AIM: The aim of this study was to observe the cardiac performance in 2-week or 4-week levothyroxine(T4)-induced cardiac hypertrophy and to elucidate the possible underlying mechanism of cardiac hypertrophy transition to heart failure in T4 treatment rats.METHODS: The blood pressure and pulse rate were measured by tail-cuff technique.The cardiac output and the preload-cardiac output were measured in working heart mode.The shortening of unloading contraction in cardiomyocytes was observed by an edge-detector system.RESULTS: Resting heart rate in T4 treatment rats increased significantly and the width of cardiomyocytes widened in T4 rats,but the length of cardiomyocytes had no difference compared with control values.The cardiac output in 2-week T4 group was higher than that in control group.The cardiac output increased when the preload increased from 5 mmHg to 15 mmHg.The unloading shortening amplitude at 1 Hz and 2 Hz increased in 2-week T4 group.No difference between 2-week T4 group and control group at 4 Hz was observed.When the stimulating frequency increased from 1 Hz to 4 Hz,the shortening amplitude also increased in control cardiomyocytes,but decreased in 2-week or 4-week T4 group.The shortening amplitude increased further in 4-week T4 group as compared with that in control.The time to peak shortening and time from peak shortening to 75% relaxation reduced at each frequency in 2-week and 4-week T4 group.The shortening and relaxation rates in 2-week or 4-week T4 group were higher than those in control group at 1 Hz and 2 Hz.The shortening and relaxation rate kept higher at 4 Hz in 2-week T4 group,but showed no difference with control at 4 Hz in 4-week T4 group.CONCLUSION: These above results suggest that shortening amplitude-frequency relationship of cardiomyocytes in 4-week T4 rats is earlier to be altered than cardiac performance in working heart.