The cardioprotective effect of sevoflurane have been proven in experimental and clinical studies. However, it has not been studied so far if this effect on the myocardium is more expressed before the onset of myocardial ischaemia (preconditioning) or after (postconditioning). The aim of this study was to determine whether the cardioprotective effect of sevoflurane was more expressed during the preconditioning or postconditioning phase of coronary bypass grafting operations.
Key words: cardioprotective effect, sevoflurane, volatile anaesthetics, myocardial ischaemia, preconditioning, postconditioning
Seventy-two patients scheduled for elective coronary artery bypass graft surgery were randomly assigned to one of three groups of equal size: a group of patients who were anaesthetized by sevoflurane before the onset of ischaemia (SEVO pre; n=24), a group of patients who were anaesthetized by sevoflurane after the ischaemic period (SEVO post; n=24) and a control group who received only propofol (Control; n=24). The effect on the myocardium was assessed by successive measurements of cardiac biomarker release in the perioperative period: troponin I (cTnI), creatine kinase (CK), CK-MB isoenzyme and lactate dehydrogenase (LD). The degree of myocardial injury was estimated quantitatively on the basis of summary values for the cardiac biomarkers of all measured concentrations and categorically on the basis of the distribution of peak troponin I concentrations in the perioperative period. The monitored summary variables were: peak value, time to reach the peak value, a difference between the peak and first measured value, percent difference between the peak and first measured value, difference between the last and first measured values, percent difference between the last and first measured values, the area under the curve of the measured values through the period. The categorical assessment of periprocedural myocardial injury was done on the basis of peak troponin I at 2, 4, 8 and 12 µg/ l.
Quantitatively estimated degree of perioperative myocardial injury, based on summary values of monitored cardiac biomarkers did not differ significantly between the groups for any of the monitored parameters. However, in the group SEVO pre there was a significantly lower value CK-MB difference between the peak and the first measured value in comparison to the SEVO post group (p=0,010). This may speak in favour of smaller periprocedural myocardial injury in the SEVO pre group. The number of patients in whom, based on peak troponin I concentrations, it was estimated to have had perioperative myocardial injury did not differ significantly between the groups, although there was a trend of a minimum number of such patients in the SEVO pre group for all monitored peak concentrations of troponin I. In the univariate analysis test of predictor variables for the development of periprocedural myocardial injury (peak troponin I > 2 µg/l), lower body surface area was found to be the only significant variable (p=0,010). In the multivariate analysis model for the same outcome in which body surface area and administration’s mode of anaesthetic were included (basic tested group), it was found that a higher body surface area (OR = 0,020, 95% CI = 0,001-0,401, p = 0,011), and SEVO pre group in regard to SEVO post group (OR = 0,277, 95% CI = 0,078-0,977, p = 0,046) were significant favourable predictors.
This research did neither establish unequivocally the cardioprotective effect of sevoflurane when it was administered before the onset of ischaemia compared to the use of propofol as an anaesthetic, nor when compared to sevoflurane administered after the ischaemic period. Some of the results indicate a possible cardioprotective effect of sevoflurane when it was administered before ischaemia compared to sevoflurane when it was administered after ischaemia, in terms of a lower periprocedural myocardial injury.
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