Asian Cardiovasc Thorac Ann 2006;14:213-218
© 2006 Asia Publishing EXchange Ltd
Right Ventricular Dysfunction Due to Right Ventricular Outflow Tract Patch
Jian-Jun Ge, MD,
Xue-Gong Shi, MS1,
Ru-Yuan Zhou, BS,
Min Lin, MS,
Sheng-Lin Ge, MS,
Shi-Bing Zhang, MS
Department of Cardiovascular Surgery
1 Department of Echocardiography, 1st Hospital of Anhui Medical University, Hefei, China
For reprint information contact: Jian-Jun Ge, MD Tel: 86 551 292 2452 Fax: 86 551 292 2008 Email: gejanjun{at}mail.hf.ah.cn, Department of Cardiovascular Surgery, 1st Hospital of Anhui Medical University, 218 Jixi Road, Hefei, Anhui 230022, China.
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ABSTRACT
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Doppler tissue imaging analysis was used to examine the relationship between right ventricular function and right ventricular outflow tract damage in 54 patients with repaired tetralogy of Fallot. The patients were divided into three groups: 16 in whom the right ventricular outflow tract was directly sutured (group DS), 23 who had transventricular patch repair (group TVP), and 15 who had transannular patch repair (group TAP). The control group consisted of 16 age-matched patients who underwent patch closure of a ventricular septal defect (group C). The Tei index was obtained from tricuspid and pulmonary Doppler flow velocities. The right ventricular Tei index was significantly greater in groups TVP and TAP than in group DS. Doppler tissue imaging analysis in groups TVP and TAP showed shorter myocardial systolic velocity, diastolic peak velocity, and atrial diastolic peak velocity, lower peak myocardial velocity and acceleration during isovolumic contraction, and prolonged isovolumic relaxation and contraction times compared to groups DS and C. Right ventricular dysfunction is due to the right ventricular outflow tract patch. Thus, the right ventricular outflow tract may be essential for right ventricular ejection and maintenance of right ventricular function.
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INTRODUCTION
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Repair of tetralogy of Fallot (TOF) has an excellent long-term prognosis and a 25-year survival of more than 94%.1 However, patients face considerable late morbidity and mortality. Right ventricular (RV) diastolic overloading due to pulmonary regurgitation results in RV enlargement and dysfunction, ventricular arrhythmia, and right heart failure.2–5 Pulmonary regurgitation is related to right ventricular outflow tract (RVOT) reconstruction, particularly using a transannular patch.6 As a result, surgical management has been modified to preserve pulmonary valve function when possible, and limit the extent of patching when a transannular type of repair is necessary. In a recent study, pulmonary regurgitation and RVOT aneurysm or akinesia were independently associated with RV dilation, and the latter with RV hypertrophy late after repair of TOF. Right ventricular outflow tract aneurysm and akinesia were common but related only in part to transannular patching. Right ventricular hypertrophy and RVOT aneurysm or akinesia were associated with lower RV ejection fraction (RVEF). Right ventricular volumes and pulmonary regurgitant volumes were equal, regardless of whether the pulmonary annulus had initially been spared.7 The risk factors for RV dilatation were not only pulmonary insufficiency but also an akinetic or dyskinetic area in the RVOT.8 Whether RV damage contributes to RV dysfunction in repaired TOF, and if patients have unnoticed developing ventricular dilatation in the early stages of follow-up, is still unclear. Therefore, we employed Doppler tissue imaging (DTI) analysis as a noninvasive technique to examine the relationship between RV dysfunction and RVOT damage in patients in the early stages of postoperative follow-up (2.9 ± 0.8 years) after TOF repair.9–12
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PATIENTS AND METHODS
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Between The period 1999 to 2003 was chosen to allow adequate postoperative follow-up while still reporting contemporary data. One hundred and fifteen patients who had undergone repair of TOF 2.9 ± 0.8 years previously, and 68 who had transatrial patch closure of a ventricular septal defect (VSD) were investigated. Twenty-six patients (23%) with TOF had direct suture of the RVOT, a transannular patch was used in 30 (26%), and a patch was placed on the infundibulum in 59 (51%). Patients were enrolled after obtaining their informed consent and the approval of the Ethics Committee of Anhui Medical University Hospital. Follow-up was completed between August and October 2004. During follow-up, almost half of the 115 patients had pulmonary insufficiency, residual outflow tract obstruction, residual VSD, or other morbidity such as right bundle branch block (RBBB) or low left ventricular ejection fraction (LVEF); it is well established that these features affect RV function.2–6,13 Therefore, to determine the relative role of RVOT damage in the genesis of RV dysfunction, these influencing factors were removed. The exclusion criteria for TOF patients were: significant pulmonary regurgitation (regurgitant fraction > 40%) or RVOT obstruction (transvalvular gradient > 30 mm Hg) and severe tricuspid regurgitation; New York Heart Association (NYHA) functional class III and IV; evidence of any resting cardiac arrhythmia; treatment with cardioactive drugs (digitalis, beta blockers, calcium-channel blockers, antiarrhythmics); and residual VSD. Fifty-four patients with repaired TOF and 16 age-matched patients with VSD were analyzed. The mean age at repair of TOF was 13.6 ± 8.3 years. Previous surgery and operative techniques in the TOF group are summarized in Table 1
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None of the 54 TOF patients had a systemic-pulmonary shunt as a palliative procedure before the operation. The operations were performed through a median sternotomy incision. Cardiopulmonary bypass was established using bicaval cannulation, a left ventricular vent through an atrial septum incision, and moderate hypothermia. The heart was arrested by antegrade administration of dilute blood cardioplegia delivered into the aortic root. After aortic crossclamping, a trans-right atrial and trans-outflow tract incision was made. All VSDs in patients with TOF were closed through a right ventriculotomy. All parieto septal and parieto parietal muscle bundles of the RVOT were widely resected. Commissurotomy was performed for pulmonary valve stenosis. To preserve pulmonary competence, transannular patching was reserved for cases in which the annulus was obviously too small, or when the systolic RV pressures obtained by direct measurement at the end of the procedure were > 80% of the systolic LV pressures. A transannular incision was used in 30 patients: incisions were extended from the right ventricle to the main pulmonary artery up to its bifurcation, and always divided the sinotubular attachment of the pulmonary valve. All transannular incisions were closed with an autologous pericardial patch. Repair was performed through an incision limited to the right ventricle in 85 patients, of whom 26 had a pulmonary infundibulum large enough to be closed directly; the right ventriculotomy was closed with a combined patch of autologous pericardium and Dacron in 59 patients (Table 1
). For VSD closure, a patch was made according to the VSD size and shape, and attached with 3 to 5 interrupted 4/0 Dacron sutures with a pledget through the tricuspid valve (atrium to ventricle). At the juncture of the VSD and the valve ring, 2 interrupted 5/0 polypropylene sutures were inserted with a pledget to the patch, and a continuous suture was made between them. In all electrocardiograms, QRS duration was measured manually and defined as the maximal QRS duration over all leads. On echocardiography, pulmonary insufficiency was described as mild if the regurgitant jet started at the valve, moderate if it started in the main pulmonary artery, and severe if it started in the pulmonary artery branches. A complete 2-dimensional and pulsed Doppler echocardiographic examination was performed using an ultrasonoscope (Hip ProSound SSD-5500; Aloka Co., Ltd., Tokyo, Japan) with a 3.5 MHz transducer. Pulsed-wave DTI was carried out by activating the DTI function in the same unit. The DTI program was set to pulsed-wave Doppler mode. Filters were set to exclude high-frequency signals. Gains were minimized to allow a clear tissue signal with minimal background noise. The DTI velocities were obtained from the 4-chamber view of each subject. A 2 mm sample volume was placed at the lateral corner of the tricuspid annulus. The peak myocardial velocities during early diastole, late diastole, systole, and isovolumic contraction were recorded at a sweep speed of 100 mm·s–1. Myocardial acceleration during isovolumic contraction (IVA) was measured by dividing the myocardial velocities during isovolumic contraction by the time interval from the onset of the myocardial velocity during isovolumic contraction (IVV) to the time at peak velocity of this wave, as described by Toyono and colleagues.11 The isovolumic contraction time was measured from the end of the myocardial velocities during late diastole to the beginning of the myocardial velocities during systole. The Tei index was calculated from the equation: Tei = (isovolumic contraction time + isovolumic relaxation time)/ejection time.
Data are reported as mean ± standard deviation or as percentages. Groups were compared using the chi-squared test for dichotomous variables and the Student t test for continuous variables.
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RESULTS
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Two patients with TOF died during follow-up after complete repair. One death occurred almost immediately after the operation, and the other was a sudden cardiac death in a 9-year-old boy. Actuarial survival was 98% at both 1 and 4 years. However, an RBBB pattern on the postoperative surface electrocardiogram was found in 77% (89/115) of patients. Poor clinical condition (NYHA functional class III) was found in cases of right atrial and RV dilatation. As was the case in approximately 50% of all subjects, echocardiography determined factors that directly affect RV function, including pulmonary regurgitation, tricuspid insufficiency, residual VSD, or RV outflow tract obstruction. Arrhythmias also related to poor condition. Three patients required further procedures because of RV dilatation due to pulmonary regurgitation (regurgitant fraction > 80%), RV outflow tract obstruction (transvalvular gradient > 60 mm Hg), and residual VSD; 94% (108/115) were in NYHA class I and II.
All patients had the characteristic pattern of RV myocardial velocities with apically directed myocardial velocities during systole and isovolumic contraction, and myocardial velocities during early and late diastole directed toward the base of the heart. As shown in Table 2, there were no significant differences in LVEF between the TOF and VSD groups ( p = 0.56). Compared to direct suture of the RVOT (group DS), DTI velocities for patients with transventricular and transannular patch repairs showed decreased myocardial velocities during early diastole (group TVP, p = 0.000067; group TAP, p = 0.00036), late diastole (TVP, p = 0.041; TAP, p = 0.023), and systole (TVP, p = 0.021; TAP, p = 0.0036), but no significant differences compared to the patch repair of the VSD group (group C, p > 0.05). In groups TVP and TAP, the peak IVA and IVV also decreased compared to group DS (TVP vs DS: IVV, p = 0.032; IVA, p = 0.0079. TAP vs DS: IVV, p = 0.023; IVA, p = 0.025). The isovolumic contraction and relaxation times for patients in group TVP and TAP were significantly longer than for those in group DS (TVP vs DS: isovolumic contraction time, p = 0.0015; isovolumic relaxation time, p = 0.00031. TAP vs DS: isovolumic contraction time, p = 0.00067; isovolumic relaxation time, p = 0.0068). The RV Tei index in groups TVP (0.64 ± 0.15) and TAP (0.62 ± 0.08) was significantly higher than in group DS (0.52 ± 0.07). There were no significant differences between groups C and DS (0.52 ± 0.07 vs. 0.52 ± 0.08, p = 0.86).
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DISCUSSION
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Most of the problems reported during the late follow-up of patients after repair of TOF have been related to abnormal RV physiology. Residual pulmonary incompetence, exercise intolerance, and malignant ventricular arrhythmias have been identified as predictors of unfavorable long-term outcome.1 As operative techniques and myocardial protection have improved in recent years, interest has centered around RV diastolic function in patients with repaired TOF. In particular, restrictive RV diastolic function has been observed early and late after repair of TOF. After 30 years, this RV dilatation was responsible for either death or re-operation in as many as 35% of patients in this study. Until a few years ago, it was thought that this problem could be controlled if incisions and patching did not extend through the pulmonary annulus. However, this policy has been shown to be ineffective as patients who had transannular patching or patching limited to the right ventricle had the same outcome.14
Pulmonary insufficiency is not the only determinant of late symptomatic RV dilatation after repair of TOF.8 Pulmonary insufficiency seems more deleterious in patients who had RVOT patching. Long-term pulmonary insufficiency alone is responsible for a slight degree of RV dilatation, but symptoms may develop much later if the contractility of the pulmonary infundibulum is preserved. The pulmonary infundibulum may be essential for RV ejection, and for maintaining pulmonary valve competence.8 Regardless of whether patching the pulmonary annulus has positive consequences on the risk of RV dilatation, it was hypothesized that pulmonary infundibular contractility might play a key role in protecting RV function after TOF repair, even if patients had unnoticed developing ventricular dilatation in the early stages of follow-up. To ascertain the validity of this hypothesis, our TOF patients with transventricular and transannular patch repair were compared with those with less RVOT impairment (transatrial patch closure of VSD and direct closure of RVOT). It was speculated that patients who had undergone surgery for less RVOT impairment were the ideal group as almost half of the 115 subjects had pulmonary insufficiency or residual outflow tract obstruction, residual VSD, RBBB, low LVEF, or arrhythmia. It is clear that all these factors are related to RV function and must be eliminated to determine the relative role of RVOT damage in the genesis of RV dysfunction.2–6 D’Andrea and colleagues15 demonstrated that RV myocardial activation delay in adults with RBBB occurred late after repair of TOF. As our TOF patients had a high incidence of RBBB, we had to find VSD patients with RBBB to remove this influence.
This study demonstrates the usefulness of TDI for analyzing the RV myocardial pattern late after repair of TOF.10,11,13,15 Compared with direct suture of the RVOT, transventricular or transannular patch repair causes: decreased myocardial velocities during early diastole, late diastole, and systole; decreased peak myocardial velocity and acceleration during isovolumic contraction; and a significantly higher RV Tei index. However, there were no significant differences between those with direct suture of the RVOT and transatrial patch repair of a VSD. These results suggest that RV dysfunction might be due to the RVOT patch.
Davlouros and colleagues7 showed the detrimental role of RV outflow aneurysms or akinesia and demonstrated their strong relationship with RV dysfunction. However, RVOT contractile dysfunction is not necessarily related to the use of a patch because RVOT akinesia or aneurysm was present in a significant number of patients (17/35, 48.5%) who did not undergo patch repair. This raises the question as to whether other factors, such as extreme myectomy (infundibular resection) and/or ischemic insult (perhaps due to conal branch interruption) are also responsible for the genesis of RVOT aneurysm or akinesia. Further support for this comes from Atallah-Yunes and colleagues16 who reported less RV dilation and preserved RV systolic function late after TOF repair with a modified approach for relieving RVOT obstruction by employing a short infundibular resection and avoiding extensive myectomy. These wall motion abnormalities were thought to be responsible for a reduction in angiographic RVEF and were more common following transventricular than transatrial repair. Recent studies have shown RV patching (RVOT or transannular) to be a significant predictor of late adverse events after repair of TOF.14 Davlouros and colleagues7 found increased RV end-diastolic and end-systolic volume indices and pulmonary regurgitant fraction in patients with transannular or RVOT patching compared to those without patch repair, whereas no such differences existed between the two patch subgroups.
Our data suggest that RVOT reconstruction with either a transannular or RVOT patch may have an immediate detrimental effect because patch repair (perhaps in conjunction with other factors such as RVOT myectomy) leads to RVOT aneurysm or akinesia, the RVOT motion is lost, or the ROVT had less systolic and diastolic function prior to the procedure. There is a striking difference between the RV function of repaired TOF patients with direct RVOT closure and those who have undergone patching. Hence it seems likely that the pulmonary infundibulum plays a role in protecting the right ventricle against the deleterious consequences of chronic pulmonary regurgitation. Thus, we suspect that damage to the RVOT during TOF repair is fundamental to the development of RV dysfunction. If the pulmonary infundibulum is not the passive conduit it was once thought to be but plays an active part in RV contraction and pulmonary valve function, then operations should be designed to preserve its integrity. In transatrial, as in transventricular repair, the annular area often requires patch enlargement. However, in transatrial repair, the incision starts from the pulmonary artery rather than the mid ventricle, such as in the transventricular approach.17,18 Although the transatrial approach necessitates wide resection of the inner muscular features of the pulmonary infundibulum, one can hope that this approach may better preserve the contractile function of the subpulmonary area. We would submit that preservation of pulmonary valve function and avoiding or limiting RVOT and transannular patching, and perhaps avoidance of extensive RVOT myectomy, are likely to preserve long-term RV systolic function.
The extent of the RV incision is very important to postoperative RV function, but to limit it to the infundibulum is incompatible with prevention of residual RVOT obstruction. So, it is insufficient to presume that the reconstructed RVOT acts as a "canal". The RVOT and RV must be reconstituted as the same "cava". The incision in the RVOT should be made as short as possible to avoid effects on RVOT function. The right ventriculotomy is closed with a combined patch (autologous pericardium and Dacron patch) and should be made short and wide. These techniques will prevent residual outflow tract obstruction and avoid RVOT aneurysm.
The pool of patients used in this study represents a very selected group of survivors of early surgical repair of TOF. To assess the effect of RV dysfunction, those with resting arrhythmias, significant pulmonary regurgitation, or RVOT obstruction were excluded. However, the effect on LV function has not been investigated. Additional predictors of biventricular dysfunction may exist and be identified with a larger patient sample and longer periods of observation, where different surgical strategies are employed. Furthermore, future studies need to address the effects of surgical intervention on biventricular function and the right-to-left interaction. It was concluded from this study that pulmonary insufficiency may not be the main factor causing RV dysfunction after TOF repair. Right ventricular dysfunction is due to the RVOT patch. The pulmonary infundibulum may be essential for complete RV ejection and maintenance of RV function. Operations should be designed to preserve its contractility.
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REFERENCES
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ABSTRACT
INTRODUCTION
