Ann Thorac Surg 2005;80:1641-1646
© 2005 The Society of Thoracic Surgeons
Original article: Cardiovascular
Late Results After PTCA for Coronary Stenosis After the Arterial Switch Procedure for Transposition of the Great Arteries
Christoph Kampmann, MD
a
,
*
,
Wlodzimierz Kuroczynski, MD
b
,
Hubert Trübel, MD
a
,
Markus Knuf, MD
a
,
Martin Schneider, MD
c
,
Markus K. Heinemann, MD, PhD
b
a Division of Pediatric Cardiology, Hospital for Sick Children, Mainz
b Clinik for Heart and Cardiovascular Surgery, University Mainz, Mainz
c University Hospital for Sick Children, Charité, Berlin, Germany
Accepted for publication November 17, 2004.
* Address correspondence to Dr Kampmann, Pediatric Cardiology, Hospital for Sick Children, University Mainz, Langenbeckstrasse 1, Mainz, D-55101 Germany (Email: kampmann{at}mail.uni-mainz.de).
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Abstract
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BACKGROUND: The arterial switch operation has become the surgical approach of choice for d-transposition of the great arteries, but there is an increased awareness of adverse sequelae in some survivors. Long-term patency and normal function of the translocated coronary arteries must be achieved. It is reported that dependent of the prior coronary status, 3% to 11% of all survivors have proximal coronary stenosis or complete occlusion develop after arterial switch operations. However, treatment of these stenoses is still a matter of debate. Late results after percutaneous transluminal coronary angioplasty (PTCA) for coronary stenosis after the arterial switch operation for d-transposition of the great arteries are reported.
METHODS: Seven children after arterial switch operation for d-transposition of the great arteries who had subsequently undergone PTCA for coronary stenosis were angiographically re-evaluated 3 to 15 months after the initial PTCA and again after 3 to 5 years.
RESULTS: All children survived the initial PTCA procedure. There were no late deaths. The degree of stenosis before PTCA ranged from 74% to 97%; immediately after PTCA from 5% to 10%; at 3 to 15 months after PTCA from zero to 6%; and at 3 to 5 years after PTCA from zero to 3%. Three to 5 years after PTCA all children showed normal development of the treated coronary artery.
CONCLUSIONS: Primary PTCA of stenotic proximal coronary arteries after the arterial switch procedure for d-transposition of the great arteries seems to be an effective treatment with excellent long-term results.
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Introduction
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Because the introduction of the arterial switch operation (ASO) by Jatene and colleagues [1] in 1975 and its modification by Lecompte and colleagues [2], the ASO has become the procedure of choice for anatomic correction of congenital heart diseases with d-transposition of the great arteries (d-TGA). The translocation of the coronary arteries from the anterior to the posterior artery is the most challenging surgical part of this procedure [3–5]. The potential risk is due to impaired coronary perfusion caused by kinking, distortion, stenosis, or compression of the coronary arteries [6, 7]. Even the early and late postoperative deaths after surgery seem to be related to coronary anomalies (eg, intramuscular coronary arteries or high takeoff from the aortic root [8]). The incidence of coronary stenoses or complete occlusion, depending on the surgical technique, is between 3% and 11%, and for type D coronary anatomy using the single orifice technique it is as much as 32.4% [9–11], and of late stenoses as much as 5.7% in asymptomatic patients [9]; therefore it is still a matter of discussion [12, 13]. However the accurate number of coronary stenoses after ASO is not exactly known, because on one hand some patients with stenoses or occlusions of the coronary arteries are without overt clinical symptoms, and also because postoperative ASO patients do not routinely undergo re-catheterization. Only selective coronary angiography is the most accurate means of assessing the patency of coronary anastomoses after the arterial switch procedure [9].
There are only a few reports of the management of these coronary stenoses, which were single patient case studies. Surgical approaches included internal mammary artery grafting [14, 15] and intraoperative angioplasty on cardiopulmonary bypass [16, 17]. In total, 13 patients are reported in literature in whom a surgical approach was successfully undertaken. A case study of percutaneous transluminal coronary angioplasty (PTCA) in a single infant with coronary stenosis was first published by Allada and colleagues [18] in 1991, and subsequently a study of 4 children by Hausdorf and colleagues [19] in 1995. The aim of the present investigation was to provide long-term follow up angiographic data on the previously reported 4 children by Hausdorf and colleagues [19] and on 3 additional children who had undergone PTCA for coronary stenosis after ASO.
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Patients and Methods
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Patients
Seven patients, aged 3 weeks to 15 months, in whom ASO had been performed between the 3rd and 9th day of life, underwent cardiac catheterization for impaired left ventricular function, bilateral pulmonary branch, or supravalvular main pulmonary artery stenosis, or for routine follow-up 3 to 15 months after ASO surgery. Before angioplasty, informed consent was obtained from all parents.
Methods
Cardiac catherization was performed during mild sedation or under anesthesia. Vascular access was routinely performed from the right femoral artery. Intravenous heparin was given between 100 and 200 IU/kg body weight (BW). Primary, left ventricular, and ascending aorta angiograms were performed. Selective coronary angiography was performed using ether a modified right Amplatz catheter (SR 3-208 [Cordis, Miami, FL]) or a right or left Judkins catheter (JL 3.5 or JR 3.5 [Cordis]). In cases of stenoses, a coronary angiography was repeated after selective intracoronary administration of 0.1 µg/kg BW of nitroglycerine to relieve coronary spasm. The degree of stenosis was determined by quantitative coronary angiography. Before PTCA, all patients received 1 mg/kg BW lidocaine. The coronary catheter was then placed with the tip in close proximity to the stenotic coronary ostium, so as not to compromize coronary blood flow. The catheter was used as a guiding catheter for a fixed-wire balloon catheter (balloon diameter, 1.5 to 2.0 mm) or a 0.014 inch floppy guide wire, which was advanced through the catheter into the stenotic coronary artery and exchanged over the wire for a balloon catheter. Overexpansion of the stenoses during angioplasty was performed in order to obtain a post-stenotic coronary diameter ratio of 0.95 to 1.55. To minimize the chance of laceration of the coronary artery, only the first one-third of the balloon was positioned within the coronary artery, just past the stenotic area. In order not to compromise coronary perfusion, inflation was kept as short as possible in patients with or without collateralization, and it did not exceed 5 seconds. After PTCA repeat angiography was performed post-intervention, all patients received 3 days intravenous heparin and 2 days nitroglycerin. In addition, 5 µg/kg BW/min nitroglycerin was administered intravenously for 48 hours. All patients received 3 to 5 mg/kg BW/d aspirin and 2 to 3 mg/kg BW/d dipyridamole for 6 months from day 1 after intervention.
Follow-up coronary angiography was first performed at 3 to 15 months after PTCA intervention, and then it was repeated 3 to 5 years after PTCA intervention. Coronary diameters were measured as previously described.
Statistical Analysis
Measurements were obtained from the coronary angiograms. Statistical analysis was performed using SPSS Version 8.0 for Windows (SPSS Inc, Chicago, IL) using a two-tailed paired t-test. P <0.05 was considered to be statistical significant.
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Results
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Patient characteristics are given in Table 1. All patients had uneventful postoperative courses after their arterial switch procedure for d-TGA. In 3 patients cardiac catherization was performed 4 weeks, 6 weeks, and 4 months after corrective surgery because of progressive impairment of left ventricular function. Fractional shortening of the left ventricle was reduced to 24%, 21%, and 19%, respectively. In 1 patient, PTCA was performed on day 9 after ASO and a type B coronary artery origin because of treatment refractory rhythm disturbances. The other patients underwent cardiac catheterization because of supravalvular main pulmonary artery stenosis (1 patient), stenosis of the bifurcation of the main pulmonary artery (1 patient) or routine follow-up examination (4 patients). In 6 of 7 patients there were no electrocardiographic changes to suggest myocardial ischemia and no elevation of cardiac enzyme levels to suggest infarction. Retrograde filling of the coronary artery was observed in 2 patients. Seven patients underwent their PTCA at a mean age of 5.6 months and were followed-up by coronary angiographies at the mean age of 13.3 months and again at a mean age of 59.1 months (Table 1). There were no intervention-related deaths. Patients survived the procedure and were available for follow-up examination.
In 1 patient, PTCA was performed only 14 months ago, so that 3 to 5-year follow ups were not available; and 1 patient did not undergo the intermediate follow-up evaluation, but did undergo the late follow-up. In those 3 patients with impaired left ventricular function, shortening fraction was shown to have normalized (ejection fraction, 71 ± 6 % [mean ± standard error of the mean]) 3 to 6 weeks after PTCA without regional wall motion abnormalities. One patient had ventricular fibrillation develop during PTCA of a right coronary artery stenosis, which was successfully treated by defibrillation. There was no need for long-term anti-arrhythmic management.
Baseline post-PTCA and follow-up stenosis measurements are given in Table 2. All stenoses could be successfully treated by PTCA (Figs 1
A–1D). Angiography performed immediately post-PTCA showed significant reduction of all dilated stenoses. Follow-up examinations performed a mean of 6.8 months after PTCA and after a mean of 50 months after PTCA revealed normal growth of the coronary arteries (Fig 2) and the treated stenoses. Paired t-test showed a significant reduction in the stenosis percentage comparing pre-PTCA with immediate post-PTCA, the stenosis percentage comparing pre-PTCA with the first and second follow-up examinations, and comparing coronary diameter pre-PTCA with the coronary diameter at the first and second follow-up examinations (Table 3). There were no statistically significant residual stenoses found at the first and second follow-up examinations.
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Fig 1. (A) A 9-day-old male child received the arterial switch operation for d-transposition of the great arteries with an originally inverted coronary artery pattern and had an uneventful early postoperative course. Subsequently, the patient was treated with digoxin and diuretics for severe ventricular dysfunction. Thirteen months after the arterial switch operation the child underwent cardiac catheterization. Selective coronary angiography revealed an 80% stenosis of the inverted left coronary artery. (B) In the same child, successful angioplasty was performed using a 2.33-mm rapid exchange balloon over a 0.014-inch floppy guide wire. (C) Angiography immediately after percutaneous transluminal coronary angioplasty without evidence of residual stenosis. (D) Follow-up control angiography at the age of 5.5 years (3.9 years after percutaneous transluminal coronary angioplasty) revealed a normal development of the coronary artery and a residual stenosis of less than 3%. Left ventricular dysfunction had normalized with time. The child was no longer receiving anti-congestive treatment.
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Fig 2. The coronary diameter at different times in box plots: at the time of percutaneous transluminal coronary angioplasty (PTCA), at the first follow-up, and at the second follow-up angiography.
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Comment
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Coronary stenosis can develop weeks to months after the ASO for anatomic correction of d-TGA, with or without overt clinical symptoms. This could be due to multiple reasons, such as kinking, distortion compression, and any unusual coronary artery anatomy in addition to thrombus formation or to intimal proliferation, but it seems more reasonable that it results from excessive scar formation surrounding the proximal part of the mobilized and translocated coronary artery. The stenoses appear to be a risk factor for late mortality [4, 7, 18, 20]. There have been previous reports suggesting up to 10% incidence of myocardial infarction or sudden death, or both, in hospital survivors [21, 22]. However, in cases of complete coronary occlusion or severe stenosis, the role of dependence on a single coronary artery blood supply with collateral circulation supporting large areas of myocardium is unclear. The capacity of neonates or of infants to collateralize, neo-vascularize, or develop cellular proliferation after an acute coronary occlusion is unknown, but it has been suggested that it may be potentially greater than in adults [10]. Nevertheless, infants with anomalous origin of the left coronary artery from the pulmonary trunk, who underwent ligation of the anomalous coronary artery on the pulmonary side had evidence of acute myocardial ischemia or infarction develop, or both develop, which impaired left ventricular function, and abnormal resting and exercise electrocardiograms [23–26]. Abnormalities are common and do not appear to be associated with symptoms, electrocardiographic changes, decreased exercise tolerance, or regional wall motion abnormalities in patients after ASO perfusion [12, 13], but unfortunately those reported patients did not undergo coronary catheterization; therefore it remains unclear if these perfusion abnormalities are related to impaired coronary blood flow. In 10 years of performing the arterial switch operation in our institution, there have been no late deaths of patients after ASO in contrast with 7.9% late deaths among those who received the atrial switch procedure (Mustard operation). Here, at the Pediatric Heart Center in Mainz, 65 patients after ASO have been re-evaluated by angiography. In all, coronary anastomosis was regularly done by the cuff method using 6-0 sutures. In our own patient population there are 3 of 65 patients (4.6%) with a complete occlusion of the right coronary artery and an additional 2 who had a coronary stenosis (3%). Coronary stenosis was not related to early ASO experience, and the coronary stenoses or occlusions were distributed almost equally during the years.
In the present patient series, PTCA was performed in those patients with severe coronary stenosis in the absence of reduced left ventricular function for fear of an increased risk of sudden cardiac death. In patients with decreased left ventricular function, it has been shown that these patients benefit from intervention. In all of these patients treated with PTCA, left ventricular function normalized within 3 to 6 weeks after intervention.
There have been no interventional related deaths reported in the literature either for a surgical or for a transcatheter approach. However the number of reported cases remains very small. Percutaneous transluminal coronary angioplasty led to an adequate growth of the coronary arteries years after intervention, and it can be speculated that normal coronary growth will continue. Long-term follow-up studies of the results of internal mammary grafting in children are not available. Results in adults would suggest that mammary graft occlusion will occur in 8.7% within 10 years.
Percutaneous transluminal coronary angioplasty for coronary stenosis after arterial switch operation differs from PTCA for atherosclerotic lesions in terms of duration of balloon inflation and balloon to vessel diameter. Although for atherosclerotic lesions, over-expansion of the vessel appears to lead to a higher degree of restenosis, it may be necessary to over-expand stenotic lesions after the ASO in order to successfully dilate a stenosis in a postoperatively scarred vessel. Balloon over-expansion was made because of the first 2 patients, with a balloon to post-stenotic coronary artery ratio of less than 1. Residual stenosis was immediately evident, and re-dilatation had to be performed with an oversized balloon and a balloon to post-stenotic coronary artery ratio of 1 to 2. Although in the following patients a balloon–vessel ratio between 1.1 and 1.4 was chosen, there was no residual stenosis evident.
Because the majority of patients with coronary stenosis after the ASO are asymptomatic, routine selective coronary angiography should be performed to detect patients with coronary stenosis, even those with normal left ventricular function by echocardiography.
In conclusion, PTCA of coronary stenosis after the ASO for d-TGA can be performed safely in infants and young children without severe procedure-related complications and with excellent long-term results. Therefore postoperative invasive diagnostic procedures seem to be mandatory to detect and treat coronary stenosis after the ASO and may contribute to a reduction in late postoperative deaths after the ASO.
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Abstract
Introduction
