Abstract:
Objective:To investigate the effectiveness of heart rate deceleration capacity (DC) measurement in predicting the car -diotoxicity of malignant tumor patients treated with epirubicin-based chemotherapy. Methods:The clinical medical records, including CK-MB and cTnI levels and dynamic electrocardiogram (ECG) parameters before and after each chemotherapy cycle, of 140 patients treated with epirubicin-based chemotherapy were analyzed. Patients were divided into the DC> 4.5 ms group and the DC≤ 4.5 ms group based on the calculated DC values. The CK-MB and cTnI levels and the dynamic ECG parameters of the two groups were compared af-ter two and four cycles of chemotherapy. Results:Patients in the two groups exhibited no statistically significant difference in their rele-vant clinical and pathological data before receiving chemotherapy ( P>0.05). However, after four cycles of chemotherapy, the DC≤ 4.5 ms group showed a significantly greater increase in serum CK-MB and cTnI concentrations over the pre-chemotherapy levels compared with the DC>4.5 ms group. After two and four cycles of chemotherapy, the DC≤ 4.5 ms group also exhibited a significantly greater in -crease in mean heart rate (beats/min) and supraventricular and ventricular arrhythmia counts (times/24h) over the pre- chemotherapy values compared with the DC> 4.5 ms group (P<0.05). After four cycles of chemotherapy, 23cases showed abnormally elevated cTnI levels in the DC ≤ 4.5 ms group. In this group, patients with elevated cTnI level exhibited no statistically significant difference in CK-MB and cTnI concentrations, mean heart rates, and supraventricular and ventricular arrhythmia counts compared with those with nor-mal cTnI level before chemotherapy (P>0.05). However, the DC values of patients with elevated cTnI were significantly lower than those with normal cTnI level (P<0.05). Conclusion:The risk of epirubicin-induced cardiotoxicity increased with decrease in DC value. The DC test was shown to be an effective predictor of the risk of epirubicin-induced cardiotoxicity.