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Asian Cardiovasc Thorac Ann 2008;16:274-277
© 2008 Asia Publishing EXchange Ltd


ORIGINAL CONTRIBUTIONS

Arterial Switch Operation: Troponin T Does Not Predict Ventilation Requirements

Madan M Maddali, MD, John Valliattu, FRCS, Taha al Delamie, FRCS, Sunny Zacharias, FRCS, Ahmed R Ahmed, MS, Shyam S Ganguly, PhD

Departments of Anesthesia and Cardiothoracic Surgery, Royal Hospital, Muscat, Sultanate of Oman

For reprint information contact: Madan M Maddali, MD, Tel: 968 2449 9759, Fax: 968 2449 9759, Email: madan{at}omantel.net.om, Royal Hospital, P.B. No. 1331, P.C: 111, Seeb, Muscat, Sultanate of Oman.


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The aim of this study was to assess whether postoperative cardiac troponin T levels could predict ventilation requirements in infants undergoing the arterial switch operation. Cardiac troponin T was measured 6 hours after aortic cross clamping and prior to tracheal extubation in 20 consecutive patients; 10 had simple and 10 had complex (with ventricular septal defect) transposition of the great arteries. The mean plasma troponin T level prior to extubation did not differ significantly in patients who were re-intubated and those who were successfully extubated. The initial cardiac troponin T levels in the complex defect group was significantly higher than in the simple transposition group. There was no correlation between initial cardiac troponin T levels and the duration of mechanical ventilation. There was no difference in mean duration of ventilation between the 2 groups. It was concluded that the postoperative cardiac troponin T level is not a predictor of successful extubation or prolonged artificial ventilation in this subset.


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Perioperative myocardial injury is a major determinant of postoperative cardiac dysfunction after pediatric open heart surgery, which might mandate postoperative ventilation and inotropic support.1 Successful discontinuation of ventilatory support might be a surrogate parameter that signifies recovery of myocardial function. Cardiac troponin T (cTnT) has been found to be an accurate predictor of complications and adverse clinical events after pediatric cardiac surgery.2 This study was designed primarily to assess prospectively whether the postoperative cTnT level might serve as an independent predictor of successful extubation in infants undergoing the arterial switch operation for transposition of the great arteries (TGA). The secondary aim was to assess whether postoperative cTnT levels might predict the duration of artificial ventilatory support in these infants. As there is direct coronary manipulation during the arterial switch operation, we restricted our interest to cTnT as a marker of myocardial injury.


    PATIENTS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
After hospital ethical committee clearance and informed consent from the parents, 20 consecutive infants who successfully underwent an arterial switch operation, with or without ventricular septal defect closure, were included in the study. Ten patients with a preoperative diagnosis of TGA alone were classified as having simple TGA, the other 10 with TGA and ventricular septal defect were classified as having complex TGA (Table 1Go). All infants in the simple TGA group had preoperative balloon atrial septostomy. Those who were hemodynamically stable preoperatively and breathing spontaneously with or without prostaglandin E1 infusion were included in the study. All babies had resting arterial oxygen concentrations > 80% on room air, with arterial blood pH ≥ 7.4. Those with elevated serum creatinine (> 1.5 mg·dL–1) either pre- or postoperatively and patients with preoperative low cardiac output requiring artificial ventilation and inotropic support were excluded.


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Table 1. Patient Characteristics According to Type of Surgery
 
All patients received narcotic-based general anesthesia with standard invasive and noninvasive hemodynamic monitoring. Hypothermic myocardial protection was provided by core cooling to a nasopharyngeal temperature of 20°C, followed by aortic cross clamping and an initial antegrade infusion of St Thomas’ Hospital crystalloid cardioplegia solution (20 mL·kg–1). Subsequent myocardial protection was achieved with retrograde crystalloid cardioplegia infusion every 20 min, using a 6F retrograde coronary sinus perfusion cannula (Medtronic DLP, Minneapolis, MN, USA). In all cases, continuous low-flow cardiopulmonary bypass (CPB) was employed during completion of the aortic and coronary anastomoses. Core rewarming was instituted during completion of the pulmonary anastomosis. Mean perfusion pressures were maintained between 30 and 70 mm Hg during rewarming, using boluses of phentolamine 100 µg·kg–1 or phenylephrine 5 µg·kg–1 as needed. Alpha stat acid-base management was adopted. Heparin was administered to maintain an activated clotting time (kaolin) of 480 sec or longer. The surgical team was the same for all the cases. Dopamine (5–10 µg·kg–1·min–1) was routinely infused to discontinue CPB; the dose was titrated to the hemodynamic and clinical state of the patient. Lactated Ringer’s solution, fresh whole blood, blood products, and increased doses of inotropics (dobutamine 5–10 µg·kg–1·min–1 or epinephrine 0.01–0.04 µg·kg–1·min–1) were given as necessary to maintain normal filling pressures and a systolic perfusion pressure of at least 60 mm Hg. All patients were admitted to the pediatric intensive care unit after surgery, and managed by surgical intensivists and pediatric cardiologists. Decisions regarding inotropic support and ventilation were based on unit protocol, hemodynamic status (arrhythmias, low mixed venous saturation, or high lactic acidosis), and clinical judgment (stable vital signs and urine output ≥ 0.5 mL–1·kg–1·hr–1). An echocardiographic study consisting of a complete 2-dimensional and Doppler evaluation with stress-velocity analysis was performed on the 2nd postoperative day to assess the adequacy of surgical correction and biventricular function. The echocardiographers were unaware of the patient’s cTnT status.

A decision to extubate was taken if the child was awake or could be aroused, neurologically intact, hemodynamically stable on reasonable inotropic support with good mixed venous oxygen saturations. Additional criteria were a satisfactory surgical result based on echocardiographic evaluation, acceptable arterial blood gas analysis results achieved with peak inspiratory pressures ≤ 16 cm H2O, positive end-expiratory pressures ≤ 5 cm H2O, intermittent mandatory ventilation rate of 15–25, and fraction of inspired oxygen ≤ 0.35. Extubation failure was defined as the need for reintubation and mechanical ventilation. Reintubation was performed in the presence of any of the following: pH < 7.25, PaCO2 > 60 mm Hg, frequent (> 2–3/hour) apnea/bradycardia spells (cessation of respiration for > 20 sec associated with heart rate <100/min), frequent desaturations ( ≥ 3 episodes/hour of SaO2 < 85%) not responding to an increase in FiO2 to 1.0, or PaO2 < 50 mm Hg despite an FiO2 of 1.0. The initial postoperative plasma cTnT values, duration of ventilation, and CPB data of all patients are shown in Table 1Go. Cardiac troponin T levels were measured 6 hours after the initial aortic cross clamp application and just prior to extubation in all patients. If the child was re-intubated, cTnT levels were again measured prior to later attempts at extubation. Immediate postoperative cTnT levels were compared between the simple and complex groups.

Results are given as mean ± standard deviation. Statistical analysis was carried out with Spearman’s rank correlation to investigate the association between continuous variables. Comparisons between groups were performed using the Mann-Whitney U test. Two-tailed significance tests were used, and a probability value < 0.05 was considered significant. All variables were processed and analyses were performed using SPSS for Windows version 11.0 (SPSS, Inc., Chicago, IL, USA).


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
All infants were alive at 30 days after the operation. Initial cTnT levels were significantly higher in the complex TGA group than in the simple TGA group (Table 1Go). The duration of ventilation was similar in both groups. Mean cross clamp and CPB times were higher in the complex TGA group. Three patients needed reintubation (1 with simple TGA and 2 in the complex TGA group). In view of the small numbers, the groups were combined for analysis. Although cTnT levels prior to extubation were higher in the 3 patients who were re-intubated (1.89 ± 2.13 ng·mL–1) than in the 17 successfully extubated (0.54 ± 0.53 ng·mL–1), the difference was not significant (p = 0.18). The possibility of an association between initial cTnT levels and the duration of ventilation, CPB time, and aortic cross clamp time was explored in all 20 patients. There was no correlation between initial cTnT and duration of ventilation (rs = 0.04; p = 0.87), CPB time (rs = 0.19; p = 0.41), or cross clamp time (rs = 0.23; p = 0.33). Similarly, there was no correlation between duration of ventilation and CPB time (rs = –0.13; p = 0.58) or cross clamp time (rs = 0.38; p = 0.10). None of the infants had ischemic changes identified by electrocardiography. Postoperative transthoracic echocardiography revealed a satisfactory correction with good biventricular contractility in all cases and no regional wall motion abnormalities, significant pulmonary valve stenosis, aortic valve regurgitation, or residual ventricular septal defect.


    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Both unsuccessful early extubation and prolonged ventilation are associated with various complications, and it is difficult to extrapolate in children the traditional weaning indices to discriminate between patients successfully extubated and those re-intubated.36 Identification of a specific indicator that could predict the duration of ventilation and the suitability of a patient for extubation would be very useful. In view of this, we explored the potential of cTnT as an independent marker of suitability for extubation and a predictor of the duration of mechanical ventilation. cTnT was selected because previous studies identified it as a reliable marker of myocardial injury and a predictor of several postoperative events in pediatric cardiac surgery.79

We were unable to demonstrate any correlation between cTnT levels prior to extubation and the success of extubation, and the mean duration of ventilation was same in both groups. The initial cTnT level was higher in the group with complex TGA, probably due to more surgical trauma; however, it did not predict prolonged mechanical ventilation postoperatively. The cTnT level at 6 hours after aortic cross clamping was chosen on the basis of a report suggesting cTnT levels become elevated 4 hours after separation from CPB.10 An association between high initial cTnT levels and failed extubation was also explored. The 3 infants who needed reintubation had initial cTnT levels of 3.95, 6.15, and 8.32 ng·mL–1; however, 2 in the simple TGA group had cTnT levels > 6.0 ng·mL–1 and neither needed reintubation. The child who needed reintubation in the simple TGA group had an initial cTnT level of 3.95 ng·mL–1. Thus infants in this group with very high initial cTnT levels did not have to be re-intubated. On the other hand, 5 patients with complex TGA had initial cTnT levels > 6.0 ng·mL–1; 2 who were re-intubated had values of 6.15 and 8.32 ng·mL–1, but 3 with cTnT levels of 8.34, 7.41, and 6.40 ng·mL–1 did not need reintubation. Mildh and colleagues2 suggested that in pediatric open heart surgery, cTnT levels > 5.9 µg·L–1 on the first postoperative day predicted death at 30 days. Taggart and colleagues8 observed that high levels of cTnT 3–6 hours after surgery were also related to reduced survival. In our study, 7 infants had initial cTnT levels > 6.0 ng·mL–1 but all were alive at 30 days postoperatively.

As for cTnT levels just prior to extubation, the one child with simple TGA who needed reintubation had a cTnT level of 4.35 ng·mL–1 and the 2 with complex TGA had values of 0.62 and 0.70 ng·mL–1. Thus a cTnT level that would predict successful or failed extubation could not be arrived at in our study. In addition, although 2 infants in the complex TGA group had initial cTnT levels > 7.5 ng·mL–1 only one with a level of 8.32 ng·mL–1 was re-intubated but was eventually extubated and doing well at 30 days. The other child in this group with an initial cTnT of 8.34 ng·mL–1 was successfully extubated after 4 days. Our observations differ from those of Taggart and colleagues8 who would have expected a disastrous outcome in these children. The vulnerability of infant myocardium depends on the duration of ischemia/hypoxia and attendant sequelae, myocardial mass index, intensity of perioperative heart failure, and anatomical extent of myocardium at risk, which could explain the disparity between our findings and previous reports.2,8 It ought to be mentioned that the absolute values of cTnT vary from one laboratory to another. Our normal level is < 0.03 ng·mL–1, and levels > 0.1 ng·mL–1 are considered to be significantly raised.

Hirsch and colleagues11 found that peak postoperative cTnT correlated with CPB and cross clamp times. Although we found that the initial cTnT level was higher in the complex TGA group, when both groups were combined, there was no association between initial cTnT level and duration of CPB or cross clamping. As elevated cTnT levels are found in patients with renal insufficiency, infants who were in renal failure or developed renal failure early postoperatively were excluded from this study.12 Preoperative hypoxemia with associated metabolic acidosis contributes to myocardial dysfunction. We believe that for comparable arterial oxygen saturations, myocardial damage would be more profound if there was associated metabolic acidosis. None of the babies in this study had preoperative metabolic acidosis.

It has been suggested that in cases of TGA, variations in coronary anatomy might influence surgical management and the postoperative course, resulting in significantly more cardiovascular morbidity and mortality because of myocardial ischemia.13 It can be expected that the resulting postoperative ischemia/infarction would lead to elevated cTnT levels along with electrocardiographic and echocardiographic changes. However, surgical coronary obstruction is independent of original anatomy, and abnormal coronary anatomy alone may not be a determinant of outcome.14 Maneuvers such as the trapdoor flap and circular buttonhole techniques might aid in coronary transfer and compensate for an unanticipated coronary artery pattern.15 It can be presumed that if there were no technical problems related to coronary transfer, most often there would be no resultant postoperative myocardial ischemia.

The obvious limitation of this study is the small number of patients. Another potential limitation is that outcome variables, such as the duration of ventilation, may depend on the intensivist managing the patient. However, clinician bias is unlikely to have been a confounding factor as the postoperative management was strictly in accordance with unit protocol, and cTnT results were not available to the intensivist. Furthermore, as the study extended over 18 months, subtle changes in surgical technique might have crept in without notice.

Although we could not demonstrate that postoperative cTnT level was a predictor of successful extubation, there was a tendency for cTnT levels to be higher in the re-intubated group, but cTnT levels > 6 ng·mL–1 did not predict a poor outcome. Good clinical judgment based on the patient’s hemodynamic parameters, ventilatory requirements, neurological status, and echocardiographic findings continue to be of prime importance in postoperative decision-making in these sick babies.


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Imura H, Modi P, Pawade A, Parry AJ, Suleiman MS, Angelini GD, et al. Cardiac troponin I in neonates undergoing the arterial switch operation. Ann Thorac Surg 2002;74:1998–2002.[Abstract/Free Full Text]

  2. Mildh LH, Pettilä V, Sairanen HI, Rautiainen PH. Cardiac troponin T levels for risk stratification in pediatric open heart surgery. Ann Thorac Surg 2006;82:1643–8.[Abstract/Free Full Text]

  3. Farias JA, Frutos F, Esteban A, Flores JC, Retta A, Baltodano A, et al. What is the daily practice of mechanical ventilation in pediatric intensive care units? A multicenter study. Intensive Care Med 2004;30:918–25.[Medline]

  4. Baisch SD, Wheeler WB, Kurachek SC, Cornfield DN. Extubation failure in pediatric intensive care incidence and outcomes. Pediatr Crit Care Med 2005;6:312–8.[Medline]

  5. Kurachek SC, Newth CJ, Quasney MW, Rice T, Sachdeva RC, Patel NR, et al. Extubation failure in pediatric intensive care: a multiple-center study of risk factors and outcomes. Crit Care Med 2003;31:2657–64.[Medline]

  6. Farias JA, Alía I, Retta A, Olazarri F, Fernández A, Esteban A, et al. An evaluation of extubation failure predictors in mechanically ventilated infants and children. Intensive Care Med 2002;28:752–7.[Medline]

  7. Lipshultz SE, Rifai N, Sallan SE, Lipsitz SR, Dalton V, Sacks DB, et al. Predictive value of cardiac troponin T in pediatric patients at risk for myocardial injury. Circulation 1997;96:2641–8.[Abstract/Free Full Text]

  8. Taggart DP, Hadjinikolas L, Wong K, Yap J, Hooper J, Kemp M, et al. Vulnerability of paediatric myocardium to cardiac surgery. Heart 1996;76:214–7.[Abstract/Free Full Text]

  9. Immer FF, Stocker F, Seiler AM, Pfammatter JP, Printzen G, Peheim E. Troponin-T: improved diagnostic assessment of myocardial damage in childhood. Acta Paediatr 1997;86:1321–7.[Medline]

  10. Hövels-Gürich HH, Vazquez-Jimenez JF, Silvestri A, Schumacher K, Minkenberg R, Duchateau J, et al. Production of proinflammatory cytokines and myocardial dysfunction after arterial switch operation in neonates with transposition of the great arteries. J Thorac Cardiovasc Surg 2002;124:811–20.[Abstract/Free Full Text]

  11. Hirsch R, Dent CL, Wood MK, Huddleston CB, Mendeloff EN, Balzer DT, et al. Patterns and potential value of elevation of cardiac troponin I after pediatric cardiac operations. Ann Thorac Surg 1998;65:1394–9.[Abstract/Free Full Text]

  12. Croitoru M, Taegtmeyer H. Spurious rises in troponin T in end-stage renal disease. Lancet 1995;346:974.[Medline]

  13. Day RW, Laks H, Drinkwater DC. The influence of coronary anatomy on the arterial switch operation in neonates. J Thorac Cardiovasc Surg 1992;104:706–12.[Abstract]

  14. Hutter PA, Bennink GB, Ay L, Raes IB, Hitchcock JF, Meijboom EJ. Influence of coronary anatomy and reimplantation on the long-term outcome of the arterial switch. Eur J Cardiothorac Surg 2000;18:207–13.[Abstract/Free Full Text]

  15. Baslaim GM. Is preoperative delineation of coronary artery pattern a prerequisite for arterial switch operation? J Card Surg 2006;21:465–70.[Medline]





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