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Ann Thorac Surg 2007;83:902-905
© 2007 The Society of Thoracic Surgeons


Original Articles: Cardiovascular

Spontaneous Closure of Small Residual Ventricular Septal Defects After Surgical Repair

Ali Dodge-Khatami, MD, PhDa,*, Walter Knirsch, MDb, Maren Tomaske, MDb, René Prêtre, MDa, Dominique Bettex, MDc, Valentin Rousson, PhDd, Urs Bauersfeld, MDb

a Division of Congenital Cardiovascular Surgery, University Children’s Hospital, Zürich, Switzerland
b Division of Pediatric Cardiology, University Children’s Hospital, Zürich, Switzerland
c Division of Anesthesiology, University Children’s 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 Children’s Hospital, University of Zürich, Steinwiesstrasse 75, CH-8032 Zürich, Switzerland (Email: ali.dodge-khatami{at}kispi.unizh.ch).


    Abstract
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
Background: Residual shunts may be detected by intraoperative or postoperative echocardiography after surgical closure of a ventricular septal defect (VSD). The hemodynamic relevance and rate of late closure are unknown.

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
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
Results after surgical closure of an isolated ventricular septal defect (VSD) are excellent, with regard to both in-hospital mortality, which reaches zero in many centers [1], and to the long-term follow-up with regard to quality of life and exercise capacity [2]. A ventricular septal defect is also a consistent component of tetralogy of Fallot (TOF) and of complete atrioventricular septal defect (AVSD), and is routinely closed during surgical correction of these more complex defects. Small residual defects are frequently described on intraoperative transesophageal echocardiography (TEE) and also on postoperative transthoracic echocardiography (TTE), but the rate of possible spontaneous closure, or the hemodynamic and clinical significance in case of a persistent residual shunt, are sparsely documented [3–5]. In a recent era of surgery we evaluated our results after surgical closure of a VSD with regard to residual defects, compared the findings of TEE with TTE in the diagnosis of residual defects, and looked at the rate of spontaneous VSD closure in time with its eventual implications for the patient in the midterm follow-up.


    Material and Methods
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
The Institutional Review Board of our hospital approved the study. Retrospective chart and echocardiography report analysis were anonymously performed, whereby patient consent was waived. Between 1994 and 2005, 198 consecutive patients underwent surgery for closure of an isolated perimembranous VSD (n = 100), a malalignment TOF VSD (n = 52), or an inlet AVSD (n = 46). Standard surgical technique using cardiopulmonary bypass with moderate hypothermia, cross-clamping, and cold blood cardioplegia were used. Patch material included xenopericardium (Edwards Xenopericardium, Edwards Lifesciences Services GmbH, Unterschleissheim, Germany, and Shelhigh Pericardial Patch, Shelhigh Inc, Union, NJ), and a running suture technique with a nonabsorbable suture was routinely employed. Exposure for VSD closure was routinely through the right atrium. For patients with complete AVSD, patch closure of the ventricular component of the defect was routine, except in two patients with very small defects in which a one-patch (atrial septal defect + VSD closure) technique was performed. In patients with TOF and isolated VSD repair, the choice of direct closure or xenopericardial patch closure of the VSD was left to the discretion of the surgeon. Direct VSD closure was performed in five patients during correction of TOF, and in 13 patients during closure of an isolated VSD. Intraoperatively, TEE was routine for all cases (Philips Sonos 5000, Philips Medical Systems, The Netherlands). In case of a large residual shunt (larger than 3 mm, or a ratio of pulmonary to systemic blood flow [Qp:Qs] > 1.5:1 as measured by intraoperative right heart saturations), cardiopulmonary bypass was resumed to achieve defect closure. Postoperatively, in the intensive care unit (ICU), at hospital discharge, and during follow-up, TTE was routinely performed (Philips Sonos 2000 or 5000, Philips Medical Systems). Echocardiographic measurements of residual VSD size were made with two-dimensional imaging and residual defects were graded as absent, between 1 and 2 mm, or larger than 2 mm. After repair of tetralogy and AVSD, patients were recommended to receive lifelong antibiotic endocarditis prophylaxis. After successful closure of an isolated VSD, endocarditis prophylaxis was recommended for six months and stopped thereafter.

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 {chi}2 test was used.


    Results
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
Median follow-up was 3.1 years (range, 0.5 to 9.7 years), and was similar in all three diagnostic groups. Discrepancy was observed between the intraoperative TEE findings and those of the first TTE performed in the intensive care unit, either on the same day as the operation or one day afterward. As seen in Table 1, the first TTE on the ICU disclosed a 30% rate of residual VSD versus only 20% on intraoperative TEE in patients after AVSD repair; 46% versus 15% after repair of tetralogy, and 30% versus 25% after isolated VSD closure, respectively. For the group as a whole (n = 198), this discrepancy between intraoperative TEE and the first TTE on the ICU with regard to residual VSD detection was significant (p = 0.002). When the analysis was performed separately for each diagnostic group these discrepancies were no longer significant for patients after AVSD repair (p = 0.27), nor for patients after isolated VSD closure (p = 0.85), while they were strongly significant for the TOF group (p < 0.0001).


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Table 1 Rate and Size of Residual VSD
 
Taking the whole group into consideration the evolution of residual defects was followed over time, with regard to either spontaneous closure or on the contrary widening of the defect, independent of the size at initial detection. When comparing the first postoperative TTE performed on the ICU to the TTE at last follow-up, 75% of all residual defects closed and 2% became larger. When comparing the TTE before hospital discharge and at last follow-up, 76% closed and no defects reopened. The same analysis was performed in the three diagnosis subgroups. From hospital discharge to last follow-up in patients with AVSD repair, 94% of residual defects closed. No defects became larger or reopened. In patients after tetralogy repair or isolated VSD closure, defects spontaneously closed in 65% and 74% of cases, respectively. Although there was a stronger trend toward spontaneous residual defect closure in patients after AVSD repair, there was no statistically significant difference in the evolution toward spontaneous closure among the three diagnostic groups (p = 0.59) in time.

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
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
Surgical closure of an isolated VSD is a routinely performed operation, using standardized surgical techniques and postoperative care management. Outcomes are excellent, with mortality and morbidity rates approaching zero in almost all centers internationally [1]. When a VSD is part of a more complex congenital heart disease, such as tetralogy of Fallot or complete atrioventricular septal defect, they are routinely closed, with surgical mortalities ranging from 1% to 5% and 3% to 16%, respectively [6, 7]. In the more modern era, elective closure is performed in infancy or early childhood, thereby reducing the potential residual long-term morbidity after successful surgical repair from long-standing preoperative pulmonary hypertension or volume overload of the ventricle. Therefore, the focus on the postsurgical history of these defects lies more in the long-term quality of life and functional status of the growing children and young adults, which will be influenced by eventual residual lesions, one of which is a VSD shunt.

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.


    References
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Mavroudis C, Backer CL, Jacobs JP. Ventricular septal defectIn: Mavroudis C, Backer CL, editors. Pediatric cardiac surgery. 3rd ed.. Philadelphia, PA: Mosby; 2003. pp. 298-320.
  2. Meijboom F, Szatmari A, Utens E, et al. Long-term follow-up after surgical closure of ventricular septal defect in infancy and childhood J Am Coll Cardiol 1994;24:1358-1364.[Abstract]
  3. Yang S-G, Novello R, Nicolson S, et al. Evaluation of ventricular septal defect repair using intraoperative transesophageal echocardiography: frequency and significance of residual defects in infants and children Echocardiography 2000;17:681-684.[Medline]
  4. Rosenfeld HM, Gentles TL, Wernovsky G, et al. Utility of intraoperative transesophageal echocardiography in the assessment of residual cardiac defects Pediatr Cardiol 1998;19:346-351.[Medline]
  5. Muhiudeen IA, Robertson DA, Silverman NH, Haas GS, Turley K, Cahalan MK. Intraoperative echocardiography for evaluation of congenital heart defects in infants and children Anesthesiology 1992;76:165-172.[Medline]
  6. Hirsch JC, Bove EL. Tetralogy of FallotIn: Mavroudis C, Backer CL, editors. Pediatric cardiac surgery. 3rd ed.. Philadelphia, PA: Mosby; 2003. pp. 383-397.
  7. Backer CL, Mavroudis C. Atrioventricular canal defectsIn: Mavroudis C, Backer CL, editors. Pediatric cardiac surgery. 3rd ed.. Philadelphia, PA: Mosby; 2003. pp. 321-338.
  8. Wienecke M, Fyfe DA, Kline CH, et al. Comparison of intraoperative transesophageal echocardiography to epicardial imaging in children undergoing ventricular septal defect repair J Am Soc Echocardiogr 1991;4:607-614.[Medline]
  9. Bol-Raap G, Weerheim J, Kappetein AP, Witsenburg M, Bogers AJJC. Follow-up after surgical closure of congenital ventricular septal defect Eur J Cardiothorac Surg 2003;24:511-515.[Abstract/Free Full Text]

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Ann. Thorac. Surg. 2007 83: 906. [Extract] [Full Text] [PDF]



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Ann. Thorac. Surg., March 1, 2007; 83(3): 906 - 906.
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