Key result
Dasatinib therapy in chronic myeloid leukemia patients was associated with a gradual increase in right ventricular systolic pressure (Spearman's r=0.2819, p<0.001), with 12.4% developing RVSP >40 mm Hg.
Why the study?
The feasibility of non-invasive transthoracic echocardiography for diagnosing dasatinib-induced pulmonary arterial hypertension in chronic myeloid leukemia needed investigation.
Does dasatinib therapy increase right ventricular systolic pressure and induce pulmonary arterial hypertension in patients with chronic myeloid leukemia?
Cohort (n=451)
Does dasatinib therapy increase right ventricular systolic pressure and induce pulmonary arterial hypertension in patients with chronic myeloid leukemia?
Effect estimate: Spearman's r = 0.2819
p-value: p=< 0.001
Routine non-invasive transthoracic echocardiography is a feasible and effective method for the early diagnosis and monitoring of dasatinib-induced pulmonary arterial hypertension in patients with chronic myeloid leukemia.
Dasatinib was associated with rising RVSP and D-PAH; leaves open whether routine echo monitoring improves CML outcomes.
BACKGROUND: We investigated the feasibility of the clinical application of non-invasive transthoracic echocardiography for diagnosis of pulmonary arterial hypertension induced by dasatinib (D-PAH) in chronic myeloid leukemia (CML). METHODS: A total of 451 CML patients who were examined by 2D-echocardiography at least once at baseline and/or during dasatinib therapy as frontline (n = 196) and subsequent line (n = 255) therapies were included in this study. D-PAH was defined as right ventricular systolic pressure (RVSP) >40 mm Hg with relevant symptoms and the absence of other specific etiologies. RESULTS: A total of 847 echocardiographies were performed including at baseline (n = 255) and during dasatinib treatment (n = 592). During the median of 36.2 (0.1-181.8) months of dasatinib therapy, the level of RVSP gradually increased (Spearman's r = 0.2819, p < 0.001) and the mean RVSP was significantly increased after taking dasatinib therapy compared with baseline. During dasatinib therapy, 56 (12.4%) patients had RVSP >40 mm Hg without (asymptomatic, n = 27, 48.2%) or with symptoms (D-PAH, n = 29, 51.8%). All asymptomatic patients maintained dasatinib therapy without further symptoms and the D-PAH patients ultimately switched to other tyrosine kinase inhibitors. After dasatinib discontinuation, 13 (45%) and 15 (52%) patients showed RVSP normalization and gradual decrease, respectively. CONCLUSIONS: Our large cohort study demonstrated that the gradual increment of RVSP might be induced by dasatinib and non-invasive echocardiography can be fast way for early diagnosis as well as for monitoring of D-PAH.
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Lee et al. (2021) conducted a cohort in chronic myeloid leukemia (n=451). dasatinib vs. baseline was evaluated on gradual increase in right ventricular systolic pressure (RVSP) (Spearman's r = 0.2819, p=< 0.001). Dasatinib therapy in chronic myeloid leukemia patients was associated with a gradual increase in right ventricular systolic pressure (Spearman's r=0.2819, p<0.001), with 12.4% developing RVSP >40 mm Hg.
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