Polycythemia vera (PV) is a chronic myeloproliferative neoplasm characterized by clonal erythrocytosis driven by JAK2 mutations, affecting more than 95% of patients. Morbidity and mortality in PV are dominated by cardiovascular complications―particularly arterial and venous thrombosis. Modern treatment approaches, including therapeutic phlebotomy, low-dose aspirin, and cytoreductive therapies (hydroxyurea, interferon-α formulations, and ruxolitinib), have reduced blood cell counts and thrombotic risk, yet concerns about treatment-associated cardiovascular toxicity have emerged. Recent cardio-oncology guidelines emphasize structured monitoring for cancer therapy-related cardiovascular toxicity. This mini review summarizes the cardiovascular burden of PV, therapeutic strategies to mitigate risk, and emerging perspectives on cardiotoxicity―including a recently reported case of reversible left ventricular dysfunction associated with ropeginterferon α-2b.
MUKAI et al. (Thu,) studied this question.