Asian Cardiovasc Thorac Ann 2005;13:24-29
© 2005 Asia Publishing EXchange Ltd
Left Ventricular Dysfunction after Closure of Large Patent Ductus Arteriosus
M Omar Galal, MD,
Mohamed Amin, MD,
Arif Hussein, MD,
Amjad Kouatli, MD,
Jameel Al-Ata, MD,
Ahmed Jamjoom, MD
Cardiovascular Department, King Faisal Specialist Hospital and Research Center, Jeddah, Saudi Arabia
For reprint information contact: M Omar Galal, MD Tel: 966 2 667 7777 Fax: 966 2 663 9581 Email: ogalal{at}yahoo.com, Cardiovascular Department, MBC J 16, King Faisal Specialist Hospital and Research Centre, P.O. Box 40047, Jeddah 21499, Saudi Arabia.
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ABSTRACT
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Changes in left ventricular dimensions and performance were studied in 43 patients after transcatheter occlusion or surgical ligation of patent ductus arteriosus. The patients were assigned to 2 groups based on their ductal diameter: 
3.1 mm to group A (n = 27) and 
3 mm to group B (n = 16). The mean age and weight of the groups were comparable. Before intervention, group A had a significantly larger mean left ventricular end-diastolic diameter than group B, while all patients had normal shortening fraction and ejection fraction. Within 1 month after intervention, left ventricular end-diastolic diameter showed a trend towards regression while shortening fraction and ejection fraction decreased significantly in group A. There were no significant changes in these parameters in group B. Between 1 and 6 months after intervention, left ventricular performance improved in most of the group A patients who were followed up. We conclude that closure of large ductus arteriosus in children leads to significant immediate deterioration of left ventricular performance, which appears to recover within a few months. Echocardiographic study before hospital discharge is recommended in these patients. Serious deterioration of ventricular performance after closure may warrant the use of angiotensin converting enzyme inhibitors.
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INTRODUCTION
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Transcatheter closure of small to moderate-sized patent ductus arteriosus (PDA) is an accepted treatment modality,1–4 but for large PDA it is only recently that transcatheter closure has emerged as a possible alternative to surgical ligation.5–8 We had noted significant deterioration of left ventricular (LV) performance in a 12-year-old patient a few hours after successful transcatheter closure of a large PDA. It took almost 3 months for the LV performance to recover. A good explanation could not be found for this observation, but a possible mechanism is Starling’s effect resulting from changes in preload and afterload subsequent to closure. This study was then conducted to investigate if changes in LV dimensions and performance do occur after closure of large PDA.
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PATIENTS AND METHODS
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All patients (n = 54) who underwent successful transcatheter closure or surgical ligation of PDA between February 2000 and April 2002 were reviewed for inclusion in this study. Patients were selected for either transcatheter occlusion or surgical ligation based on their weight and echocardiographic evaluation. Those with a very large PDA (narrowest diameter > 7 mm) and weighing below 5 kg were referred directly for surgical ligation. The inclusion criteria for this study were patients who had an isolated problem of PDA that was successfully closed surgically or by transcatheter closure as well as patients who underwent surgical ligation after transcatheter closure failed (1 patient had a failed Amplatzer occlusion). The exclusion criteria were the following: premature babies and neonates regardless of weight; patients who, after transcatheter closure, were left with a more than moderate amount of residual left-to-right shunt (a residual PDA > 2 mm and a jet reaching the pulmonary valve, as judged by color Doppler echocardiography); patients with other congenital heart defects in addition to PDA; and patients who underwent concomitant PDA occlusion and other interventions. It was assumed that in these patients the associated lesions would affect LV volume and function. A total of 11 patients were excluded from the study.
The 43 patients who qualified for this study were divided into 2 groups according to the narrowest diameter of their PDA as measured by angiography in the descending aorta: 3.1 mm to group A (27 patients) and 3 mm to group B (16 patients). In 4 patients who were sent for surgery without cardiac catheterization, the narrowest diameter as determined by 2-dimensional echocardiography was used. All 4 patients had a narrowest diameter that was much larger than 3 mm. The PDA was restrictive in group B patients.
In group A, PDA closure was achieved with an Amplatzer occluder device (AGA Medical, Golden Valley, MN, USA) in 17 patients, with 2 detachable coils (William Cook Europe, Bjaeverskov, Denmark) in 1 patient, and by surgical ligation in 9. All group B patients underwent coil closure.
All patients underwent complete physical examination and detailed echocardiographic study before intervention. LV end-diastolic diameter (LVEDD), LV end-systolic diameter (LVESD), interventricular septal thickness in diastole (IVSd), LV posterior wall thickness in diastole (PWd), aortic diameter, and left atrial diameter were measured by M-mode echocardiography in the parasternal long-axis view as recommended by the American Society of Echocardiography.9 From these measurements, the following LV parameters were computed: shortening fraction (SF) = [(LVEDD – LVESD) / LVEDD] x 100; ejection fraction (EF) = [(LVEDD volume – LVESD volume) / LVEDD volume] x 100, where LVEDD volume = (7 x LVEDD3) / (2.4 + LVEDD) and LVESD volume = (7 x LVESD3) / (2.4 + LVESD); LV mass index = 1.04 [(LVEDD + IVSd + PWd)3 – LVEDD3] / body surface area. The narrowest diameter of the PDA was measured in the ductal view.
Follow-up was incomplete because many patients either came from remote regions of the country or were foreigners who left the country after treatment. Echocardiographic study was performed at least once in 34 patients (23 group A and 11 group B) within 1 month (a few hours to < 1 month) after intervention and in 23 patients (18 group A and 5 group B) within 6 months (> 1 month to < 6 months) after intervention. Overall, 23 out of 27 group A patients (85%) and 11 out of 16 group B patients (69%) had at least 1 echocardiographic study after PDA closure. Since M-mode echocardiographic measurements are observer-dependent, we defined changes in LV indices as clinically relevant if they were 10% greater than the baseline (preclosure) level. Accordingly, instead of reporting the difference from baseline, we elected to present the percentage difference from baseline. We defined changes of < 10% as no change, changes between 10% and < 20% as mild changes, between 20% and < 30% as moderate, and 30% as severe.
Signed consent for undergoing cardiac catheterization was obtained from the parents of all patients. Patients were sedated with ketamine and midazolam during the procedure. None needed general anesthesia or intubation. Heparin was administered only in patients who were given an Amplatzer device, as recommended by the manufacturer. Angiograms taken in a straight lateral position were reviewed to determine the type and diameter of PDA. The PDA was considered restrictive if the peak systolic pulmonary artery pressure recorded during cardiac catheterization was < 40% of the systemic value. The narrowest diameter was measured using a software program pre-installed in the Cathcor system (Siemens, Erlangen, Germany), which involves the use of electronic calipers for accurate measurement and for minimizing error. The diameter of the catheter was used as a reference point to correct for the magnification factor. In cases where the angiograms were already transferred out of the Cathcor, PDA measurements were obtained manually. When there was discrepancy between angiographic and echocardiographic measurements, the former was used to assign the patient to group A or B.
Coil occlusion of the PDA was performed through either a retrograde (n = 12) or an antegrade approach (n = 5), while Amplatzer occlusion was undertaken using an antegrade approach. These procedures have been described elsewhere.2,10–12 In patients undergoing transcatheter closure, a dose of cefuroxime (30 mg·kg–1) was administered intravenously 20 to 30 minutes before device implantation, and 2 more doses were given in the next 24 hours.
Surgical ligation was performed under general anesthesia. With the patient in a right lateral decubitus position, a standard left posterolateral thoracotomy was performed through the fourth intercostal space. The lung was gently retracted, and the posterior pleura was incised. The left superior intercostal vein was ligated and divided. The edges of the posterior pleura were cauterized, care being taken not to injure the vagus nerve and the thoracic duct. Stay sutures were then placed on the anterior edge of the pleura. Sharp dissection was continued above and below the level of the PDA. The recurrent laryngeal nerve was left on the pleural flap, which was retracted medially. A sharp dissection above and below the PDA opened access into the right tissue plane. A curved dissector was then used, and the branches were opened parallel to the duct to avoid injury. An attempt to come around the duct with a fully curved dissector was made only when the dissection was deep enough both above and below the duct. When the instrument passed freely behind the PDA, a braided silk ligature was passed around the duct. When it was safely ligated, we checked that the thrill had disappeared. A 2nd Ligaclip was applied if necessary. In case of a large PDA, fine vascular clamps were applied, and the PDA was divided. Both ends were oversewn, usually with a running mattress suture in 1 layer and then a continuous over-and-over stitch in the 2nd layer using polypropylene suture. All bleeding points were carefully stopped, and the posterior pleura was approximated with 2 or 3 single stitches. The chest was then closed in a routine manner with an intercostal drain in place.
Data are presented as mean ± standard deviation. Paired Student’s t test was used to compare the results. A p-value < 0.05 was considered statistically significant.
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RESULTS
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Table 1
compares the demographic data of the groups. While mean age, weight, height, and the centile for weight were comparable, the centile for height was significantly lower in group A patients, who had larger PDA, indicating their failure to thrive. The narrowest diameter of the PDA was 5.7 ± 2.1 mm in group A, compared with 1.8 ± 0.6 mm in group B.
Echocardiographic studies after the intervention showed that 20 out of 23 group A patients (87%) and all 11 group B patients (100%) examined had complete PDA closure. Only mild leaks occurred in the 3 group A patients with residual shunt. No complications were reported either during the intervention or during follow-up.
Table 2 compares the echocardiographic measurements between the groups before intervention and within 1 month after, while Table 3 compares these results within group A. Before intervention, LVEDD and LV mass index in group A were significantly larger than in group B, while SF and EF were normal in all patients in both groups. When examined within 1 month after intervention, LVEDD showed a trend towards regression in group A, while it remained unchanged in group B, with no significant difference between the groups. In group A, both SF and EF fell significantly after intervention, from 37.4% to 27.7% and from 67.8% to 54.5%, respectively. There was no significant change in group B in either parameter.
In terms of changes in SF within 1 month after PDA closure in the 23 group A patients evaluated, there was no change in 7 patients (30%), mild changes in 2 (9%), moderate changes in 9 (39%), and severe changes in 5 (22%). It is worth mentioning that in the patients with "no" change, SF fell by between 4.2% and 9.7%. Among the 11 group B patients who were examined, there was either improvement or no change in SF except for 1 patient who had mild changes.
Between 1 and 6 months after intervention, LV function improved in most of the group A patients evaluated (Table 3
last column), although the differences between these results and those obtained within 1 month after intervention were not statistically significant. Two patients had a SF below 28% but a normal pulmonary artery pressure as determined by tricuspid regurgitation velocity. One of these 2 patients was given an angiotensin converting enzyme (ACE) inhibitor, as the deterioration in LV function was felt to be clinically significant.
The echocardiograms of a group A patient are shown in Figure 1, revealing an initially increased LVEDD decreasing after Amplatzer occlusion and an initially normal SF of 36.7% dropping 1 week after intervention to 17% and 3 months later normalizing to 29%. Figure 2 shows that SF fell by more than 10% in most of the group A patients examined after intervention, even falling by over 40% in a few cases. Some patients continued to show SF depression 1 to 6 months after intervention, but most showed improvement.
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Figure 1. M-mode echocardiograms of left ventricular function in a patient with a large patent ductus arteriosus (A) before intervention (B) 1 week and (C) 3 months after Amplatzer occlusion.
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Figure 2. Left ventricular shortening fraction of group A patients before and at various intervals after closure of their large patent ductus arteriosus.
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DISCUSSION
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There have been numerous reports addressing the safety and efficacy of surgical ligation13,14 and transcatheter closure of PDA using various devices.4,15,16 Our study, in contrast, looks at the effect of PDA closure on LV systolic performance. The study was planned after observing deterioration in LV function immediately after successful closure of a very large PDA using an Amplatzer device. One possible explanation for this observation is that a large PDA is associated with a large left-to-right shunt and increased LV preload. According to Starling’s law, an increased preload stretches LV muscle fibers, resulting in increased contractility and therefore increased SF. Closure of a large PDA results in a sudden reduction in LV volume overload, thereby reducing muscle fiber stretch and decreasing SF.
We also hypothesize that following PDA closure, changes in afterload may be another contributory factor adversely affecting LV systolic performance. Prior to closure, the left ventricle ejects blood both into the high-resistance systemic circulation and via the PDA into the low-resistance pulmonary circulation, while after PDA closure it ejects blood into the high-resistance systemic circulation only. Therefore, we speculate that LV afterload increases after closure, which might contribute to the reduced SF observed in our patients with large PDA. Thus, closure of large PDA unmasks the pre-existing but unrecognized LV dysfunction.
A few studies have evaluated cardiac performance after PDA ligation, but only in the newborn period.17,18 One study showed that although ductal ligation increased blood pressure and systemic resistance, wall stress and ventricular performance were maintained.17 In contrast, SF dropped significantly in our patients with larger PDA. The major, and probably most important, difference between these studies and ours is that our patients were older.
The circulatory physiology in a large PDA shares characteristics of significant aortic insufficiency and more so of mitral regurgitation. All of these lesions result in LV volume overload, dilation, and hypertrophy that progressively increase with time. Studies of both aortic insufficiency19 and mitral regurgitation have shown that significant volume overload over prolonged periods of time adversely affects LV contractile function and leads to irreversible loss of myocardial function if surgical intervention is delayed. Moreover, similar reduction in LV systolic function as in our patient group with large PDA has been observed postoperatively in patients with significant mitral regurgitation.20 It seems appropriate to extrapolate these data and assume that patients with large PDA are at similar risk of developing LV dysfunction over time as those with significant aortic and mitral regurgitation, and our results support this speculation.
Therefore, while LV function might be preserved in neonates and young infants even with large PDA,17 these patients’ LV performance is probably at risk of deterioration if the PDA remains open and LV volume overload persists for a longer period of time. Occasionally, we have noticed that acute deterioration in LV function after closure of large PDA is so significant that the patient may experience symptoms of reduced exercise tolerance. Use of afterload-reducing drugs (such as ACE inhibitors) should be considered.
Our comparative study shows that, while patients with large PDA develop significant LV dysfunction after ductal closure, those with small PDA do not. It is interesting to note that over 60% of the patients with large PDA had at least a moderate to severe drop in SF, indicating that this may be a very frequent occurrence. However, LV function seems to recover fairly quickly. In our study, LV performance normalized within 3 to 6 months in most of the patients who were followed up, although 1 patient had a SF that was below 28% even after 1 year and was prescribed an ACE inhibitor.
Although we believe that LV systolic performance deteriorates immediately following PDA closure, we had complete short-term (up to 6 months) follow-up echocardiographic data in only 34 out of a total of 43 patients (79%), making it difficult to establish a firm conclusion and to propose recommendations regarding the timing of PDA closure. Nevertheless, as the measurements had initially been made for clinical use, rather than for proving or disproving any hypothesis, they were free from investigator bias.
Another concern is that some patients might have been inadvertently assigned to the wrong group, as the difference between the cutoff points of the groups was only 0.1 mm, but this would only underestimate the depression in SF after closure of large PDA (group A) rather than overestimating it. Hence, the acute changes in LV parameters might have been even more pronounced than we have reported in this group. It would also be helpful if we had calculated Qp / Qs ratio for the patients who underwent transcatheter closure and correlated it with the size of the PDA. But this information was available for only a very few patients in group B.
We conclude that significant LV systolic changes may occur after closure of large PDA either surgically or by transcatheter occlusion. Echocardiographic evaluation before discharge from hospital is recommended. LV function usually recovers within a few months in these patients. In some patients, the reduction in LV performance can be large enough to require the use of ACE inhibitors. Patients with small PDA are not at risk of such deterioration after closure. Larger, prospective studies are warranted to confirm our findings and to produce more conclusive evidence.
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ACKNOWLEDGMENTS
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We are much thankful to Mr. Omar Isak and Ghassan Baslaim, MD for their contributions to this paper.
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ABSTRACT
INTRODUCTION
