Ventricular repolarization dynamics in arsenic trioxide treatment of acute promyelocytic leukemia

Arsenic trioxide is the first-line treatment for acute promyelocytic leukemia (APL); however, abnormalities of ventricular repolarization and QT interval prolongation are the most common adverse effects. We explore ventricular repolarization dynamic changes and the influence of clinical factors in APL patients during arsenic trioxide induction therapy.

APL patients receiving arsenic trioxide induction therapy were included. Arsenic trioxide effects on ventricular repolarization-related indicators such as QTc, QT interval dispersion (QTd), heart rate-corrected J to T-peak (JTpC), and T-peak to T-end covariate (TpTec) interphase were statistically analyzed. Furthermore, logistic regression analysis was conducted to explore the correlation between various clinical factors and changes in repolarization indexes.

Ninety-three patients were recruited finally. Seven patients with QTc > 500 ms after arsenic trioxide treatment were discontinued from the study. QTc, QTd and JTpC interphase prolonged on day 8; TpTec prolongation was observed at the late induction stage. The risk factors were disease risk, hemoglobin and lactate dehydrogenase for QTc; hemoglobin for QTd; disease risk and hemoglobin for JTpC and TpTec.

QTc, QTd and JTpC were prolonged in the early use of arsenic trioxide and in contrast with TpTec. Hypothrombinemia was a common risk factor of ventricular repolarization prolongation and should be considered in preventing cardiac adverse effects of arsenic trioxide in APL patients.