RESUMEN
OBJECTIVE: To study the cardiac toxicity of arsenic trioxide (As(2)O(3)). METHODS: To investigate and analyze the probable mechanisms of cardiac toxicity of As(2)O(3) by dynamic monitoring of clinical manifestations, basal cardiac rate and electrocardiographic data of acute promyelocyte leukemia (APL) patients during As(2)O(3) therapy. The instant change of the action potential, the I(Ca-L) and I(k) of single cardiac myocyte of guinea pig was also observed with patch clamp dynamically. RESULTS: Approximately 71.4% of the 28 cases of APL showed cardiac toxic reaction in different degree in the first week after As(2)O(3) intravenous infusion in general dose, mainly expressing rapid heart rate or prolonged QT interval. As(2)O(3) could prolong the action potential duration from (563.0 +/- 55.8) ms to (737.7 +/- 131.7) ms (P < 0.05) and increased the I(Ca-L) and I(k) of single cardiac myocyte of guinea pig in vitro. CONCLUSION: As(2)O(3) intravenous infusion in general therapeutic dose can cause tachycardia and prolong QT interval in some of the APL patients. The probable mechanism of these side-effects may be due to instant involvement of ionic channel of cardiac myocyte.