Warm induction cardioplegia and reperfusion dose influence the occurrence of the post CABG TnI level
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《血管的通路杂志》
a Department of Cardiopulmonary Bypass, Cardiovascular Institute & Fuwai Hospital, PUMC & CAMS, Beijing, China
b Department of Pediatrics, Pediatrics Penn State College of Medicine-085, 500 University Drive, P.O. Box 850, Hershey, PA 17033-0850, USA
c Department of Cardiac Surgery, Cardiovascular Institute & Fuwai Hospital, PUMC & CAMS, Beijing, China
d Department of Anesthesiology, Cardiovascular Institute & Fuwai Hospital, PUMC & CAMS, Beijing, China
Abstract
As a new biochemical marker cardiac troponin-I (CTnI) is a more sensitive and specific marker for detection of differences in myocardium injuries than other chemical enzymes. This study investigates the effect of warm induced and reperfusion blood cardioplegia on the release of troponin-I during the CABG. In our research, 24 three-vessel coronary artery disease (CAD) patients underwent CABG and were divided into two groups randomly: Group of warm induction and reperfusion blood cardioplegia (Group W N=12); Group of simple warm induction and no reperfusion (Group C N=12). The effect of myocardium protection of the two methods of myocardium protection were evaluated by clinical outcome, CTnI. Serial venous blood samples were obtained before and after surgery. In both groups, there were no differences in operative parameters. The level of CTnI increased from postoperative 6 h (P<0.05), reached peak in 2472 h and recovered postoperatively on 6th day in both groups. Compared with group C, the plasma concentrations of CTnI in group W were significantly lower at 6 h, 24 h and 72 h (P<0.01). The results suggest that the method of warm induction and reperfusion blood cardioplegia reduces the leakage of CTnI than group of simple warm blood cardioplegia in CABG patients.
Key Words: Myocardial protection; Troponin-I; Cardioplegia; Cardiopulmonary bypass
1. Introduction
In a previous prospective randomized study [1] involving 28 patients with myocardial protection undergoing an elective first cardiac operation, we evaluated the myocardial protection of warm blood cardioplegia induction and simple cool blood cardioplegia induction during cardiopulmonary bypass and using cardiac troponin T (CTnT) as the criteria for evaluating the adequacy of myocardial protection. The results clearly showed, compared with cold blood cardioplegia induction, that warm blood cardioplegia induction provides better myocardial protection during cardiopulmonary bypass. Then we tried to find out another way to do it better. We applied both the warm induction and reperfusion during the CABG, compared with the simple warm induction without reperfusion and using troponin-I as the marker for evaluating the results of the myocardial injury during CABG.
Warm blood cardioplegia using the antegrade intermittent technique was more recently proposed to overcome the disadvantage of a continuous blood flow in the operative field.
Also, cardiac troponin-I (CTnI) has been introduced in clinical work to test myocardial injury, showing higher specificity and sensitivity than other routinely used biochemical markers of cardiac damage and also it has been used to assess the effectiveness of different methods of myocardial protection [2,3]. The purpose of this study was, therefore, to compare warm induction and reperfusion with simple warm blood cardioplegia using troponin-I to assess the injury to cardiac tissues.
2. Methods
2.1. Patients selection
The study was approved by Fuwai Heart Hospital, Beijing, China. All the patients were operated by the same group in Fuwai hospital, including the surgeons, anesthesiologist and perfusionist. From May 2002 to October 2002, 24 CAD patients operated on CABG were randomized to warm blood cardioplegia (group W; n=12), simple warm blood cardioplegia induction (group C; n=12). Preoperative and operative clinical parameters are shown in Table 1. Randomization was performed by the method described by Altman and Bland [4]. All the patients were three-vessel coronary artery disease without valve disease with normal left ventricle function, and the first time to receive CABG. Not included were patients with an ejection fraction below 0.30 and recent myocardial infarction (<2 months). The left internal mammary artery was used in all patients.
2.2. Cardiopulmonary bypass
The Stockert-II heart-lung machine with roller pump and Medtronic membrane oxygenator Affinity was used. Tubing pack with cardioplegia delivery (blood: crystalloid=4:1) system (Perfect, Beijing, China), and an arterial filter (Xi Jing, Xi an, China). Non-pulsatile CPB was used at a flow rate of 2.63.0 l/min/kg. Mean arterial pressure was maintained 6585 mmHg) by adjusting blood flow rate. Anesthesia Standard general anesthesia was achieved in all groups with fentanyl, isofurane and enfurane.
2.3. Method of myocardium protection
Institution cardioplegia was administered in both groups. The cardioplegia were administered every 30 min for a period of 2 min with the same infusion rate as the first time. Group of warm induction and reperfusion blood cardioplegia (Group W, n=12); Group of simple warm blood cardioplegia induction (Group C, n=12). The route of delivery was exclusively antegrade in the two groups. The temperature of cardioplegia ranged from 4 to 6 °C in groups and was applied during clamp off. In both groups the heart was induced by the warm blood cardioplegia (35 °C) into the line, during clamping using the cold blood cardioplegia maintaining. Also before clamp off, in Group W the warm reperfusion was applied. Warm reperfusion was started immediately after the last distal anastomosis, and was performed with a constant flow rate of 150 ml/min. Warm reperfusion was carried out in two steps and took 6 min: (1) during the first 2 min, the blood hyperkalemic mixture defined above was injected and progressively rewarmed to 20 °C, and (2) during the last 4 min, the infusate used was exclusively composed of oxygenated blood, which increased to 35 °C at the end of the reperfusion.
2.4. Laboratory assay
Plasma level marker of myocardial damage (CTnI) was obtained from serial venous blood samples before induction, after cardiopulmonary bypass (CPB), postoperative 6 h, 24 h, 72 h and 6th day, respectively. Cardiac troponin-I concentrations were measured by a specific immunoenzymometric assay developed. Test sample was incubated with monoclonal antibody 8E1 for 15 min. After washing, following the addition of a substrate (tetramethylbenzydine), enzyme activity was measured. The reaction was stopped by adding H2SO4 and the absorbance was read at 450 nm on the status spectrophotometer.
2.5. Electrocardiogram
A 12-lead electrocardiogram was recorded preoperatively at 2 h, at 2 h postoperatively and then daily postoperatively. The electrocardiographic diagnosis criteria for perioperative myocardial infarction (PMI) were new Q-waves >0.04 ms or a reduction in R-waves >25% in at least two leads.
2.6. Statistical analysis
Statistical analysis was performed with SPSS statistical software. One-way analysis of variance (ANOVA) was performed to test the effect of the type of cardioplegia and time on CTnI concentration. Two-way analysis of covariance with repeated measures was performed to test the effect of the type of cardioplegia on CTnI concentration. Statistical significance was accepted at a P<0.05. All data are expressed as mean±standard deviation (S.D.) (Table 2).
3. Results
Preoperative, operative, and postoperative data are shown in Table 1. The preoperative status was nearly identical in the two groups according to age, sex ratio, weight, C/T and EF%.
In the operative data there was no significant difference between the two groups in cardiopulmonary bypass time, clamp time, graft number, total amount of cardioplegic solution, lowest temperature during bypass and auto-resuscitation.
All patients survived, and no differences were observed in groups with regard to postoperative incidences of renal, respiratory, and neurological complications. The level of CTnI in both groups (group W 5.21±0.48 μg/l and group C 6.20±1.15 μg/l) increased from postoperative 6 h (P<0.05) compared with before induction (group W 0.43±0.27 μg/l, group C 0.40±0.29 μg/l), and this indicates that in both groups the myocardium was injured. The value reached peak in 2472 h and recovered on the postoperative 6th day. Compared with group C, the plasma concentration of CTnI in group W was significantly lower at 6, 24 and 72 h (P<0.01) (Fig. 1).
4. Discussion
Cardiac troponin-I is a specific and sensitive marker of myocardial injury. CTnI was found exclusively in cardiac muscle and clearly was different from skeletal isoforms, so making it a specific marker for myocardial damage. This specificity is particularly beneficial for patients undergoing cardiac surgery because the value of measurements of serum creatinine kinase and lactate dehydrogenase is limited by enzyme release from noncardiac tissues [5,6]. The CTnI increases in all patients after cardiac surgery. This fact shows the inevitable myocardial damage caused by myocardial arrest. The CTnI measurements can detect these small differences in myocardial tissue damage. We have already used it to assess the myocardium injury in our research [7]. The purpose of our present prospective randomized study was to determine the extent to which warm induction and reperfusion cardioplegia, and simple cool blood cardioplegia, contribute to the improvement of myocardial protection using CTnI as the criteria for evaluating the adequacy of myocardial protection.
In a previous study, cold blood cardioplegia with warm induction was clearly better than simple cool blood cardioplegia induction [1]. In our present study, we add the warm reperfusion before the clamp off. Comparison of the results of these two methods shows that with the addition of warm reperfusion to simple warm cardioplegia induction makes it as effective.
Therefore, it is acceptable that hypothermia has been routinely used as it reduces oxygen demand by decreasing the basal metabolic rate. However, hypothermia may have side effects like ‘cold contracture’ of microcirculation in coronary arteries to cause additional ischemia and reperfusion injury [8], rapid cooling during cardioplegia increasing left ventricular pressure, [Ca2+]i and coronary resistance, and is energy consuming [9] inhibiting the sodium pump to cause edema, and shifting the oxygen–hemoglobin dissociation curve leftward [10]. So warm induction reduces damage by avoiding cool contracture. In our previous study we learnt that warm induction is better than the cool blood induction. We could hypothesise that with the additional warm reperfusion before the clamp off, the better the result we could get, because of washing out the substances produced by the anaerobic metabolism and by bringing free radical scavengers to a heart at rest. Kawasuji's results suggest that terminal warm blood cardioplegia also may enhance myocardial reoxygenation and optimize the oxygen supply/demand balance of the myocardium during reperfusion [11].
In Teoh's study [12] he compared cold blood cardioplegia (11 patients) to cold blood cardioplegia followed by a ‘hot shot’ (9 patients). They showed that with the hot shot, myocardial metabolic recovery was improved, high-energy phosphates were better preserved, metabolic response to stress was normal, and diastolic function was preserved. Reperfusion damage is thought to be caused in part by oxygen free radicals produced during the early phases of reoxygenation. For Teoh and colleagues, the hot shot improves cold blood cardioplegia protection by washing out the products of anaerobic metabolism. In Caputo's study [13], thirty-five patients undergoing primary elective coronary revascularisation were randomized to one of two different techniques of myocardial protection. The data suggest that warm blood hyperkalemic reperfusion hot shot prevents myocardial metabolic derangement seen during coronary artery surgery.
Our data showed a significant higher grade of myocardial protection exerted by warm induction and reperfusion in comparison to simple warm blood cardioplegia induction. This finding supports the hypothesis of a high protective effect of warm induction and reperfusion. Warm reperfusion accelerated myocardial metabolic recovery, preserved high-energy phosphates, improved the metabolic response to postoperative hemodynamic stresses, and reduced left atrial pressures.
In summary, our study showed that with the additional warm reperfusion to simple warm cardioplegia induction offers advantage in low risk patients. This conclusion cannot be extended to high risk patients (e.g. redo CABG, combined surgery, ejection fraction under 0.30, unstable angina). Whether the higher release of CTnI in both the groups might be predictive of an adverse clinical outcome in a larger patient population or in higher-risk patients remains to be investigated.
References
Li S, Long C, Chang Q, Zhang D, Strickler AG, Nussmeier NA. Myocardial protection of warm blood cardioplegic induction during cardiopulmonary bypass. J Extra Corpor Technol 2001; 33:2106–110.
Sadony V, Korber M, Albes G, Podtschaske V, Etgen T, Trosken T, Ravens U, Scheulen ME. Cardial troponin-I plasma levels for diagnosis and quantitation of perioperative myocardial damage in patients undergoing coronary artery bypass surgery. Eur J Cardiothorac Surg 1998; 13:157–62.
Etievent JP, Chocron S, Toubin G, Taberlet C, Alwan K, Clement F, Cordier A, Schipman N, Kantelip JP. Use of cardiac troponin-I as a maker of perioperative myocardial ischemia. Ann Thorac Surg 1995; 59:51192–1194.
Altman DG, Bland JM. How to randomize. Br Med J 1999; 319:703–704.
Mair J, Wagner I, Puschendorf B, Mair P, Lechleitner P, Dienstl F, Calzolari C, Larue C. Cardiac troponin-I to diagnose myocardial injury. Lancet 1993; 341:838–839.
Adams JE 3rd, Sicard GA, Allen BT, Bridwell KH, Lenke LG, Davila-Roman VG, Bodor GS, Ladenson JH, Jaffe AS. Cardiac troponin-I a marker with high specificity for cardiac injury. Circulation 1993; 88:101–106.
Ji BY, Feng ZY, Liu JP, Long C. Myocardial protection related to magnesium content of cold blood hyperkalemic cardioplegic solutions in CABG. Extra Corpor Technol 2002; 34:2107–110.
Cannon MB, Vine AJ, Kantor HL, Lahorra JA, Nickell SA, Hahn C, Allyn JW, Teplick RS, Titus JS, Torchiana DF. Warm and cold blood cardioplegia. Comparison of myocardial fuction and metabolism using 31P magnetic resonance spectroscopy. Circulation 1994; 90:328–338.
Lahorra JA, Torchiana DF, Tolis G Jr, Bashour CA, Hahn C, Titus JS, Geffin GA, Daggett WM. Rapid cooling contracture with cold cardioplegia. Ann Thorac Surg 1997; 63:51353–1360.
Buckberg GD. Update on current techniques of myocardial protection. Ann Thorac Surg 1995; 60:805–814.
Kawasuji M, Tomita S, Yasuda T, Sakakibara N, Takemura H, Watanabe Y. Myocardial oxygenation during terminal warm blood cardioplegia. Jpn Ann Thorac Surg 1998; 65:51260–1264.
Teoh KH, Christakis GT, Weisel RD, Fremes SE, Mickle DA, Romaschin AD, Harding RS, Ivanov J, Madonik MM, Ross IM. Accelerated myocardial metabolic recovery with terminal warm blood cardioplegia. J Thorac Cardiovasc Surg 1986; 91:888–895.
Caputo M, Dihmis WC, Bryan AJ, Suleiman MS, Angelini GD. Warm blood hyperkalaemic reperfusion (‘hot shot’) prevents myocardial substrate derangement in patients undergoing coronary artery bypass surgery. Eur J Cardiothorac Surg 1998; 13:5559–564.(Bingyang Ji, Mingzheng Li)
b Department of Pediatrics, Pediatrics Penn State College of Medicine-085, 500 University Drive, P.O. Box 850, Hershey, PA 17033-0850, USA
c Department of Cardiac Surgery, Cardiovascular Institute & Fuwai Hospital, PUMC & CAMS, Beijing, China
d Department of Anesthesiology, Cardiovascular Institute & Fuwai Hospital, PUMC & CAMS, Beijing, China
Abstract
As a new biochemical marker cardiac troponin-I (CTnI) is a more sensitive and specific marker for detection of differences in myocardium injuries than other chemical enzymes. This study investigates the effect of warm induced and reperfusion blood cardioplegia on the release of troponin-I during the CABG. In our research, 24 three-vessel coronary artery disease (CAD) patients underwent CABG and were divided into two groups randomly: Group of warm induction and reperfusion blood cardioplegia (Group W N=12); Group of simple warm induction and no reperfusion (Group C N=12). The effect of myocardium protection of the two methods of myocardium protection were evaluated by clinical outcome, CTnI. Serial venous blood samples were obtained before and after surgery. In both groups, there were no differences in operative parameters. The level of CTnI increased from postoperative 6 h (P<0.05), reached peak in 2472 h and recovered postoperatively on 6th day in both groups. Compared with group C, the plasma concentrations of CTnI in group W were significantly lower at 6 h, 24 h and 72 h (P<0.01). The results suggest that the method of warm induction and reperfusion blood cardioplegia reduces the leakage of CTnI than group of simple warm blood cardioplegia in CABG patients.
Key Words: Myocardial protection; Troponin-I; Cardioplegia; Cardiopulmonary bypass
1. Introduction
In a previous prospective randomized study [1] involving 28 patients with myocardial protection undergoing an elective first cardiac operation, we evaluated the myocardial protection of warm blood cardioplegia induction and simple cool blood cardioplegia induction during cardiopulmonary bypass and using cardiac troponin T (CTnT) as the criteria for evaluating the adequacy of myocardial protection. The results clearly showed, compared with cold blood cardioplegia induction, that warm blood cardioplegia induction provides better myocardial protection during cardiopulmonary bypass. Then we tried to find out another way to do it better. We applied both the warm induction and reperfusion during the CABG, compared with the simple warm induction without reperfusion and using troponin-I as the marker for evaluating the results of the myocardial injury during CABG.
Warm blood cardioplegia using the antegrade intermittent technique was more recently proposed to overcome the disadvantage of a continuous blood flow in the operative field.
Also, cardiac troponin-I (CTnI) has been introduced in clinical work to test myocardial injury, showing higher specificity and sensitivity than other routinely used biochemical markers of cardiac damage and also it has been used to assess the effectiveness of different methods of myocardial protection [2,3]. The purpose of this study was, therefore, to compare warm induction and reperfusion with simple warm blood cardioplegia using troponin-I to assess the injury to cardiac tissues.
2. Methods
2.1. Patients selection
The study was approved by Fuwai Heart Hospital, Beijing, China. All the patients were operated by the same group in Fuwai hospital, including the surgeons, anesthesiologist and perfusionist. From May 2002 to October 2002, 24 CAD patients operated on CABG were randomized to warm blood cardioplegia (group W; n=12), simple warm blood cardioplegia induction (group C; n=12). Preoperative and operative clinical parameters are shown in Table 1. Randomization was performed by the method described by Altman and Bland [4]. All the patients were three-vessel coronary artery disease without valve disease with normal left ventricle function, and the first time to receive CABG. Not included were patients with an ejection fraction below 0.30 and recent myocardial infarction (<2 months). The left internal mammary artery was used in all patients.
2.2. Cardiopulmonary bypass
The Stockert-II heart-lung machine with roller pump and Medtronic membrane oxygenator Affinity was used. Tubing pack with cardioplegia delivery (blood: crystalloid=4:1) system (Perfect, Beijing, China), and an arterial filter (Xi Jing, Xi an, China). Non-pulsatile CPB was used at a flow rate of 2.63.0 l/min/kg. Mean arterial pressure was maintained 6585 mmHg) by adjusting blood flow rate. Anesthesia Standard general anesthesia was achieved in all groups with fentanyl, isofurane and enfurane.
2.3. Method of myocardium protection
Institution cardioplegia was administered in both groups. The cardioplegia were administered every 30 min for a period of 2 min with the same infusion rate as the first time. Group of warm induction and reperfusion blood cardioplegia (Group W, n=12); Group of simple warm blood cardioplegia induction (Group C, n=12). The route of delivery was exclusively antegrade in the two groups. The temperature of cardioplegia ranged from 4 to 6 °C in groups and was applied during clamp off. In both groups the heart was induced by the warm blood cardioplegia (35 °C) into the line, during clamping using the cold blood cardioplegia maintaining. Also before clamp off, in Group W the warm reperfusion was applied. Warm reperfusion was started immediately after the last distal anastomosis, and was performed with a constant flow rate of 150 ml/min. Warm reperfusion was carried out in two steps and took 6 min: (1) during the first 2 min, the blood hyperkalemic mixture defined above was injected and progressively rewarmed to 20 °C, and (2) during the last 4 min, the infusate used was exclusively composed of oxygenated blood, which increased to 35 °C at the end of the reperfusion.
2.4. Laboratory assay
Plasma level marker of myocardial damage (CTnI) was obtained from serial venous blood samples before induction, after cardiopulmonary bypass (CPB), postoperative 6 h, 24 h, 72 h and 6th day, respectively. Cardiac troponin-I concentrations were measured by a specific immunoenzymometric assay developed. Test sample was incubated with monoclonal antibody 8E1 for 15 min. After washing, following the addition of a substrate (tetramethylbenzydine), enzyme activity was measured. The reaction was stopped by adding H2SO4 and the absorbance was read at 450 nm on the status spectrophotometer.
2.5. Electrocardiogram
A 12-lead electrocardiogram was recorded preoperatively at 2 h, at 2 h postoperatively and then daily postoperatively. The electrocardiographic diagnosis criteria for perioperative myocardial infarction (PMI) were new Q-waves >0.04 ms or a reduction in R-waves >25% in at least two leads.
2.6. Statistical analysis
Statistical analysis was performed with SPSS statistical software. One-way analysis of variance (ANOVA) was performed to test the effect of the type of cardioplegia and time on CTnI concentration. Two-way analysis of covariance with repeated measures was performed to test the effect of the type of cardioplegia on CTnI concentration. Statistical significance was accepted at a P<0.05. All data are expressed as mean±standard deviation (S.D.) (Table 2).
3. Results
Preoperative, operative, and postoperative data are shown in Table 1. The preoperative status was nearly identical in the two groups according to age, sex ratio, weight, C/T and EF%.
In the operative data there was no significant difference between the two groups in cardiopulmonary bypass time, clamp time, graft number, total amount of cardioplegic solution, lowest temperature during bypass and auto-resuscitation.
All patients survived, and no differences were observed in groups with regard to postoperative incidences of renal, respiratory, and neurological complications. The level of CTnI in both groups (group W 5.21±0.48 μg/l and group C 6.20±1.15 μg/l) increased from postoperative 6 h (P<0.05) compared with before induction (group W 0.43±0.27 μg/l, group C 0.40±0.29 μg/l), and this indicates that in both groups the myocardium was injured. The value reached peak in 2472 h and recovered on the postoperative 6th day. Compared with group C, the plasma concentration of CTnI in group W was significantly lower at 6, 24 and 72 h (P<0.01) (Fig. 1).
4. Discussion
Cardiac troponin-I is a specific and sensitive marker of myocardial injury. CTnI was found exclusively in cardiac muscle and clearly was different from skeletal isoforms, so making it a specific marker for myocardial damage. This specificity is particularly beneficial for patients undergoing cardiac surgery because the value of measurements of serum creatinine kinase and lactate dehydrogenase is limited by enzyme release from noncardiac tissues [5,6]. The CTnI increases in all patients after cardiac surgery. This fact shows the inevitable myocardial damage caused by myocardial arrest. The CTnI measurements can detect these small differences in myocardial tissue damage. We have already used it to assess the myocardium injury in our research [7]. The purpose of our present prospective randomized study was to determine the extent to which warm induction and reperfusion cardioplegia, and simple cool blood cardioplegia, contribute to the improvement of myocardial protection using CTnI as the criteria for evaluating the adequacy of myocardial protection.
In a previous study, cold blood cardioplegia with warm induction was clearly better than simple cool blood cardioplegia induction [1]. In our present study, we add the warm reperfusion before the clamp off. Comparison of the results of these two methods shows that with the addition of warm reperfusion to simple warm cardioplegia induction makes it as effective.
Therefore, it is acceptable that hypothermia has been routinely used as it reduces oxygen demand by decreasing the basal metabolic rate. However, hypothermia may have side effects like ‘cold contracture’ of microcirculation in coronary arteries to cause additional ischemia and reperfusion injury [8], rapid cooling during cardioplegia increasing left ventricular pressure, [Ca2+]i and coronary resistance, and is energy consuming [9] inhibiting the sodium pump to cause edema, and shifting the oxygen–hemoglobin dissociation curve leftward [10]. So warm induction reduces damage by avoiding cool contracture. In our previous study we learnt that warm induction is better than the cool blood induction. We could hypothesise that with the additional warm reperfusion before the clamp off, the better the result we could get, because of washing out the substances produced by the anaerobic metabolism and by bringing free radical scavengers to a heart at rest. Kawasuji's results suggest that terminal warm blood cardioplegia also may enhance myocardial reoxygenation and optimize the oxygen supply/demand balance of the myocardium during reperfusion [11].
In Teoh's study [12] he compared cold blood cardioplegia (11 patients) to cold blood cardioplegia followed by a ‘hot shot’ (9 patients). They showed that with the hot shot, myocardial metabolic recovery was improved, high-energy phosphates were better preserved, metabolic response to stress was normal, and diastolic function was preserved. Reperfusion damage is thought to be caused in part by oxygen free radicals produced during the early phases of reoxygenation. For Teoh and colleagues, the hot shot improves cold blood cardioplegia protection by washing out the products of anaerobic metabolism. In Caputo's study [13], thirty-five patients undergoing primary elective coronary revascularisation were randomized to one of two different techniques of myocardial protection. The data suggest that warm blood hyperkalemic reperfusion hot shot prevents myocardial metabolic derangement seen during coronary artery surgery.
Our data showed a significant higher grade of myocardial protection exerted by warm induction and reperfusion in comparison to simple warm blood cardioplegia induction. This finding supports the hypothesis of a high protective effect of warm induction and reperfusion. Warm reperfusion accelerated myocardial metabolic recovery, preserved high-energy phosphates, improved the metabolic response to postoperative hemodynamic stresses, and reduced left atrial pressures.
In summary, our study showed that with the additional warm reperfusion to simple warm cardioplegia induction offers advantage in low risk patients. This conclusion cannot be extended to high risk patients (e.g. redo CABG, combined surgery, ejection fraction under 0.30, unstable angina). Whether the higher release of CTnI in both the groups might be predictive of an adverse clinical outcome in a larger patient population or in higher-risk patients remains to be investigated.
References
Li S, Long C, Chang Q, Zhang D, Strickler AG, Nussmeier NA. Myocardial protection of warm blood cardioplegic induction during cardiopulmonary bypass. J Extra Corpor Technol 2001; 33:2106–110.
Sadony V, Korber M, Albes G, Podtschaske V, Etgen T, Trosken T, Ravens U, Scheulen ME. Cardial troponin-I plasma levels for diagnosis and quantitation of perioperative myocardial damage in patients undergoing coronary artery bypass surgery. Eur J Cardiothorac Surg 1998; 13:157–62.
Etievent JP, Chocron S, Toubin G, Taberlet C, Alwan K, Clement F, Cordier A, Schipman N, Kantelip JP. Use of cardiac troponin-I as a maker of perioperative myocardial ischemia. Ann Thorac Surg 1995; 59:51192–1194.
Altman DG, Bland JM. How to randomize. Br Med J 1999; 319:703–704.
Mair J, Wagner I, Puschendorf B, Mair P, Lechleitner P, Dienstl F, Calzolari C, Larue C. Cardiac troponin-I to diagnose myocardial injury. Lancet 1993; 341:838–839.
Adams JE 3rd, Sicard GA, Allen BT, Bridwell KH, Lenke LG, Davila-Roman VG, Bodor GS, Ladenson JH, Jaffe AS. Cardiac troponin-I a marker with high specificity for cardiac injury. Circulation 1993; 88:101–106.
Ji BY, Feng ZY, Liu JP, Long C. Myocardial protection related to magnesium content of cold blood hyperkalemic cardioplegic solutions in CABG. Extra Corpor Technol 2002; 34:2107–110.
Cannon MB, Vine AJ, Kantor HL, Lahorra JA, Nickell SA, Hahn C, Allyn JW, Teplick RS, Titus JS, Torchiana DF. Warm and cold blood cardioplegia. Comparison of myocardial fuction and metabolism using 31P magnetic resonance spectroscopy. Circulation 1994; 90:328–338.
Lahorra JA, Torchiana DF, Tolis G Jr, Bashour CA, Hahn C, Titus JS, Geffin GA, Daggett WM. Rapid cooling contracture with cold cardioplegia. Ann Thorac Surg 1997; 63:51353–1360.
Buckberg GD. Update on current techniques of myocardial protection. Ann Thorac Surg 1995; 60:805–814.
Kawasuji M, Tomita S, Yasuda T, Sakakibara N, Takemura H, Watanabe Y. Myocardial oxygenation during terminal warm blood cardioplegia. Jpn Ann Thorac Surg 1998; 65:51260–1264.
Teoh KH, Christakis GT, Weisel RD, Fremes SE, Mickle DA, Romaschin AD, Harding RS, Ivanov J, Madonik MM, Ross IM. Accelerated myocardial metabolic recovery with terminal warm blood cardioplegia. J Thorac Cardiovasc Surg 1986; 91:888–895.
Caputo M, Dihmis WC, Bryan AJ, Suleiman MS, Angelini GD. Warm blood hyperkalaemic reperfusion (‘hot shot’) prevents myocardial substrate derangement in patients undergoing coronary artery bypass surgery. Eur J Cardiothorac Surg 1998; 13:5559–564.(Bingyang Ji, Mingzheng Li)