| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Cardiac Imaging |
1 From the Departments of Radiology (A.v.S., A.d.R.), Cardiology (H.W.V., J.J.B., E.E.v.d.W.), Cardiothoracic Surgery (M.G.H., P.H.S.), and Pediatric Cardiology (J.O.), Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, the Netherlands. From the 2002 RSNA scientific assembly. Received May 22, 2003; revision requested August 4; final revision received February 25, 2004; accepted April 1. Address correspondence to A.d.R. (e-mail: a.de_roos@lumc.nl).
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
|---|
MATERIALS AND METHODS: The medical ethics committee approved this study, and informed consent was obtained. Cardiac magnetic resonance (MR) imaging was performed before, 7 months after, and 19 months after PVR in 25 consecutive patients with tetralogy of Fallot with a 1.5-T MR imager. RV function was assessed with gradient-echo sequences in the short-axis plane. Pulmonary flow was assessed with a velocity-encoded phase-contrast sequence. Paired t test was used to evaluate follow-up data. Independent samples t test was used to assess differences based on the presence of recurrent pulmonary regurgitation (PR).
RESULTS: Mean indexed RV end-diastolic volume decreased from 166.9 mL/m2 ± 41.3 before PVR to 113.5 mL/m2± 35.7 (P < .001) at 7-month follow-up and 111.7 mL/m2± 41.1 (P = .46) at 19-month follow-up. The RV ejection fraction was corrected for PR and improved from 25.0% ± 7.7 before surgery to 44.1% ± 11.9 (P < .001) and 45.2% ± 11.1 (P = .39), at 7- and 19-month follow-up, respectively. Recurrent PR after PVR was found in 11 patients; 14 patients did not have recurrent PR. Total reduction of indexed RV end-diastolic volume at 19 months follow-up was more prominent in patients who did not have recurrent PR than in patients who did have recurrent PR (P < .05). Furthermore, improvement of RV ejection fraction corrected for regurgitation was more marked in patients who did not have recurrent PR than in patients who did have recurrent PR (P < .05).
CONCLUSION: In patients with tetralogy of Fallot, RV function improves rapidly after PVR and is sustained at 19-month follow-up in most patients; however, recurrence of PR after PVR appears to reduce recovery of RV systolic function.
© RSNA, 2004
Index terms: Heart, function, 523.145 • Heart, MR, 523.121412 • Heart, surgery, 51.45 • Heart, ventricles, 523.145 • Tetralogy of Fallot, 52.145
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
|---|
Pulmonary valve replacement (PVR) is often performed in patients with tetralogy of Fallot who have longstanding PR and severe RV dilatation and leads to direct volumeunloading of the RV. In a recent study by Vliegen et al (13), the early hemodynamic effects of PVR in adults were evaluated 24 years after initial repair of tetralogy of Fallot. A significant decrease of RV dilatation of approximately 30% and an improvement of systolic function and validity according to the New York Heart Association classification was found in these patients 7 months after surgery. Mid- and long-term outcome in patients after PVR is largely unknown. Several reports have mentioned residual or recurrent PR after surgery (14,15); however, we are unaware of any studies that have systematically evaluated the clinical importance of recurrent PR and the time course of RV recovery.
Accordingly, the purpose of this study was to assess the time course of RV function improvement after pulmonary PVR in patients long after repair of tetralogy of Fallot.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
|---|
|
MR Imaging
MR studies were performed with a 1.5-T system (NT15 Gyroscan; Philips Medical Systems, Best, the Netherlands). The MR protocol has been described previously (13). In summary, a multiphase electrocardiographically triggered multishot echoplanar gradient-echo technique was used to acquire short-axis images. Images were acquired during breath holds. Section thickness was 10 mm, with a section gap of 0.8–1.0 mm. The flip angle was 30°, and the echo time was 5–10 msec. A total of 18–25 frames were obtained per cycle and resulted in a temporal resolution of 22–35 msec.
Velocity mapping was performed with a velocity-encoded phase-contrast sequence. For velocity mapping of the pulmonary artery, sagittal and coronal spin-echo scout images were used to construct a double-oblique plane perpendicular to the vessel. Pulmonary flow measurements were obtained halfway between the pulmonary valve and the bifurcation or approximately 2 cm proximal to the bifurcation when no pulmonary valve was present. The sequence was encoded for through-plane velocities of up to 200 cm/sec. For velocity mapping of flow through the tricuspid valve, two- and four-chamber gradient-echo images were used to construct a parallel plane through the valve. The flip angle was 20°, echo time was 12 msec, and temporal resolution was 25–35 msec. No sedation was used in any of the patients.
Postprocessing
All images were quantitatively analyzed at a Sun workstation (Sun Microsystems, Mountain View, Calif) with two software packages that were developed and validated at our institution (16). Image analysis can be performed with low inter- and intraobserver variability (17,18). All contours were drawn manually by the same observer (A.v.S.). Velocity maps were analyzed by using the analytic software package (Flow; Medis, Leiden, the Netherlands). Contours were drawn for the main pulmonary artery, and flow data were obtained from the velocity data of each voxel in all phases. Flow curves were obtained with this method for flow in the main pulmonary artery during a cardiac cycle. The regurgitant fraction was calculated with the following formula: (regurgitant flow dived by systolic forward flow) times 100. PR was considered statistically significant if the regurgitant fraction was more than 5% of the systolic forward flow. In addition, flow curves for flow through the tricuspid valve were assessed by using the same method.
The transverse gradient-echo images of the ventricles were analyzed with software (Mass; Medis) (16). The RV end-diastolic and end-systolic volumes were assessed by drawing contours around the lumen of the RV at end diastole and end systole in all sections, as described previously (19). Section summation was used, and the total RV end-diastolic and end-systolic volumes were calculated with the software. RV stroke volume was then calculated with the software by deducting the RV end-systolic volume from the RV end-diastolic volume. RV ejection fraction was calculated by dividing the RV stroke volume by the RV end-diastolic volume. RV ejection fraction was then corrected for regurgitation of the tricuspid and pulmonary valves by dividing the net pulmonary flow by the RV end-diastolic volume, thus the corrected RV ejection fraction was equal to the net pulmonary flow, which was calculated by subtracting regurgitant flow from pulmonary forward flow and then dividing by the RV end-diastolic volume (13). RV end-diastolic volume and RV end-systolic volume were indexed for body surface area.
Statistical Analysis
All data are presented as mean values ± 1 standard deviation, unless stated otherwise. Data were analyzed by using SPSS for Windows (version 10.0; SPSS, Chicago, Ill). The paired samples Student t test was used to evaluate changes in MR parameters after PVR, and the independent samples Student t test was used to identify differences between patients with and those without recurrent PR. Statistical significance was indicated by a P value of less than .05. Repeated measuring of the variables of interest (eg, end-diastolic volume) was accounted for with a repeated-measures model (linear mixed model). Testing for equality of slopes for regression lines of variables of interest versus time was performed for the indexed RV end-diastolic volume and corrected ejection fraction. Because the latter variable is a percentage, it did not show gross violations of normality with the Kolmogorov-Smirnov test or at visual inspection.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
|---|
|
Baseline characteristics for both groups were similar (Table 2). Surgical techniques, however, were different between patients who had recurrent PR and those who did not. Ten patients received a pericardial patch to adapt the homograft to the RV outflow tract, and only one of them had early recurrent PR. Surgical reduction of the RV outflow tract in case of aneurysm formation was performed in four patients. No early recurrence of PR was seen in these patients. Three patients underwent surgical reduction of the RV outflow tract and insertion of a pericardial patch in the RV outflow tract. In this group, no patient had early recurrent PR. Late recurrent PR, however, was discovered in four patients with a pericardial patch and in one patient with surgical reduction of the RV outflow tract.
|
|
Three patients with recurrent PR (early recurrent PR, n = 2; late recurrent PR, n = 1) did not experience a reduction in indexed RV end-diastolic volume. These three patients had neither improvement of RV systolic function nor improvement of validity. These observations indicate that recurrent PR has a negative effect on the recovery of RV function.
RV systolic function improved along the same time course as the improvement of RV dilatation. The mean indexed RV end-systolic volume before PVR was 95.2 mL/m2± 34.7 in patients without recurrent PR and 102.4 mL/m2± 40.7 in patients with recurrent PR. In patients without recurrent PR, mean indexed RV end-systolic volume decreased to 58.3 mL/m2± 16.3 at 7-month follow-up (P < .01 compared with that obtained at baseline MR imaging); this was followed by a further decrease to 50.6 mL/m2± 12.8 at 19-month follow-up (P = .02 compared with that obtained at 7-month follow-up). The patients with recurrent PR had a mean indexed RV end-systolic volume of 73.9 mL/m2± 50.7 at 7-month follow-up (P = .02 compared with that obtained at baseline MR imaging) and 75.2 mL/m2± 54.4 at 19-month follow-up (P = .82 compared with that obtained at 7-month follow-up).
The RV ejection fraction corrected for PR increased from 25.2% ± 8.8 to 48.9% ± 9.3 at 7-month follow-up (P < .01 compared with that obtained at baseline) and 49.8% ± 5.8 at 19-month follow-up (P = .14 compared with that obtained at 7-month follow-up) in patients who did not have recurrent PR. The RV ejection fraction corrected for PR increased from 24.6% ± 6.1 to 38.3% ± 12.5 at 7-month follow-up (P = .03 compared with that obtained at baseline) and 38.4% ± 13.1 at 19-month follow-up (P = .86 compared with that obtained at 7-month follow-up) in patients who did have recurrent PR. Moreover, the results of repeated-measures analysis (linear mixed model) showed that the time course of improvement of RV ejection fraction corrected for PR is different (P = .04).
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
|---|
RV Dilatation
We found a significant decrease in RV dilatation after PVR. This observation is in accordance with observations of previous researchers, who have found a decrease in RV dilatation of approximately 30% in patients with tetralogy of Fallot after PVR in children (14,20) in follow-up studies performed up to 2 years after surgery. These reports suggest that volume unloading due to elimination of PR may be the most important factor. In these studies, however, no distinction was made between patients with and those without recurrent PR.
In our population, the time course of decrease of RV dilation was influenced by the recurrence of PR. Furthermore, if recurrent PR was detected at early follow-up, decrease of RV volumes was limited, and little additional decrease of RV volumes was found at 17-month follow-up. Moreover, the late recurrence of PR coincided with a late increase of RV volumes, although the initial decrease of RV volumes was in the normal range. This finding supports the concept that recurrent PR has a detrimental effect on RV function after PVR.
RV Systolic Function
RV systolic function was measured with the RV ejection fraction and the RV end-systolic volume. Systolic performance was corrected for the degree of PR, as previously reported (13). In a previous study by Bove et al (20), a significant reduction of RV dilatation after PVR was found in 11 patients with tetralogy of Fallot; only a marginal increase in the EF was found, although most patients reported a subjective improvement in exercise tolerance. The improvement of systolic function was possibly obscured in the study by Bove et al (20), because RV ejection fraction was not corrected for the change in loading conditions.
In the present study, both RV dilatation and systolic function improved along the same time course. In case of recurrence of PR after PVR, there is less decrease of RV volume and subsequently, less improvement of systolic function when compared with that in patients who did not experience recurrence of PR. Thus, we speculate that improvement of systolic function is a direct consequence of volume unloading after valve replacement.
Recurrent PR after PVR
The recurrence of PR after PVR has been reported by several other authors. Therrien et al (15) studied 70 patients before and after PVR by using echocardiography. In their study, 92% of patients had at least moderate PR before surgery. In 11 (20%) patients, at least moderate recurrent PR was found after PVR. Warner et al (14) studied 16 patients with tetralogy of Fallot who underwent PVR for moderate or severe PR. After PVR, four patients had moderate recurrent PR. All four had a unilateral or bilateral stenosis of the pulmonary artery branches, as indicated by postoperative pulmonary artery pressure gradients of more than 20 mm Hg, which indicates that residual pulmonary stenosis after surgery might induce the recurrence of PR. In our study, five patients had significant pulmonary stenosis before PVR, but all were treated during subsequent surgery; therefore, we conclude that pulmonary stenosis does not contribute to the recurrence of PR.
Causes for recurrent PR are largely unknown. Different mechanisms could play a role in the early and late recurrence of PR. We believe that early recurrent PR is likely due to surgical technical factors, such as distortion of the homograft at implantation. Distortion may be caused by an imperfect fit of the graft when the RV outflow tract diameter and homograft diameter show a substantial discrepancy in size. We propose the hypothesis that failure to reduce a grossly enlarged RV outflow tract may result in lack of central leaflet coaptation and subsequent regurgitation. The detrimental role of akinesia or aneurysm formation in the RV outflow track of RV dilatation and systolic function, independent of the presence of PR, has recently been shown by Davlouros et al (11). By using a small RV outflow tract patch (autologous or xenopericardium), the adaptation of the homograft may be improved in some cases. Perioperative reduction of the RV outflow tract was performed in four of our patients, and the fact that none of them had residual or early recurrent PR supports this hypothesis. Furthermore, of the 10 patients who received a pericardial patch to obtain a better fit between the RV outflow tract and the homograft, early recurrent PR was found in only one.
In our study, one patient showed deterioration of RV function and validity after PVR. In this patient, a mismatch between the grossly enlarged RV outflow tract and the homograft led to severe recurrent PR shortly after PVR. During a PVR procedure that was performed 2 years after initial PVR, the RV outflow tract volume was significantly reduced. In the first 6 months after this second PVR, recurrent PR was not found, and RV function was greatly improved in this patient.
The mechanism of late recurrent PR might be different from that of early recurrent PR. Oei et al (21) reported that the insertion of allograft valve conduits in both children and adults leads to an increase of T-lymphocyte precursor cells with a potentially damaging effect toward the heart valve homograft. Immunologic mechanisms of homograft dysfunction seem to occur mainly in small infants, whereas degenerative processes in homografts of adult patients are less related to immunologically mediated inflammatory responses. Slow calcific graft degeneration due to fiber rupture and infiltration of several blood components and calcium seems to be the predominant mechanism in adults (22,23).
Limitations
Since patients were not randomized before surgery, definite conclusions on the relationship between surgical technique and recurrence of PR cannot be made. Furthermore, longer follow-up is needed to evaluate the long-term effects of recurrent PR on RV function and overall validity and the possible need for additional surgery. A multicenter study with a large patient group and long follow-up could provide more insight into the factors that influence recovery of RV function after PVR.
PVR in adults with tetralogy of Fallot who have moderate to severe PR leads to a rapid recovery of RV function. At midterm follow-up as much as 19 months after surgery, RV function recovery is sustained in the majority of patients; however, recurrence of PR after PVR appears to reduce recovery of RV systolic function. Baseline characteristics do not predict recovery of RV function, whereas surgical techniques appear to be relevant to prevent recurrence of PR and thereby may affect recovery of RV function.
|
FOOTNOTES |
|---|
Authors stated no financial relationship to disclose.
Author contributions: Guarantors of integrity of entire study, all authors; study concepts and design, all authors; literature research, A.v.S.; clinical studies, A.v.S., A.d.R.; data acquisition, all authors; data analysis/interpretation, A.v.S., H.W.V., A.d.R., M.G.H.; statistical analysis, A.v.S.; manuscript preparation and definition of intellectual content, all authors; manuscript editing, A.v.S., A.d.R.; manuscript revision/review and final version approval, all authors
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTSDISCUSSIONREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  S. Chua, R. A. Levine, C. Yosefy, M. D. Handschumacher, J. Chu, A. Qureshi, J. Neary, T.-T. Ton-Nu, M. Fu, C. J. Wu, et al. Assessment of right ventricular function by real-time three-dimensional echocardiography improves accuracy and decreases interobserver variability compared with conventional two-dimensional views Eur J Echocardiogr, July 1, 2009; 10(5): 619 - 624. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H B Grotenhuis, L J M Kroft, S G C van Elderen, J J M Westenberg, J Doornbos, M G Hazekamp, H W Vliegen, J Ottenkamp, and A de Roos Right ventricular hypertrophy and diastolic dysfunction in arterial switch patients without pulmonary artery stenosis Heart, December 1, 2007; 93(12): 1604 - 1608. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Coats, S. Khambadkone, G. Derrick, M. Hughes, R. Jones, B. Mist, D. Pellerin, J. Marek, J. E. Deanfield, P. Bonhoeffer, et al. Physiological consequences of percutaneous pulmonary valve implantation: the different behaviour of volume- and pressure-overloaded ventricles Eur. Heart J., August 1, 2007; 28(15): 1886 - 1893. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Oosterhof, A. van Straten, H. W. Vliegen, F. J. Meijboom, A. P.J. van Dijk, A. M. Spijkerboer, B. J. Bouma, A. H. Zwinderman, M. G. Hazekamp, A. de Roos, et al. Preoperative Thresholds for Pulmonary Valve Replacement in Patients With Corrected Tetralogy of Fallot Using Cardiovascular Magnetic Resonance Circulation, July 31, 2007; 116(5): 545 - 551. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Oosterhof, H. W Vliegen, F. J Meijboom, A. H Zwinderman, B. Bouma, and B. J M Mulder Long-term effect of pulmonary valve replacement on QRS duration in patients with corrected tetralogy of Fallot Heart, April 1, 2007; 93(4): 506 - 509. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. R. Henkens, A. van Straten, M. J. Schalij, M. G. Hazekamp, A. de Roos, E. E. van der Wall, and H. W. Vliegen Predicting Outcome of Pulmonary Valve Replacement in Adult Tetralogy of Fallot Patients Ann. Thorac. Surg., March 1, 2007; 83(3): 907 - 911. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Oosterhof, F. J. Meijboom, H. W. Vliegen, M. G. Hazekamp, A. H. Zwinderman, B. J. Bouma, A. P.J. van Dijk, and B. J.M. Mulder Long-term follow-up of homograft function after pulmonary valve replacement in patients with tetralogy of Fallot Eur. Heart J., June 2, 2006; 27(12): 1478 - 1484. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P A Davlouros, K Niwa, G Webb, and M A Gatzoulis The right ventricle in congenital heart disease Heart, April 1, 2006; 92(suppl_1): i27 - i38. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. I. Norton, C. Tong, R. B. J. Glass, and J. C. Nielsen Cardiac MR Imaging Assessment Following Tetralogy of Fallot Repair RadioGraphics, January 1, 2006; 26(1): 197 - 211. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. van Straten, H. W. Vliegen, H. J. Lamb, S. D. Roes, E. E. van der Wall, M. G. Hazekamp, and A. de Roos Time Course of Diastolic and Systolic Function Improvement After Pulmonary Valve Replacement in Adult Patients With Tetralogy of Fallot J. Am. Coll. Cardiol., October 18, 2005; 46(8): 1559 - 1564. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Kuehne, B. K. Gleason, M. Saeed, D. Turner, J. Weil, D. F. Teitel, C. B. Higgins, and P. Moore Combined pulmonary stenosis and insufficiency preserves myocardial contractility in the developing heart of growing swine at midterm follow-up J Appl Physiol, October 1, 2005; 99(4): 1422 - 1427. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. P. Graham Jr The Year in Congenital Heart Disease J. Am. Coll. Cardiol., June 7, 2005; 45(11): 1887 - 1899. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| RADIOLOGY | RADIOGRAPHICS | RSNA JOURNALS ONLINE |
