Eur J Cardiothorac Surg 2004;26:767-772
© 2004 Elsevier Science NL
Functional biventricular repair using left ventriclepulmonary artery conduit in patients with discordant atrioventricular connections and pulmonary outflow tract obstructiondoes conduit obstruction maintain tricuspid valve function?
Masahiro Koh*,
Toshikatsu Yagihara,
Hideki Uemura,
Koji Kagisaki,
Soichiro Kitamura
Department of Cardiovascular Surgery, National Cardiovascular Center, 5-7-1 Fujishiro-dai, 565-8565 Suita, Osaka, Japan
Received 4 September 2003;
received in revised form 17 April 2004;
accepted 28 May 2004.
* Corresponding author. Tel.: +81-6-6833-5012; fax: +81-6-6872-7486
e-mail: masahiro.koh{at}nifty.ne.jp
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Abstract
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Objective: The aim of the study is to determine whether function of the tricuspid valve placed for the systemic circulation is related to left ventricular pressure supporting the pulmonary circulation after functional repair for atrioventricular discordance. Methods: Right ventricular volume and tricuspid regurgitation (TR) were investigated, in relation to left ventricular pressure, in 15 patients with this malformation who underwent functional biventricular repair with left ventriclepulmonary artery conduit. Results: After the functional biventricular repair, ratio of systolic left ventricular pressure to right ventricular one (LVP/RVP) was 0.58±0.24 and right ventricular end-diastolic pressure (RVEDV) significantly increased from 104±24 to 137±39% of normal predicted value (P=0.015). Five patients with LVP/RVP>0.6 were free from TR, however, six of seven with LVP/RVP<0.6 developed TR. Three patients required eventual tricupid valve replacement. Conduit replacement was required in seven patients and five were assessed similarly. After the conduit replacement, LVP/RVP decreased from 1.08±0.34 to 0.58±0.14 and RVEDV increased significantly from 87±24 to 129±19% (P=0.011). One patient with postoperative LVP/RVP of 0.36 developed moderate TR. Conclusion: Mild obstruction at the pulmonary channel is not necessarily an evil after functional biventricular repair for this malformation, in terms of TR and right ventricular dilatation.
Key Words: Discordant atrioventricular connection Functional biventricular repair Conduit obstruction Tricuspid regurgitation
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1. Introduction
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The morphologically right ventricle as well as its inlet valve possess one of the important keys for an efficient circulation after classical biventricular repair for hearts with discordant atrioventricular connections, since these are to be placed to support the systemic circulation. In some patients, in fact, the right ventricle does function rather well with good competence of the tricuspid valve, and dysfunction of the ventricle or haemodynamically significant regurgitation across the tricuspid valve becomes obvious by means of clinical examinations in others [14]. This sort of functional deterioration would probably reflect morphological backgrounds. Musculature of the right ventricle should differ from that of the morphologically left ventricle, and Ebstein's malformation of the tricuspid valve is known to be frequent in this particular setting of atrioventricular connections [5,6]. Another cause of deterioration, nonetheless, could be the interaction between the left and the right ventricles. There are some reports found stating that relatively high pressure of the left ventricle seems beneficial to the function of the tricuspid valve when the pulmonary trunk is banded in patients with complete transposition previously undergoing intra-atrial redirection of blood as a definitive repair [710]. To determine whether this is also the case in those patients having discordant atrioventricular connections and having the circulation repaired in a functional biventricular fashion, our present investigation was carried out.
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2. Methods
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We reviewed the records of 15 patients (nine males and six females) with discordant atrioventricular connection and pulmonary outflow tract obstruction who underwent functional biventricular repair using external left ventriculepulmonary artery conduit since October 1978 at National Cardiovascular Center, Osaka, Japan.
2.1. Assessment of RV function
Tricuspid Regurgitation (TR) was assessed by color Doppler transthoracic echocardiography. TR was subjectively graded as follows: none, slight, mild, moderate, and severe. Right ventricular end-diastolic volume (RVEDV) was assessed quantitatively by angiography using biplane Simpson method. Normal predicted value was calculated from body surface area (81.95xBSA1.47). Ratio of systolic left ventricular pressure to right ventricular one (LVP/RVP) was measured in catheterization study.
2.2. Patients' clinical characteristics
Clinical data are summarized in Table 1. Age at operation ranged from 2.8 to 49 years (median 5.6 years), and follow-up period ranged from 17 months to 24 years (median 15 years). In 10 patients, systemic-to-pulmonary shunting operations had been carried out as palliative procedures. In terms of cardiac morphology, atrial situs was solitus in 12, and inversus in 3. Solitary outlet of the aorta from the morphologically RV with pulmonary atresia was seen in seven, double-outlet right ventricle with pulmonary stenosis in five, and ventriculoarterial discordance with pulmonary stenosis in two. Associated malformations were ventricular septal defect (VSD) in 14, and criss-cross atrioventricular connection in one. Preoperative TR was moderate in one, however, other patients had no significant TR. No patient had either Ebstein's anomaly or apparent tricuspid valve abnormality. Preoperative RV and LV pressures were equal in all patients.
2.3. Surgical technique
The surgical procedure was carried out via a median sternotomy using cardiopulmonary bypass, moderate systemic hypothermia, and cardioplegic cardiac arrest. As an external left ventriclepulmonary artery conduit, a valved conduit was used in seven (IonescuShiley bovine pericardial valved conduit in five and Hancock composite Dacron-porcine valved conduit in two), a hand-made trileaflet pericardial roll, which we call valved pericardial roll, in five (Rygg swine pericardium in three, Xenomedica equine pericardium in one, ePTFE sheet in one), and an autologous pericardial roll in two (Table 2). All but one required concomitant VSD closure. VSD was closed via aortotomy in eight, via right atriotomy in three, and via left ventriculotomy in three.
2.4. Data analysis
Changes of parameters were tested by use of paired Student's t-test (Statview 5.0; SAS Institute Inc., Cary, North Carolina). Values of P<0.05 were considered significant at the 95% confidence level.
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3. Results
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There was no early death. During the follow-up period, one patient died suddenly 17 months after the operation possibly due to arrhythmia, and another patient died after 12 years because of progressive RV failure (Table 3). Including these patients, six patients developed significant TR after the functional biventricular repair, and three of them required replacement of the tricuspid valve (TVR). Conduit replacement was carried out in other five patients (No. 6, 10, 11, 12, 13, 15) having progressive conduit obstruction. One patient required concomitant aortic valve replacement. Pacemaker implantation was needed in two patients because of complete atrioventricular block.
In 12 patients, excluding one who underwent early TVR (No. 10) and two patients who did not undergo preoperative angiography (Nos. 5 and 14), changes of LVP/RVP and RVEDV were assessed. Postoperative catheterization was carried out 13.3±7.5 months after the functional biventricular repair (range: 231 months). LVP/RVP decreased from 1.00±0.05 (range: 0.861.06) to 0.58±0.21 (range: 0.270.99) properly (Fig. 1) . Preoperative RVEDV was 104±24% of normal predicted value (range: 65145%), and postoperative angiography showed significant increase in RVEDV with the value of 137±39% (range: 100199%; P=0.015). Six of seven patients having postoperative LVP/RVP less than 0.6 developed TR greater than moderate. However, five patients with postoperative LVP/RVP over 0.6 were free from significant TR.

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Fig. 1. Right ventricular end-diastolic volume and ratio of systolic left ventricular pressure to right ventricular one were assessed both before and after the functional biventricular repair in 12 patients. Asterisk represents that tricuspid regurgitation was induced after the surgery.
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Similar evaluation was carried out in five patients who required conduit replacement (Fig. 2)
. All five patients had good tricuspid valve function before conduit replacement. They were catheterized 10.6±5.9 months after conduit replacement (range: 117 months). LVP/RVP was 1.08±0.34 (range: 0.791.67) before conduit replacement and was reduced to 0.58±0.14 (range: 0.360.72). RVEDV increased from 87±24% (range: 71128%) to 129±19% (range: 112154%), and this change was statistically significant (P=0.011). One patient with postoperative LVP/RVP of 0.36 developed moderate TR associated with right ventricular dilatation after conduit replacement, while other four patients with moderately elevated LVP/RVP maintained good tricuspid valve function.

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Fig. 2. Similar assessment was carried out both before and after the conduit replacement in five patients. Asterisk represents that tricuspid regurgitation was induced after the surgery.
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4. Discussion
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Since 1987, we have employed anatomical biventricular repair, the so-called double switch procedure, in patients with discordant atrioventricular connections [1117], and this alternative procedure has been our principal surgical choice in this setting. This is because the procedure, although rather extensive, can provide the systemic circulation supported by the morphologically left ventricle, and we consider that the circumstance has potential advantages. The tricuspid valve, even with some morphological abnormalities, is placed, and is likely to function reasonably, within the pulmonary circulation relatively low-pressured. Of course, the alternative procedure may pose some deleterious aspects in the future, such as atrial arrhythmia related to the surgical maneuver of intra-atrial redirection of blood. Apart from the logical assumptions concerning anatomical biventricular repair, we have to seek for better functional status in patients who are or who were not submitted for the double switch procedure because of morphological or other impediments, and also in those who underwent functional biventricular repair as a definitive procedure before 1987 at our institution.
Between 1978 and 1986, 24 patients with discordant atrioventricular connections underwent functional biventricular repair, and, between 1987 and 2003, of 56 patients with this particular atrioventricular connections submitted for definitive repair, 13 patients underwent functional biventricular repair because of morphological reasons which would have militated against successful establishment of the anatomical biventricular repair, such as VSD remote from the aortic orifice or small end-diastolic volume of the left ventricular chamber. Among all these 37 patients undergoing functional biventricular repair, we chose, in the present study, 15 patients whose channel from the left ventricle to the pulmonary arteries was reconstructed by placement of an external conduit.
A conduit with a valve structure is apt to become obstructive in the longer terms after repair, resulting in progressive elevation of the left ventricular pressure. Its influence on the interaction between the left ventricle and the right ventricle somehow resembles to that of banding of the pulmonary trunk after the atrial switch procedure in patients with complete transposition. In a clinical aspect, furthermore, the paediatricians commonly require the surgeons to reoperate on the patients demonstrating obvious pressure gradient between the left ventricle and the pulmonary arteries, based on the criteria that is applied for conduit stenosis between the morphologically right ventricle and the pulmonary arteries subsequent to anatomical biventricular repair, such as for tetralogy of Fallot with pulmonary atresia [18,19]. We, the surgeons, should know more precisely regarding the role of similar reoperation in those with functional biventricular repair physiology. These are the reasons of our patients' selection this time.
Our present retrospective review indicated that left ventricular pressure lower than 60% of the systemic right ventricular pressure at the systolic phase could be among deleterious factors in terms of TR and dilatation of the right ventricular cavity. In these respects, reoperation under the conventional criteria for obstruction between the right ventricle and the pulmonary arteries is not necessarily justifiable when employed completely leaving no pressure gradient between the left ventricle and the pulmonary arteries. Although we are unable to determine alternative criteria in this particular setting on the basis of the present investigation in this series, it is not unfair to suggest that the surgeon can choose a smaller conduit than usually used so as to provide some pressure gradient after reoperation. Similarly, at the time of initial functional biventricular repair, an external conduit, if needed, could better be designed smaller than a fully unobstructed channel. Even not intended, the channel may remain slightly or potentially obstructive. Because of the particular morphological features of the coronary arteries [20] and the papillary muscles, an incision to the left ventricle is often made at its middle or apical portion, rather than its outlet portion, and an external conduit from the left ventricle to the pulmonary arteries can be long. In reality, postoperative LVP/RVP appeared somewhat high (0.58±0.21), the value being greater than 0.6 in five patients (Fig. 1), although this series included some patients who underwent surgical procedures during recent years and in whom the surgeon intentionally left pressure gradient at the outflow from the pulmonary ventricle. Anyway, the surgeon might not be blamed for mild obstruction across the channel between the left ventricle and the pulmonary arteries after either reoperation for conduit stenosis or initial functional biventricular repair, since such a circumstance can benefit postoperative cardiac performance, at least in terms of TR.
Doty et al. suggested posterior pulmonary outflow tract resection and reconstruction placing operative manipulation posterior to the pulmonary annulus so as to preserve the conduction tissue [21]. As this technique usually leaves some pressure gradient, it might be attractive alternative to conduit repair in some selected circumstances in terms of preventing TR. However, we think it is also somewhat difficult to achieve intentional residual pressure gradient.
Mechanism of well-maintained function of the tricuspid valve, or relevance between TR and left ventricular pressure, remains speculative. In some articles reporting placement of pulmonary arterial banding after the atrial switch for complete transposition, they speculated that elevated left ventricular pressure would cause a shift of septal orientation and non-circular geometry of annular attachment of the tricuspid valve would protect against regurgitation across its orifice. Also for patients with discordant atrioventricular connections, there are reports of anatomical biventricular repair mentioning change in TR [22,23]. We could not quantify such features in our current series. Change in RVEDV could be one of the parameters, which imply a shift of the ventricular septum after decompression of the left ventricle. But, it unlikely expresses direct participation of geometrical change in structural shape of the annular attachment of the tricuspid valve.
In conclusion, on the basis of the present investigation, tricuspid insufficiency, regurgitation across the systemic inlet valve, can be promoted by usual entire decompression of the morphologically left ventricle for the pulmonary circulation in patients with discordant atrioventricular connections undergoing functional biventricular repair. We recommend to leave some degree of pressure gradient at the pulmonary channel so as to maintain appropriate left ventricular pressure, and not to apply a conventional and standard criteria for reoperation treating obstruction of the right ventricular outflow tract after anatomical biventricular repair.
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Footnotes
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Presented at the joint 17th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 11th Annual Meeting of the European Society of Thoracic Surgeons, Vienna, Austria, October 1215, 2003.
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Appendix A. Conference discussion
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Dr T. Ebels (Groningen, The Netherlands): Do you think that we should place a restrictive conduit at the time of the first operation?
Dr Koh: Yes, at the time of initial functional repair and at the time of reoperation as well.
Dr O. Ghez (Marseille, France): Could you tell us if your increase in LV volume was due to septal displacement or to annular dilatation of the tricuspid, please.
Dr Koh: This study was a retrospective study. And we could not quantify the septal shift or geometric change of the tricuspid valve. But in our study, in all patients left ventricular volume significantly increased associated with LVPA pressure depression. And some of them actually developed tricuspid regurgitation.
Dr R. Cesnjevar (Erlangen, Germany): In those patients developing tricuspid valve regurgitation, were there any anatomic abnormalities of the tricuspid valve or were they morphologically normal beforehand?
Dr G. Ziemer (Tuebingen, Germany): You used in all your patients LV-to-pulmonary artery conduit. Now, seeing your results, you may even go and forget about the conduit and try to resect the subpulmonary stenosis even if you were left with a 50 or 60-mm gradient, and then you could come to the same conclusions. So seeing your results, I would not be worried just to try to get rid of some of the stenosis and then you have not to use a conduit.
Dr Koh: Could you repeat your question.
Dr Ziemer: After you did some of your surgery and you got your findings, why did you continue to use a conduit in order to have no obstruction to start with but rather resect the subpulmonary stenosis although you may have left a certain gradient?
Dr Koh: During recent years, we intentionally used smaller conduit than was usually used.
Dr Ziemer: The question is, why don't you just resect the subpulmonary stenosis without putting the conduit?
Dr Koh: Oh, subpulmonary stenosis?
Dr Ziemer: Yes.
Dr Koh: In this series, all patients had subpulmonary stenosis.
Dr Ziemer: Of course, yes, but there are two possibilities, either you put a conduit or to resect the subpulmonary stenosis. And the question is, maybe it is better just to resect, thus leaving some gradient.
Dr Koh: Actually, it's a little bit difficult and unreasonable to obtain adequate pressure gradient with subpulmonary stenosis.
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