) in individuals with chronic myeloid leukaemia (CML) has evolved; (2) evaluate the risk of MACE associated with the prescription of different CML tyrosine kinase inhibitors (TKI). METHODS: A population-based retrospective study including all patients (n=4238) diagnosed with CML in Ontario, Canada between 1986 and 2017 and and age-matched and sex-matched individuals who received healthcare but who did not have CML (controls: n=42 380). The cohort was divided into those entering before 2001 vs from 2001 onwards (when TKIs were introduced). We developed competing risks models to compare time-to-event in CML cases versus controls. We adjusted for baseline comorbidities and present subdistribution HRs and 95% CIs. The relationship between TKI use and MACE was assessed by logistic regression. RESULTS: Before 2001 and from 2001 on, patients with CML had a higher crude incidence of MACE than patients without CML (19.8 vs 15.3 and 20.3 vs 12.6 per 1000 person-years, respectively). After adjustment for cardiovascular risk factors, patients with CML had a lower subdistribution hazard for MACE (0.59, 95% CI 0.46 to 0.76) before 2001; but from 2001, the adjusted subdistribution HR for MACE (1.27, 95% CI 0.96 to 1.43) was similar to age-matched and sex-matched patients. The incidence (9.3 vs 13.8 per 1000 person-years) and subdistribution hazard for cardiovascular death (0.43, 95% CI 0.36 to 0.52) were lower in patients with CML than controls before 2001. From 2001 on, the incidence (6.3 vs 5.4 per 1000 person-years) and subdistribution hazard for cardiovascular death (0.99, 95% CI 0.84 to 1.18) were similar to age-matched and sex-matched patients without CML with a higher risk of cerebrovascular events (8.6 vs 5.6 per 1000 person-years; 1.35, 95% CI 1.00 to 1.83) and peripheral arterial events (6.9 vs 3.0 per 1000 person-years; 1.66 95% CI, 1.15 to 2.39) in patients with CML than patients without CML. Compared with imatinib, there was no difference in the risk of MACE among those prescribed dasatinib (OR 0.67, 95% CI 0.41 to 1.10) or nilotinib (OR 1.22, 95% CI 0.70 to 1.97). CONCLUSIONS: In a contemporary CML population, the risk of MACE and cardiovascular death is at least as high as among age-matched and sex-matched patients without CML and may be higher for cerebrovascular and peripheral arterial events. No difference in the risk of MACE between imatinib, dasatinib and nilotinib was observed.
Leong et al. (Fri,) conducted a cohort in Chronic myeloid leukaemia (n=46,618). Chronic myeloid leukaemia (contemporary era from 2001) vs. Age-matched and sex-matched individuals without CML was evaluated on Major adverse cardiovascular events (MACE) (HR 1.27, 95% CI 0.96-1.43). Chronic myeloid leukaemia in the contemporary era (from 2001) was associated with a similar adjusted risk of MACE compared to matched controls without CML (HR 1.27; 95% CI 0.96-1.43).
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