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JAKis play a key role in the treatment of MPN. However, emerging evidence suggests that JAKis can lead to adverse cardiovascular events. Results from a first-of-a-kind meta-analysis evaluating the cardiovascular safety of JAKis in MPN were published in eJHaem by Dunn et al.1 The analysis included 23 publications with a pooled population of 2,198 patients; 1,145 in the JAKi group and 1,053 in the control group.1 The analysis aimed to compare rates of arterial and venous thrombosis, MACE, and hypertension in patients with MPN treated with a JAKi compared to those treated with BAT or placebo, and to review the clinical significance of cardiovascular safety in these patients.1 |
Key learnings |
Patients in the JAKi group experienced significantly fewer thromboembolic events vs those in the control group (IRR, 0.52; 95% CI, 0.28–0.98; p = 0.04). |
This was primarily driven by ruxolitinib inpatients with MF and PV, with a subgroup analysis of ruxolitinib studies demonstrating an even more significant reduction in thromboembolic events in the JAKi group vs the control group (IRR, 0.41; 95% CI, 0.26–0.64; p < 0.001). |
No difference was observed in the rates of MACE (IRR, 0.97; 95% CI, 0.52–1.82; p = 0.93) or hypertension (IRR, 0.81; 95% CI, 0.48–1.35; p = 0.42) between the JAKi and control groups. |
JAKis were associated with a reduced risk of thromboembolic events compared to the control group in patients with MPN. Further prospective trials may elucidate the cardiovascular profiles of various JAKs across different MPN subtypes. |
Abbreviations: BAT, best available therapy; CI, confidence interval; IRR, incidence rate ratio; JAKi, Janus kinase inhibitor; MACE, major adverse cardiovascular events; MF, myelofibrosis; MPN, myeloproliferative neoplasms; PV, polycythemia vera.
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