Correspondence  |   April 2003
Propofol Preservation of Myocardial Function in Patients Undergoing Coronary Surgery Using Cardiopulmonary Bypass is Dose Dependent
Author Affiliations & Notes
  • David M. Ansley, M.D.
  • *University of British Columbia, Vancouver, British Columbia, Canada.
Article Information
Correspondence   |   April 2003
Propofol Preservation of Myocardial Function in Patients Undergoing Coronary Surgery Using Cardiopulmonary Bypass is Dose Dependent
Anesthesiology 4 2003, Vol.98, 1028. doi:
Anesthesiology 4 2003, Vol.98, 1028. doi:
To the Editor:—
We read with great interest the article recently published by De Hert et al.  1 entitled “Sevoflurane but Not Propofol Preserves Myocardial Function in Coronary Surgery Patients.” In this study, the authors based their conclusion primarily on myocardial mechanics measured before and 15 min after cardiopulmonary bypass. Hearts were paced at 90 beats/min during the measurements. This approach makes the cardiac mechanics measured more comparable between groups.
It would be very helpful for us to know if the plasma concentration of propofol is available and/or if the hemodynamic data are comparable at 12 h or more postoperatively in this study. An experimental study has shown that the protective effect of propofol on myocardial function following global myocardial ischemia and reperfusion is dose dependent, being effective at concentrations of 30 μm or more and not effective at concentrations of 10 μm or less. 2 This may explain why propofol is not cardiac protective at “clinically relevant” concentrations of 1 μg/ml (5.6 μm) 3 or up to 10 μm. 4 Our preliminary clinical study indicated that propofol is cardiac protective in a dose-dependent manner in coronary surgery patients when applied at “clinically achievable” concentrations of 4 and 11.8 μg/ml during surgery. This was evident when the cardiac index beyond 12 h post–cardiopulmonary bypass was compared. 5 
To understand this we conducted an experiment in an isolated heart model, applying 12 μg/ml (67 μm) propofol during global myocardial ischemia and during the early phase of reperfusion and then 5 μg/ml after 15 min of reperfusion (to avoid the depressant effect of high-dose propofol on myocyte contraction). We have observed that this approach provides better long-term myocardial functional recovery than 5 μg/ml propofol applied throughout ischemia and reperfusion. 6 
De Hert et al.  should be congratulated for their efforts. They provided evidence that cardiac troponin I was significantly lower in the sevoflurane group than in the propofol group up to 36 h postoperatively, a cardiac protection probably related to the preconditioning effects of sevoflurane. It should be noted, however, that from 24 to 36 h postoperatively, cardiac troponin I levels decreased in all 10 patients in the propofol group, while they increased in 2 or 3 patients (2 of 10 or 3 of 10) in the sevoflurane group. This is a significant difference between groups.
We must point out that a decrease in heart rate and/or the depression of cardiac contraction during the early phase of reperfusion might be an integral part of the cardiac-protective effect of propofol in the long run. Given that cardiac output increased from post–cardiopulmonary bypass to the end of the operation only in the propofol group and that there was no difference in clinical outcome between groups, we feel that the statement “propofol is not myocardial protective,” as implied in the title of the article by De Hert et al.  , 1 is somewhat misleading.
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