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Ann Thorac Surg 2007;83:902-905
© 2007 The Society of Thoracic Surgeons
a Division of Congenital Cardiovascular Surgery, University Childrens Hospital, Zürich, Switzerland
b Division of Pediatric Cardiology, University Childrens Hospital, Zürich, Switzerland
c Division of Anesthesiology, University Childrens Hospital, Zürich, Switzerland
d Department of Biostatistics, Institute for Social and Preventive Medicine, University of Zürich, Zürich, Switzerland
Accepted for publication September 25, 2006.
* Address correspondence to Dr Dodge-Khatami, University Childrens Hospital, University of Zürich, Steinwiesstrasse 75, CH-8032 Zürich, Switzerland (Email: ali.dodge-khatami{at}kispi.unizh.ch).
| Abstract |
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Methods: Between 1994 and 2005, 198 consecutive patients underwent surgical correction of an isolated VSD (n = 100), tetralogy of Fallot (n = 52) or atrioventricular septal defect (n = 46). Intraoperative transesophageal echocardiography (TEE) was routine, and postoperative transthoracic echocardiography was performed in the intensive care unit, at hospital discharge, and during follow-up. Residual defects were graded as absent, between 1 and 2 mm, or greater than 2 mm.
Results: Shunt-related discrepancy was observed between intraoperative TEE and intensive care unit transthoracic echocardiographic findings; significantly so after Fallot repair (p < 0.0001). After discharge, 83% of all residual defects less than 2 mm closed. Of nine residual defects greater than 2 mm, only three closed after a median follow-up of 3.1 years. In patients with residual shunts, they were hemodynamically insignificant, required no medication, and no endocarditis was noted. At last follow-up, there was no significant difference between the percentage of residual shunts among the three groups (p = 0.135).
Conclusions: Postsurgical residual VSDs less than 2 mm closed spontaneously in the majority within a year. Defects greater than 2 mm are unlikely to close spontaneously. Residual shunts after atrioventricular septal defect repair almost always close, whereas one third will remain open after Fallot or isolated VSD repair. At midterm follow-up, residual shunts remained hemodynamically and clinically irrelevant. Revision of a residual defect greater than 2 mm on cardiopulmonary bypass at initial repair, guided by TEE, may spare late redo surgery and lifelong antibiotic prophylaxis.
| Introduction |
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| Material and Methods |
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Statistical analysis included a sign test to compare the grade of residual defects at different follow-up time points. To compare different diagnostic groups with respect to a binary endpoint (percentage of residual defects at any given follow-up point), a
2 test was used.
| Results |
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Patch closure of the VSD was performed in 178 cases, whereas direct VSD closure was judged feasible in 20 patients. A residual defect was significantly more frequent after direct closure (5 of 20; 25%) as compared with after-patch closure of a VSD (12 of 178; 6.7%) (p = 0.006). The small numbers of residual defects in each diagnostic group with regard to closure technique were too small to perform a meaningful subgroup analysis.
After hospital discharge, 83% of all residual defects less than 2 mm closed. Of the nine residual defects greater than 2 mm, only three closed after a median follow-up of 3.1 years. In all other patients with persistent residual defects at last follow-up the shunts were hemodynamically insignificant, as documented by TTE and electrocardiogram (neither enlargement of cardiac chambers nor signs of ventricular strain, respectively), the patients required no medication, and no endocarditis was noted. At last follow-up, there was no statistically significant difference between residual VSDs among the three diagnostic groups (p = 0.135).
| Comment |
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We found a global residual shunt rate ranging between 15% and 25% on intraoperative TEE, compared with a 30% to 46% rate of residual defects detected by postoperative TTE in the ICU, and a rate between 35% and 38% on TTE by hospital discharge. This incidence may seem high but includes a majority of 1 mm defects, which are clearly hemodynamically insignificant. After subgroup analysis, the discrepancy between TEE and first TTE in the ICU was significant only for patients after TOF repair (p < 0.0001). There are two possible interpretations of this observation: (1) either the TEE disclosed a "false-negative" finding, whereby a residual VSD was incorrectly missed in the operating room; or (2) TEE provided a "true-negative" observation, whereby an accurate TEE correctly excluded a residual shunt in the operating room [4, 5, 8] but which unfortunately "reopened" by the time of the subsequent TTE in the ICU. An explanation for the defects incorrectly missed by intraoperative TEE could be due to the tachycardia and hypovolemia that are frequent immediately after coming off cardiopulmonary bypass. There is often turbulence in the various cardiac chambers, owing to indwelling cannulae of the cardiopulmonary bypass system, to jets against intracardiac patch material, to jets in the resected muscle bundles of the right outflow tract, or to jets created by a newly reconstructed pulmonary valve, which may make the distinction with a residual shunt more difficult. Furthermore, transiently elevated right ventricular pressures, shadowing by the anteriorly positioned patch material, or peripatch swelling in the operating room may lead to unmasking of small residual defects only days after surgery [3]. In our series, this is illustrated by the significant discrepancy between TEE and TTE findings after complete repair of tetralogy, as compared with that after isolated VSD closure or AVSD repair.
Similar to our study and findings, Yang and colleagues [3] looked at the frequency and significance of residual defects in 294 patients undergoing surgical closure of a simple VSD, or that with associated complex congenital heart disease. The intraoperative TEE detected a residual VSD in 96 of 294 patients (33%), being slightly higher in patients after closure of an isolated VSD (41%) as compared with that after correction of more complex defects with a VSD component (30%), although the difference was not significant. From the 96 of 294 residual defects seen by intraoperative TEE, only 33 had a residual VSD detected by TTE at hospital discharge (34%). Interestingly, 15 patients who had no VSD in the operating room were noted to have a residual defect within 18 months of follow-up after surgery, although these were all small defects less than 2 mm. Yang and colleagues [3] concluded as to the utility of TEE as an assessment tool of residual defects in the operating room, stating that one third of patients will have a residual defect detected immediately after surgery but that two thirds of these will spontaneously close by hospital discharge. For them, defects larger than 4 mm should undergo immediate surgical revision, and those with tetralogy of Fallot with a small residual defect at the superior aspect of the VSD patch should be followed closely for defect enlargement and a late significant shunt [3].
In our study population, 83% of all residual shunts less than 2 mm closed spontaneously, and the vast majority did so within a year after the initial operation. Those larger than 2 mm closed in only three of nine patients, after a median follow-up of 3.1 years. Patients with residual defects were asymptomatic, medication-free, and had no episodes of endocarditis at last follow-up, so that their quality of life was judged normal to excellent. Similar to our findings, in a retrospective study including 109 patients operated for closure of an isolated VSD after a mean follow-up of 14.5 years, Meijboom and colleagues [2] found 84% of patients to subjectively assess their health as good or very good. Mean exercise capacity was normal in 84% of patients and 89% were free of any medical or surgical intervention since the operation. Residual VSDs were found in 7% of patients and none had signs of pulmonary hypertension or symptomatic arrhythmias. The incidence of late death was 2%. The authors concluded that, despite the presence of many anatomic, hemodynamic, or electrophysiologic sequelae, virtually all patients are asymptomatic [2]. In a more recent study, Bol-Raap and colleagues [9] studied 188 consecutive patients undergoing surgical closure of an isolated VSD, with a mean follow-up of 2.6 years (range, 0.1 to 9.4). During follow-up, no reoperations were necessary for closing a residual VSD, and 37 of 73 (51%) of the residual trivial shunts disappeared spontaneously at a median time of 3.9 years. By actuarial analysis, all trivial shunting had disappeared by 8.4 years.
We found a significant difference between residual shunts after direct or patch closure of a VSD, namely a more than threefold incidence after direct closure. This may intuitively be explained by the excessive tension pulling on the suture lines at the edges of the VSD, after an attempt at direct closure. Currently, this is only undertaken in our unit with small defects in older patients who have sufficiently fibrosed margins of their VSD, which allows for a secure and permanent defect closure. Patch closure is otherwise the norm.
Residual shunts closed spontaneously more frequently after complete repair of AVSD, as compared with after correction of TOF and closure of an isolated VSD, although this did not reach statistical significance. We speculate that the increased "surgical traffic," namely the neo-crux cordis of the heart, consisting of the interface of two patches for VSD and atrial septal defect closure, and the suture abundance with reconstruction of two atrioventricular valves, will lead to more inflammation and subsequent fibrosis, which may allow for eventual closure of a residual shunt. The use of xenopericardium in our series, rather than more inert material such as Dacron or Gore-Tex, may have induced more postoperative inflammation leading to closure of small residual defects, although this remains speculative.
Limitations of this study are inherent foremost to its retrospective nature. Although not influencing the postoperative results with regard to spontaneous defect closure or being a focus of this study, there were instances where we went back on cardiopulmonary bypass to close larger residual shunts, as detected by TEE or intraoperative saturation measurements, although the exact incidence cannot be quantified due to missing observations. Interobserver variability may have biased the quality and precision of the findings as our team consists of two anesthesiologists specialized in pediatric cardiac anesthesia and TEE, and seven pediatric cardiologists performing the postoperative TTE in the intensive care unit, during the in-hospital stay, and at out-patient follow-up.
In conclusion, residual shunts smaller than 2 mm will almost always close spontaneously, and more surely so after AVSD repair, most often by one year after surgical repair. Defects greater than 2 mm are unlikely to close but are hemodynamically and clinically irrelevant for the patient. Even after a perfect repair of AVSD and TOF, lifelong endocarditis prophylaxis is indicated. At our institution, for patients after successful closure of an isolated VSD, endocarditis prophylaxis is discontinued after six months. In this subgroup, revision of a residual shunt greater than 2 mm, as detected by intraoperative TEE, may spare lifelong endocarditis prophylaxis and(or) avoid subsequent reoperation.
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