proposal and the same as our previous relevant doubleblinded randomised controlled trial conducted in thoracoscopic surgery. 4 The dexmedetomidine and control group showed comparable baseline heart rate of 79.0 AE 14.3 beats per minute (bpm) and 77.3 AE 11.7 bpm (P ¼ 0.424). Comparable cardiac index results were also observed in the dexmedetomidine and control group at 2.8 AE 0.9 and 2.9 AE 0.8 l min À1 m À2 (P ¼ 0.650). Therefore, the infusion of dexmedetomidine indeed resulted in the differences in the heart rate and cardiac index between the two study groups. The exclusion of patients with pre-operative sinus bradycardia (less than 50 bpm) 4 was not conducted, as this may be frequently observed in patients taking beta-adrenergic blockers for the management of hypertension. However, no patient presented baseline sinus bradycardia in this study.When comparing the baseline and average haemodynamic states of the goal-directed haemodynamic therapy, dexmedetomidine reduced the heart rate and the cardiac index by approximately 10%. Theoretically, the effect on the heart rate may have alerted the attending anaesthesiologist to the use of dexmedetomidine. Yet, the lowered heart rates ($10%) were minimal. We believe that the average heart rate difference between the two groups (70.6 vs. 77.7 bpm), which was difficult to detect during clinical care, did not indicate clinically meaningful bradycardia. By comparison, the stronger propofol and opioid-sparing effects (>20%) were easier to detect because the anaesthesiologist might have been aware of a significantly lower concentration of target-controlled propofol infusion to maintain a bispectral index between 40 and 60. However, this may be an inevitable condition in relevant dexmedetomidine studies, and the outcome assessors were blinded to the group allocation. Therefore, we consider that this may be irrelevant to the findings of the present study.
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