Figure 3.
IRs of new-onset CV-AEs, AT-AEs, overall hypertension, new-onset hypertension, and CV-AEs and AT-AEs according to the number of risk factors per 100 person-years by the frontline TKI modality. (A-B) The IR of patients with new-onset CV-AEs (A) and AT-AEs (B) was significantly higher with ponatinib therapy compared with other TKI modalities; P < .001 in both panels. (C-D) IR of patients with hypertension (overall [C] and new-onset [D]) was highest with ponatinib followed by imatinib 400 mg followed by other TKI modalities; P < .001 in both panels. (E-F) As the number of cardiovascular risk factors increases, the IRs of new-onset CV-AEs (E) and AT-AEs (F) increase within each TKI modality. Patients who received ponatinib had the highest IR (compared with other TKIs) with ≥2 risk factors; P < .001 in both panels.

IRs of new-onset CV-AEs, AT-AEs, overall hypertension, new-onset hypertension, and CV-AEs and AT-AEs according to the number of risk factors per 100 person-years by the frontline TKI modality. (A-B) The IR of patients with new-onset CV-AEs (A) and AT-AEs (B) was significantly higher with ponatinib therapy compared with other TKI modalities; P < .001 in both panels. (C-D) IR of patients with hypertension (overall [C] and new-onset [D]) was highest with ponatinib followed by imatinib 400 mg followed by other TKI modalities; P < .001 in both panels. (E-F) As the number of cardiovascular risk factors increases, the IRs of new-onset CV-AEs (E) and AT-AEs (F) increase within each TKI modality. Patients who received ponatinib had the highest IR (compared with other TKIs) with ≥2 risk factors; P < .001 in both panels.

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