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Anesth Analg 2006;103:289-296
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000226097.22384.f4

CARDIOVASCULAR ANESTHESIA

Cardioprotective Properties of Sevoflurane in Patients Undergoing Aortic Valve Replacement with Cardiopulmonary Bypass

Stefanie Cromheecke, MD*, Veronik Pepermans, MD*, Ellen Hendrickx, MD*, Sur Lorsomradee, MD*, Pieter W. ten Broecke, MD*, Bernard A. Stockman, MD{dagger}, Inez E. Rodrigus, MD, PhD{dagger}, and Stefan G. De Hert, MD, PhD*

From the Departments of *Anesthesiology and {dagger}Cardiac Surgery, University Hospital Antwerp, Belgium.

Address correspondence and reprint requests to Stefan G. De Hert, MD, PhD, Department of Anesthesiology, University Hospital Antwerp, Wilrijkstraat 10, B-2650 Edegem, Belgium. Address e-mail to stefan.dehert{at}ua.ac.be.


   Abstract
Top
 Abstract
Introduction
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
In coronary surgery patients the use of a volatile anesthetic regimen with sevoflurane was associated with a better recovery of myocardial function and less postoperative release of troponin I. In the present study we investigated whether these cardioprotective properties were also apparent in the cardiac surgical setting of aortic valve replacement (AVR) surgery for the correction of aortic stenosis. Thirty AVR surgery patients were randomly assigned to receive either target-controlled infusion of propofol or inhaled anesthesia with sevoflurane. Cardiac function was assessed perioperatively using a pulmonary artery catheter. Perioperatively, a high-fidelity pressure catheter was positioned in the left ventricle. Postoperative concentrations of cardiac troponin I were followed for 48 h. After cardiopulmonary bypass (CPB), stroke volume and dP/dtmax were significantly higher in the patients with sevoflurane. Post-CPB, the effects of an increase in cardiac load on dP/dtmax were similar to pre-CPB in the sevoflurane group (1.0 % ± 5.4% post-CPB versus 1.3% ± 8.6% pre-CPB) but more depressed in the propofol group (–8.2% ± 4.4% post-CPB versus 0.1% ± 4.9% pre-CPB). The rate of relaxation was significantly slower post-CPB in the propofol group. Postoperative levels of troponin I were significantly lower in the sevoflurane group. Our data indicate that the use of a volatile anesthetic regimen in AVR surgery was associated with better preservation of myocardial function and a reduced postoperative release of troponin I.


   Introduction
Top
 Abstract
 Introduction
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Cardiac surgery is associated with a transient depression of myocardial function postoperatively (1). Recently, several studies have reported cardioprotective effects of volatile anesthetics in coronary surgery patients. In these studies, the use of a volatile anesthetic resulted in better myocardial performance and decreased release of troponin I postoperatively. However, these studies involved coronary surgery that was performed either by using intermittent cross-clamping (2–4) or off-pump surgery (5–6).

Patients undergoing aortic valve replacement (AVR) surgery for aortic stenosis do not have coronary stenosis requiring coronary surgery. Instead they have left ventricular (LV) hypertrophy (LVH), which may render cardioprotection with cardioplegia unpredictable. This population of patients may be exposed to myocardial ischemia as a result of aortic cross-clamping and thus cardioprotection by inhaled anesthetics would be valuable in this setting.

We hypothesized that if the cardioprotective effects observed with a volatile anesthetic regimen were related to a direct effect of the anesthetic drug on the extent of postoperative myocardial dysfunction and/or damage, this phenomenon should also be observed in other types of cardiac surgery involving a prolonged period of myocardial ischemia during the period of aortic cross-clamping. To test this hypothesis we compared preoperative and postoperative cardiac function and postoperative troponin I release in patients undergoing AVR anesthetized either with an IV anesthetic regimen or with a volatile anesthetic regimen.


   METHODS
Top
 Abstract
 Introduction
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
The study was approved by the institutional Ethical Committee (University Hospital Antwerp, Edegem, Belgium) and written informed patient consent was obtained. Thirty patients scheduled to undergo elective AVR for aortic stenosis were enrolled in this study. Preoperative exclusion criteria included previous coronary surgery or valve replacement, combined operations (simultaneous valve repair and coronary surgery, carotid endarterectomy, or LV aneurysm repair), critical aortic stenosis (aortic valve area >0.5 cm2, unstable angina, occurrence of coronary stenosis on coronary angiography, documented myocardial infarction within the previous 6 wk, active congestive heart failure, hemodynamic instability with the need for medical or mechanical support, severe hepatic disease (alanine aminotransferase or aspartate aminotransferase >150 U/L), renal insufficiency (creatinine concentration >1.5 mg/dL), severe chronic obstructive pulmonary disease (forced expired volume in 1 s <0.8 L), or history of neurologic disturbance.

Antiplatelet therapies were stopped 1 wk before the operation and replaced by a SC daily dose of nadroparine (Fraxiparine®; Sanofi-Synthelabo, Brussels, Belgium), 0.6 mL (7500 U anti-Xa). Sulfonylurea derivatives were stopped 2 days before the operation and replaced by insulin therapy if necessary.

Patients were randomly allocated to two different anesthetic protocols. A computer-generated random code determined which anesthetic protocol was identified by each treatment number. Subjects were assigned the treatment numbers in ascending chronological order of admission in the study. The participant randomization assignment was concealed in an envelope until the start of anesthesia.

All preoperative cardiac medication except for angiotensin-converting enzyme inhibitors and the angiotensin II receptor antagonists was continued until the morning of surgery. In the operating room patients received routine monitoring, including 5-lead electrocardiogram, radial and pulmonary artery catheters with continuous cardiac output measurement, pulse oximetry, capnography, and blood and urine bladder temperature monitoring. In group A, anesthesia was induced with a continuous infusion of remifentanil at 0.4 µg ·kg–1 ·min–1 and a target-controlled infusion of propofol set at a target plasma concentration of 2 µg/mL. In group B, anesthesia was induced with a continuous infusion of remifentanil at 0.4 µg ·kg–1 ·min–1, sevoflurane was initially started at 8% and when the patient was anesthetized, decreased to a concentration of 0.5%–1% end-tidal. In all groups, muscle paralysis was obtained with pancuronium bromide 0.1 mg/kg. In group A, anesthesia was maintained with remifentanil 0.2–0.4 µg ·kg–1 ·min–1 and target-controlled infusion of propofol set at a plasma target concentration of 2–4 µg/mL. In group B, anesthesia was maintained with remifentanil 0.2–0.4 µg ·kg–1 ·min–1 and sevoflurane 0.5%–1% end-tidal. Depth of anesthesia was determined with bispectral index (BIS XP®; Aspect Medical Systems, Newton, MA) and aimed at a BIS between 40 and 50 during surgery. Standard median sternotomy and pericardiotomy were performed. After administration of 300 U/kg heparin, the aortic cannula was secured in place. Activated coagulation time was kept above 450 s throughout cardiopulmonary bypass (CPB). Routine surgical techniques and cardioprotective strategies were used in all patients in both groups. This included IV administration of 2 g methylprednisolone after induction of anesthesia and large-dose aprotinin (Trasylol®; Bayer, Leverkusen, Germany) scheme (bolus of 2 x 106 kallikrein-inhibiting units (KIU) followed by a continuous infusion of 5 x 105 KIU/h until the end of CPB plus an additional 2 x 106 KIU in the priming fluid of the CPB circuit). Cardioprotection was obtained with cardioplegic solution (Custodiol®; HTK – Bretschneider solution for cardioplegia, dr Franz Köhler Chemie GMBH, Alsbach-Hähnlein, Germany). During CPB, anesthesia was maintained in group A with remifentanil (0.4 µg ·kg–1 ·min–1) and target-controlled infusion of propofol (2–4 µg/mL). In group B, anesthesia was maintained with remifentanil (0.4 µg ·kg–1 ·min–1) and sevoflurane (0.5%–1% measured at the outlet of the oxygenator) through the fresh gas flow on the CPB circuit. Body temperature was cooled to 28°C on CPB. After the surgical procedure, the heart was reperfused (reperfusion time was set at 50% of the aortic cross-clamp time in all patients) and the bladder was rewarmed to a temperature of 35°C. The heart was paced in atrioventricular mode at a rate of 90 bpm and the patients were separated from CPB. Post-CPB, anesthesia was maintained with remifentanil (0.4 µg ·kg–1 ·min–1) combined with propofol (2–4 µg/mL) in group A and sevoflurane (0.5%–1% end-tidal) in group B. After removal of the aortic cannula, heparin activity was neutralized with protamine at a ratio of 1 mg protamine for 100 U heparin. Protamine administration was further guided by activated coagulation time measurements aiming at a value of 140 s. At the end of the procedure, patients were transferred to the intensive care unit (ICU), where they were kept sedated for 4 h with a continuous infusion of remifentanil 0.3 µg ·kg–1 ·min–1 and propofol at 2 µg/mL. The patients were then weaned from the ventilator and tracheally extubated.

In each patient, a sterilized, prezeroed electronic tip manometer (MTCP3Fc catheter; Dräger Medical Electronics, Best, The Netherlands; frequency response = 100 KHz) was inserted in the ventricle. The catheter was connected to a Hewlett Packard monitor (HP78342A; Hewlett Packard, Brussels, Belgium). The output signals of the pressure transducer system were digitally recorded together with the electrocardiographic signals at 1-ms intervals (Codas; DataQ, Akron, OH). Zero and gain-setting of the tip manometer were checked against a high-fidelity pressure gauge (Druck Ltd., Leicester, UK) after removal.

For the invasive measurements and all measurements post-CPB, heart rate was kept constant by atrioventricular sequential pacing at a rate of 90 bpm. All measurements were obtained with mechanical ventilation suspended at end-expiration. The measurements consisted of recordings of consecutive electrocardiographic and LV pressure tracings during an increase of systolic and diastolic blood pressures obtained by raising the caudal part of the surgical table by 45 degrees, thereby raising the legs. Leg elevation resulted in a rapid beat-to-beat increase in ventricular pressures (Fig. 1).


Figure 15
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  		Figure 1. Leg elevation resulted in a rapid beat-to-beat increase in ventricular pressure.

 

A first set of measurements was obtained before CPB. After this measurement, the catheter was removed, the venous cannula inserted, and CPB initiated. After a stabilization period of 15 min to allow for recovery of systolic and diastolic data after CPB, the post-CPB measurements were obtained (7).

In this study, filling pressures were kept constant (central venous pressure >10 mmHg and pulmonary capillary wedge pressure >12 mm Hg) throughout the entire observation period by the administration of IV fluids (crystalloids and hydroxyethyl starches). Hypotension was defined as a mean arterial blood pressure <60 mm Hg. Inotropic support was provided with dobutamine and vasopressive support with norepinephrine (4).

Global hemodynamic data (mean arterial blood pressure, mean pulmonary artery pressure, central venous pressure, cardiac output) were recorded just before the start of surgery, before the start of CPB, 15 min after the end of CPB, at the end of the operation, at arrival at the ICU, and 6 h and 12 h later in the ICU.

Ventricular data were recorded before and 15 min after the end of CPB. End-diastolic pressure (EDP) was timed at the peak of the R-wave on the electrocardiogram. The effects of leg elevation on cardiac function in the different conditions of cardiac load were evaluated by the changes in EDP, peak ventricular pressure, ventricular pressure at dP/dtmin (end-systolic pressure [ESP]), and dP/dtmax before and at the end of leg elevation. The effects of leg elevation on rate of ventricular pressure decrease were evaluated by dP/dtmin and the time constant {tau} of isovolumic relaxation. {tau} was calculated based on the monoexponentional model with a nonzero asymptote using LV pressure values from dP/dtmin to a pressure 10 mmHg above LVEDP (8,9). The following equation was used: ln Pt = ln Po – time/{tau}. Time constant {tau} was linearly fit to the corresponding ESP, and the slope R (ms/mm Hg) of this relation was calculated. R quantified changes in {tau}, induced by changes in ESP and quantified afterload dependence of the rate of LV pressure decrease. At least 10 consecutive beats were taken for the calculation of R. Sample correlation coefficients of the ESP-{tau} relationships yielded values of more than 0.92 in all patients. Analysis of cardiac performance data was completed in a blinded fashion with the person completing the analysis having no knowledge of the anesthetic regimen used.

Blood was sampled in all patients for determination of cardiac troponin I. These samples were obtained before the start of surgery (base), at arrival in the ICU (T0) and at 6, 12, 24, and 48 h (T6, T12, T24, and T48) after arrival in the ICU. Troponin I was measured using an immunoassay method (Vitros ECI®; Orthoclinical Diagnostics, Beerse, Belgium). The limit of quantification of cardiac troponin I determination was 0.04 ng/mL. When values below the detection limit were reported, zero was retained as the value. The coefficient of variation of the measurements is 15% for troponin I values up to 0.06 ng/mL, 7% for values between 0.77 and 3.37 ng/mL, and 5% for values above 3.37 ng/mL.

Sample size of the study was calculated based on the two outcome variables also used in previous studies (2–3), a biochemical marker of postoperative myocardial damage: cardiac troponin I level and a measure of myocardial function: the dP/dtmax post-CPB. For the cardiac troponin I level, a minimum detected difference of 2 ng/mL between the 2 groups was considered a clinically important difference. For a power of 0.8 and {alpha} = 0.05, a sample size of 10 patients in each group was calculated to be appropriate. For the dP/dtmax post-CPB, a minimum detected difference of 100 mm Hg/s between the 2 groups was considered statistically significant. These differences together with the sd were based on previous observations (2–3). For a power of 0.8 and {alpha} = 0.05, a sample size of 14 patients in each group was calculated to be appropriate.

Patient characteristics were compared using Fisher’s exact test and a one-way analysis of variance where appropriate. Medians were compared using the Kruskal-Wallis one-way analysis of variance test on the ranks. Hemodynamic data were tested for normal distribution. Data before and after CPB were compared using analysis of variance for repeated measurements. Posttest analysis was performed using the Bonferroni-Dunn test. Relations in hemodynamic variables were analyzed using linear regression analysis computing Pearson’s correlation coefficient. Slopes and intercepts of the relationships before and after CPB within each group were compared using Student’s t-test. All hemodynamic data were expressed as mean ± sd. Statistical significance was accepted at P < 0.05. All P values were two-tailed.


   RESULTS
Top
 Abstract
 Introduction
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
There was no significant difference in the characteristics of the patients (Table 1). BIS values were similar in both groups. Surgery and postoperative recovery were uneventful in all patients. None of the patients developed myocardial infarction postoperatively. Six patients in the propofol group developed atrial fibrillation after 24 h postoperatively compared with 1 patient in the sevoflurane group (P < 0.05).


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  		Table 1. Patient Characteristics

 

Mean pulmonary artery pressure and central venous pressure were kept stable throughout the observation period. Post-CPB and at the end of the operation, stroke volume index was significantly lower in the propofol group, whereas it remained stable in the sevoflurane group. From timepoint ICU 6 the transient decrease in stroke volume index in the propofol group had normalized (Table 2).


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  		Table 2. Preoperative and Postoperative Hemodynamic Data

 

Need for inotropic (4 patients in the propofol group versus 1 patient in the sevoflurane group) and vasoconstrictive (6 patients in the propofol group versus 2 patients in the sevoflurane group) support was not significantly different between groups after CPB, nor in the ICU (inotropic support: 6 patients in the propofol group versus 3 patients in the sevoflurane group; vasoconstrictive support: 8 patients in the propofol group versus 4 patients in the sevoflurane group).

The arterial blood gas values and hemoglobin concentrations at the different times were similar in both groups.

LVEDP was significantly increased after CPB in both groups. LV dP/dtmax decreased post-CPB in the propofol group but not in the sevoflurane group. ESP decreased post-CPB in both groups. Post-CPB, the time constant of isovolumic relaxation ({tau}) was increased in the propofol group but not in the sevoflurane group (Table 3).


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  		Table 3. Left Ventricular Pressure Data Before and After CPB

 

Leg elevation increased EDP. The increase in EDP was similar before and after CPB in both groups (Table 4). Before CPB, the increase in dP/dtmax with leg elevation was similar in both groups (0.1% ± 4.9% versus 1.3% ± 8.6%). After CPB, the effects of leg elevation on dP/dtmax significantly differed between groups (P < 0.05) (–8.2% ± 4.4% in the propofol group versus 1.0% ± 5.4% in the sevoflurane group (Fig. 2). Peak LV pressure increased similarly with leg elevation in both groups before CPB. The increase in ESP with leg elevation was similar for both groups before and after CPB. The increase in {tau} with leg elevation was similar before and after CPB in the sevoflurane group but not in the propofol group. In the propofol group the increase in {tau} with leg elevation was significantly more pronounced than before CPB. Load dependence of LV pressure decrease (R) was similar in both groups before CPB. After CPB, R was increased in the propofol group but not in the sevoflurane group.


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  		Table 4. Changes in Left Ventricular Pressure Data with Leg Elevation Before and After CPB

 

Figure 25
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  		Figure 2. Percentage change in maximal rate of pressure development (dP/dtmax) with leg elevation before and after cardiopulmonary bypass (CPB) with the different anesthetic regimens. With sevoflurane the response to leg elevation is similar before and after CPB. With propofol, there is a decrease in dP/dtmax with leg elevation after CPB, whereas there was an increase in dP/dtmax before CPB.

 

Variables of contraction ({Delta} dP/dtmax) and relaxation (R) were coupled. A close relationship was found between individual changes in dP/dtmax and R in all experimental conditions (Fig. 3). Before CPB, the relationship between changes in dP/dtmax and the individual values of R were comparable in both groups. (propofol group: y = 0.47 – (0.009*x), r = 0.89, P < 0.001; sevoflurane group: y = 0.39 – (0.007*x), r = 0.88, P < 0.001). After CPB, the relationship between changes in dP/dtmax and individual values of R was not significantly altered in the sevoflurane group, but in the propofol group both slope and intercept differed significantly from before CPB (propofol group: y = 0.39 – (0.007*x), r = 0.88, P = 0.003; sevoflurane group: y = 0.38 – (0.005*x), r = 0.74, P < 0.001).


Figure 35
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  		Figure 3. Plots relating individual values of R (load dependence of left ventricle pressure decrease) to corresponding changes in dP/dtmax with leg elevation. On each plot, the data before (filled circles) are compared with the data after (open triangles) cardiopulmonary bypass (CPB). For sevoflurane, the relationships are similar before and after CPB. With propofol both intercept as slope have changed after CPB.

 

Figure 4 illustrates the evolution of cardiac troponin I levels during the first 48 h postoperatively. Troponin I levels increased in all patients throughout the observation period. From T6, troponin I levels were significantly higher in the propofol group compared with the sevoflurane group.


Figure 45
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  		Figure 4. Evolution of cardiac troponin I in both groups before surgery (base), at arrival in the intensive care unit (T0), and after 6 (T6), 12 (T12), 24(T24), and 36 (T36) h. Concentration was significantly larger in the propofol group at T6, T12 and T24.

 

All patients in both groups were weaned from the ventilator in the first 6 h after arrival in the ICU. In the sevoflurane group, the duration of the stay in the ICU was significantly less than the propofol group (45.0 ± 4.5 h in the propofol group versus 23.0 ± 4.6 h in the sevoflurane group) (P < 0.005), but the difference in hospital length of stay between groups did not reach statistical significance (9.7 ± 4.6 days in the propofol group versus 7.0 ± 0.8 days in the sevoflurane group).


   DISCUSSION
Top
 Abstract
 Introduction
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The results of the present study indicated that in AVR the patients anesthetized with sevoflurane had a better preservation of cardiac function after surgery and smaller concentrations of postoperative cardiac troponin I than the patients anesthetized with propofol.

Many factors determine the occurrence of myocardial damage and outcome after cardiac surgery. Among these, patient characteristics and surgery-related events are the most common reasons for possible complications. Patient characteristics were similar in both groups, as were type of cardioprotection, duration of aortic cross-clamp, and CPB time. This suggested that the differences in cardiac function between groups were not caused by differences in patient characteristics and intraoperative events but seemed instead to be related to the choice of the anesthetic drug.

Experimental observations have extensively shown that volatile anesthetics administrated before and after ischemia improve cardiac function. These properties have been attributed to an anesthetic preconditioning effect (10–15), but volatile anesthetics may also have a protective action when administrated only during the reperfusion period (16–18).

In contrast to the experimental studies, the results from clinical studies on the cardioprotective effects of anesthetic drugs are less straightforward. Preconditioning protocols showed variable results on postoperative cardiac function and variables of myocardial damage (19–23). Although other studies have analyzed the effect of administration of volatile anesthetics during ischemia (24) and during early reperfusion (Wolfgang Buhre, MD, PhD, University of Aachen, Aachen, Germany, PhD thesis, 2001) and observed some beneficial effects, the most straightforward protective effects were observed when the volatile anesthetic was administered throughout the entire procedure (2–6,25).

This issue was debated in a study by De Hert et al. (25) that looked at the effects of the different modalities of administration of the volatile anesthetic on cardiac function after CPB. This study clearly demonstrated that the protective effects were most pronounced when the volatile anesthetic was administered during the whole procedure.

All the currently available clinical data were obtained in specific settings of coronary surgery either on CPB with the use of intermittent cross clamping (2–4), or in off-pump coronary artery bypass (5) and minimally invasive direct coronary artery bypass (6) surgery. It cannot be excluded that in these protocols part of the protective effect could also be related to an ischemic preconditioning effect. The present study extends the observation obtained in coronary surgery patients that the use of a volatile anesthetic results in better cardiac function and less evidence of myocardial damage to a patient population with no coronary stenosis. Patients undergoing isolated AVR for aortic stenosis do not have coronary stenosis requiring coronary artery bypass grafting. However, if they have LV hypertrophy, it may render cardioprotection with cardioplegia unpredictable. Subendocardial ischemia is always a concern. Regardless, this population of patients will be exposed to myocardial ischemia because of aortic cross-clamping. Cardioprotection by volatile anesthetics would be valuable in these patients. Only one report by Van der Linden et al. (26) also mentioned a beneficial effect of the use of sevoflurane during AVR. In these patients, a difference was seen in postoperative troponin T release between the patients anesthetized with an IV drug protocol and those anesthetized with inhaled sevoflurane. Although these observations lack the power of a prospective randomized study, they suggest the beneficial effects of a volatile anesthetic regimen in valve surgery also.

The results of the present study confirmed this protective effect because a preserved cardiac function and less postoperative release of troponin I was observed in AVR patients anesthetized with sevoflurane.

A number of methodologic issues deserve attention. Propofol and sevoflurane were used as a part of a multidrug anesthetic regimen. Opioids also have been shown to have a preconditioning effect (27,28). In the present study, anesthesia was based in part on a continuous infusion of remifentanil. However, the dosages of remifentanil (and other drugs used in the present study) were similar in both groups, suggesting that the observed differences in cardiac function between groups were related to the choice between sevoflurane and propofol. In both groups, a number of patients needed inotropic and vasoconstrictive support after CPB and in the first hours in the ICU. Obviously, this treatment influenced the analysis of cardiac function in both groups. The current data may, therefore, not be interpreted as the sole effects of propofol or sevoflurane on cardiac function after CPB.

In conclusion, in AVR surgery patients, the use of a volatile anesthetic regimen was associated with preserved cardiac function after CPB and less postoperative release of troponin I compared with a total IV anesthetic regimen. These data indicate that the clinical protective properties of volatile anesthetics observed in coronary surgery are also present during AVR surgery. Further studies should determine whether these properties are also applicable to for other types of cardiac surgery.


   Footnotes
 
Accepted for publication April 10, 2006.


   REFERENCES
Top
 Abstract
 Introduction
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press