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Ann Thorac Surg 2006;81:2250-2258
© 2006 The Society of Thoracic Surgeons
a Department of Cardiovascular Surgery, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts
b Department of Cardiology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts
Accepted for publication November 4, 2005.
* Address correspondence to Dr Mayer, Department of Cardiovascular Surgery, Children's Hospital Boston-Bader 273, 300 Longwood Ave, Boston, MA 02115 (Email: john.mayer{at}cardio.chboston.org).
Presented at the Forty-first Annual Meeting of The Society of Thoracic Surgeons, Tampa, FL, Jan 24–26, 2005.
| Pediatric cardiac surgery:
The Annals of Thoracic Surgery CME Program is located online at http://cme.ctsnetjournals.org. To take the CME activity related to this article, you must have either an STS member or an individual non-member subscription to the journal.
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Abstract |
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METHODS: Retrospective review of patients admitted to our institution with the diagnosis of PA/IVS-RVDCC from 1989 to 2004. All angiographic imaging studies, operative reports, and follow-up information were reviewed. Right-ventricle–dependent coronary circulation was defined as situations in which ventriculocoronary fistulae with proximal coronary stenosis or atresia were present, putting significant left ventricle myocardium at risk for ischemia with right ventricle decompression.
RESULTS: Thirty-two patients were identified with PA/IVS-RVDCC. All underwent initial palliation with modified Blalock-Taussig shunt (BTS). Median tricuspid valve z-score was -3.62 (-2.42 to -5.15), and all had moderate (n = 13) or severe (n = 19) right ventricular hypoplasia. Median follow-up was 5.1 years (9 months to 14.8 years). Overall mortality was 18.8% (6 of 32), with all deaths occurring within 3 months of BTS. Aortocoronary atresia was associated with 100% mortality (3 of 3). Of the survivors (n = 26), 19 have undergone Fontan operation whereas 7, having undergone bidirectional Glenn shunt, currently await Fontan. Actuarial survival by the Kaplan-Meier method for all patients was 81.3% at 5, 10, and 15 years, whereas mean survival was 12.1 years (95% confidence interval: 10.04 to 14.05). No late mortality occurred among those surviving beyond 3 months of age.
CONCLUSIONS: In patients with PA/IVS-RVDCC, early mortality appears related to coronary ischemia at the time of BTS. Single-ventricle palliation yields excellent long-term survival and should be the preferred management strategy for these patients. Those with aortocoronary atresia have a particularly poor prognosis and should undergo cardiac transplantation.
Pulmonary atresia with intact ventricular septum (PA/IVS) is a rare yet morphologically heterogeneous lesion characterized by absence of egress from the right ventricle (RV) into the pulmonary artery or through a ventricular septal defect into left ventricle (LV). Varying degrees of tricuspid valve (TV) and RV hypoplasia as well as considerable abnormalities in coronary circulation, such as sinusoids, fistulae, coronary stenosis, or atresia, are common [1]. Right ventricle-to-coronary artery fistulae have been reported to occur in 31% to 68% of patients with PA/IVS [2–9], while a right-ventricle–dependent coronary circulation (RVDCC), the situation in which a significant portion of the LV is supplied by ventriculocoronary fistulae fed by a hypertensive RV, has been described in anywhere from 3% to 34% of these patients [2, 3, 5, 6, 9–11].
Previous surgical management strategies for patients with PA/IVS and RVDCC have included right ventricle decompression (RVD) regardless of coronary anatomy, RV thromboexclusion with TV closure and ligation of ventriculocoronary fistulae, systemic-to-pulmonary artery shunting, aorto-right ventricular shunting, staged single-ventricle palliation, and cardiac transplantation [3, 5, 9, 12–16].
Until 1986, it had been our institutional bias to decompress all patients with PA/IVS regardless of TV size, RV size and anatomy, or coronary anatomy until it was realized that RVD in the setting of RVDCC carried a 100% mortality rate as a result of significant LV dysfunction from irreversible myocardial ischemia [3, 17]. Since that time, it has been our practice to selectively manage all patients with PA/IVS and RVDCC along the single-ventricle pathway [10, 11].
Because of the relative infrequency of this anomaly as well as limited numbers of patients with RVDCC who have been included in published series, little is known about the mid or longer-term outcome of such patients managed by the single-ventricle approach [5, 10, 13, 18]. It has been suggested that patients with ventriculocoronary fistula and extensive, or even less extensive, coronary anomalies are at risk for ongoing ischemia that may predispose them to higher interim and late mortality; however, there are no known data to substantiate this theory [10, 19, 20]. Controversy still exists as to the optimal management algorithm for these patients.
The purpose of this study was to assess longer-term outcome in patients with PA/IVS-RVDCC managed along the single-ventricle pathway, to provide a basis for comparison with management strategies that include systemic-to-pulmonary artery shunt or prolonged prostaglandin administration followed by cardiac transplantation, and to gain a better understanding of the natural history of RVDCC in terms of LV function and the fate of associated coronary fistulae and stenoses.
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Data Collection
All available echocardiograms, angiograms, operative reports, and medical records from our institution as well as reports from outside institutions, when original studies were not available, were reviewed. Additionally, all available follow-up angiograms were reviewed and compared with initial angiograms by a single angiographer to further understand the natural history of ventriculocoronary fistulae and associated coronary artery stenoses in this patient population.
Echocardiographic measurements included maximum TV annulus diameter (expressed as z-score to adjust for body surface area), degree of RV hypoplasia (graded as absent, mild, moderate, or severe), and status of LV function (graded as normal, mildly depressed, moderately depressed, or severely depressed). Qualitative judgments of the extent of RV hypoplasia were taken from the echocardiographic report. All echocardiograms were read by a faculty echocardiographer, but the echocardiograms were not re-reviewed for this study.
Coronary angiographic technique included right ventriculography, balloon occlusion aortogram, and selective coronary injections to determine presence and location of ventriculocoronary fistulae, coronary stenoses or coronary atresia, or both, or interruption. Right ventricular pressure was directly measured by catheter. All angiograms were re-reviewed by one interventional cardiologist (L.B.A.) for the purpose of this study.
Definitions
Right-ventricle–dependent coronary circulation was defined by either (1) the presence of ventriculocoronary artery fistulae with angiographically severe obstruction of at least two major coronary arteries (eg, right or left main coronary artery [RCA, LCA], left anterior descending [LAD], circumflex or posterior descending coronary arteries); (2) complete aortocoronary atresia; or (3) situations in which a significant portion of the LV myocardium was supplied by the RV and was judged to be at risk for ischemia with RVD (eg, single coronary artery with stenosis), or clinical deterioration with associated ischemia by electrocardiogram (ECG) upon RVD intraoperatively in instances when a diagnosis of RVDCC was not correctly made on the initial interpretation of the angiogram. A representative angiogram demonstrating RVDCC is shown in Figures 1 and 2.
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Statistical Analysis
All analyses were performed with SPSS statistical software (version 12.0; SPSS, Chicago, Illinois). Data are presented as frequencies or medians with ranges as appropriate. Median values between survivors versus nonsurvivors were compared using the Mann-Whitney U test. Categorical data were compared using the 
2 test or Fisher's exact test where appropriate. Actuarial survival was estimated with 95% confidence interval using the Kaplan-Meier product-limit method. All p values less than 0.05 were considered statistically significant.
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Results |
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Patient characteristics are depicted in Table 1. In this cohort, median age at BTS was 2 days (range, 0 to 38), and median weight was 3.2 kg (range, 1.8 to 3.8 kg). Median age at BDG was 7.2 months (range, 3.5 to 24), and median age at Fontan was 3.4 years (range, 1.7 to 9.6).
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Anatomic Features
The median TV z-score for these patients was -3.62 (range, -2.42 to -5.15) with no difference between survivors and nonsurvivors (p = 0.26; Table 2). All patients had either moderate or severe RV hypoplasia, but there was no difference in degree of RV hypoplasia between survivors and nonsurvivors (p = 0.36; Table 2).
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Mortality
The overall mortality rate was 18.8% (6 of 32). All deaths occurred within 3 months of BTS, with the majority (5 of 6, 83%) occurring within the first month. Actuarial survival for the entire cohort was 81.3% at 5, 10, and 15 years (Fig 3). There were no perioperative or late deaths after either BDG or Fontan; thus, actuarial survival for those surviving beyond the first 3 months was 100%.
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The remaining 2 deaths were of patients in whom progressive LV dysfunction developed after BTS and who were referred to our institution for transplant evaluation. One patient, who was initially doing well, had cardiorespiratory failure 6 days after BTS. He had anterolateral ischemia by ECG and severely depressed LV function by echocardiography. He was referred for transplant evaluation, but the family decided against transplantation and requested withdrawal of support on postoperative day 8. The last patient also had an uneventful postoperative course after BTS and was doing well at home until postoperative day 82, when he became irritable with poor oral intake. He was found to have new-onset severe LV dysfunction by echocardiogram as well as intermittent atrioventricular block by ECG. Upon transfer to our institution, he suffered a cardiac arrest requiring emergent extracorporeal membrane oxygenation cannulation, and during cardiac catheterization was found to have a large thrombus obliterating his RV cavity. He had refractory ventricular fibrillation, and support was withdrawn.
Of the remaining patients, 19 have undergone Fontan operation, with 8 extracardiac and 11 lateral tunnel procedures performed based on surgeon preference (Fig 4). All patients had either normal (n = 18) or low-normal (n = 1) LV systolic function as documented by most recent echocardiogram at a median age of 7.2 years (range, 1.8 to 14.8) and at a median time of 2.5 years (range, 3 weeks to 10.3 years) since Fontan. There was no difference in survival or ventricular function based on Fontan approach. Seven patients, having already undergone successful BDG, are currently awaiting their Fontan procedures (Fig 4).
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The generally accepted mechanism for development of these anomalous communications is that abnormally elevated RV pressure forces preexisting channels or sinusoids in the developing fetal myocardium to remain patent and communicate with epicardial coronary arteries to become fistulae [7, 19]. Coronary stenoses are hypothesized to result from endothelial injury sustained as a result of turbulent flow generated by retrograde coronary perfusion from the RV [25]. Coronary stenosis and hypoplasia distal to fistulae have also been described suggesting that competitive flow may play a role in promoting these lesions [25]. Whether flow of less saturated blood through these persistent ventriculocoronary fistulae plays a role in progression of coronary stenoses is unknown.
Right-ventricle–dependent coronary circulation results when coronary stenoses or atresia occur proximal to these fistulae, making the myocardium solely dependent upon the RV for adequate perfusion. Although the primary pathology is related to the RV, the myocardium of the functionally single LV is also at risk for ischemia and subsequent ventricular dysfunction. In the setting of ventriculocoronary fistulae without proximal stenosis, or dual coronary supply, there is theoretical potential for RV "steal" upon RVD that could lead to underperfusion of myocardium distal to the fistulae [20]. In the setting of RVDCC, RVD results in significant infarction of the RV-dependent LV if there are not sufficient collateral arteries to the region and is usually fatal [3, 17, 25, 26].
The true prevalence of RVDCC is unknown, but is likely in the range between the 5% and 9% reported in multi-institutional studies [2, 6] and the 25% to 35% described in single-institution studies where referral patterns and angiographic practices may be different [4, 10, 11]. Nevertheless, management strategies for such patients are largely dependent on accurate delineation of coronary anatomy at the time of initial diagnosis of PA/IVS. Improved outcome for patients with PA/IVS has been attributed to appropriate surgical stratification of patients based on coronary anatomy [11].
While RVDCC was found to be risk factor for death by multivariate analysis in the Congenital Heart Surgeon's Society 1993 report [6] assessing outcomes in neonatal PA/IVS, the same did not hold true for coronary abnormalities assessed in their 2004 report investigating determinants of mortality and type of repair in these neonates [2]. Detailed neonatal angiography, required for definitive diagnosis of RVDCC, is difficult to perform. In addition there may be significant variation in interpretation of angiographic studies both between and even within institutions making objective assessments from large multi-institutional studies challenging.
Our current institutional understanding of the significance of RVDCC was elucidated by Giglia and colleagues [3] in 1992 in an angiographic study of 16 patients with PA/IVS and ventriculocoronary fistulae who had undergone RVD between 1979 and 1990. All 7 patients with ventriculocoronary fistulae but without coronary stenosis or atresia survived RVD. Four of 6 patients with a single coronary stenosis survived whereas all 3 patients with stenosis of two major coronary artery branches died of acute LV dysfunction shortly after RVD. The authors concluded that presence of coronary stenosis in at least two major coronary arteries was a contraindication to RVD, but that the presence of ventriculocoronary fistulae alone or with a single proximal coronary stenosis did not preclude RVD but was associated with a less favorable outcome.
In a more recent angiographic study in 2000 from our institution by Powell and coworkers [10], 12 patients with PA/IVS-RVDCC who underwent single-ventricle palliation from 1986 to 1997 were found to have an 83% 5-year actuarial survival. The 2 deaths (17%) in that series occurred within 4 months from presumed coronary ischemia. Both of these patients are included in the current report, with 4 additional cases added.
Our current results with single-ventricle palliation in this more contemporary series are practically identical, with 18.8% overall mortality and 81.3% 5, 10 and 15-year actuarial survival. All deaths in this series occurred within 3 months of BTS from similarly presumed coronary ischemia. In both current series and the earlier series, there were no perioperative or late deaths after BDG or Fontan. In this cohort, survival was comparable with that reported for other congenital heart lesions managed along the single-ventricle pathway [26] and is somewhat better than that reported after cardiac transplantation (81% versus 75% 1-year survival, 81% versus 65% 5-year survival) [28, 29]. Although the inclusion of patients referred from other institutions after neonatal shunting makes it difficult to know the true denominator for the population at risk, it does make clear that a single-ventricle management strategy can be carried out in institutions other than our own. Furthermore, in the follow-up period ranging up to 15 years, patients with PA/IVS-RVDCC who were managed with a single-ventricle approach have been able to avoid the ongoing risks associated with transplantation. More detailed analysis and longer-term follow-up are necessary to determine whether this survival benefit persists and whether there are important differences in quality of life over time. It is clear that at least the intermediate term transplantation is likely not necessary except in the patients with complete aortocoronary atresia or in those with significant left ventricular dysfunction.
The exact mechanism of this presumed coronary ischemia is unclear but may be related to presence of ventriculocoronary fistulae that impede normal diastolic antegrade coronary flow. Coronary perfusion with undersaturated RV blood may contribute to the insult. In addition, there may be coronary steal from the presence of the patent ductus arteriosus because of the effect on antegrade diastolic coronary perfusion. Finally, addition of a systemic-to-pulmonary artery shunt to this physiologic situation may present a larger volume load to the heart than would a patent ductus arteriosus, and may result in lower diastolic blood pressure from increased runoff into the pulmonary arteries as pulmonary vascular resistance decreases postnatally.
The effect of less extensive coronary anomalies (ie, non-RVDCC) was analyzed in an echocardiographic series by Gentles and colleagues [20] in 1993. The authors found that while regional LV dysfunction was unusual in patients without coronary artery abnormalities, it was common before and increased after RVD, although global LV dysfunction was rare.
During CPB, the RV preload may be reduced unless care is taken to keep the heart filled, resulting in reduced coronary perfusion in areas that are either completely or partially dependent on the RV ejection. Although venovenous bypass has been proposed to keep the RV beating and ejecting and to provide oxygenated blood for the RV dependent myocardium in an effort to prevent myocardial ischemia during right heart bypass operation [29], we have found no contraindication to standard CPB at the time of BDG or Fontan as long as adequate RV filling and ejection are maintained. We do not routinely use CPB at the time of BTS construction, when the neonatal myocardium may arguably be at highest risk.
Unlike situations in which coronary ostia are present, myocardial perfusion occurs only during systole in the unique situation where there is complete aortocoronary atresia or proximal coronary stenosis coronary with RVDCC. With the observation that there has been 100% mortality in patients with PA/IVS and aortocoronary atresia at our institution since 1986 (n = 3), as well as in the few cases reported in the literature [31–35], we have altered our management strategy so that these patients are now listed for primary cardiac transplantation. This anatomic subgroup appears to be particularly vulnerable to coronary ischemia with very limited myocardial reserve. Since implementation of this change as of January 2005, we have diagnosed, listed and successfully transplanted 1 neonate with complete aortocoronary atresia (severe RV hypoplasia, TV z-score -4.0) who was maintained on prostaglandin (PGE1) for 5 days while awaiting a donor heart.
While a short waiting time is certainly desirable, it is not always possible, and the new challenge becomes how to best manage these patients on the waiting list for what may be weeks to months. Whether BTS, prolonged PGE1 administration, a combination of both strategies (PGE1 for several weeks followed by BTS if no donor heart becomes available), or perhaps even ductal stenting is the optimal strategy is unknown. In an attempt to increase the donor pool for neonates, cardiac transplantation with ABO-incompatible donors has been performed with encouraging early results [36]. Patients with aortocoronary atresia appear to be suitable candidates for this approach.
Finally, we have not observed regression of ventriculocoronary fistulae or coronary stenoses to the point that an RV-dependent circulation has evolved into a "non–RV-dependent circulation" in the 20 patients in whom we had adequate follow-up angiography. The observed regression in fistulae (n = 5) and coronary stenosis (n = 1) may be related to lower measured RV pressures over time (median right ventricle pressure 170% versus 137% systemic, pre-BTS versus post-BTS) but while plausible, cannot be explained by the development of a more extensive collateral circulation based on our findings. Interestingly, dynamic collapse of the RCA during systole was observed in 2 patients with an atretic RCA and similar collapse of the LAD in 1 patient with proximal-mid LAD interruption, supporting the finding by Calder and colleagues [7] that there is some intrinsic structural abnormality inherent to RV-dependent coronary arteries. In their autopsy series, loss of normal coronary arterial wall structure and replacement with fibrocellular tissue containing irregular strands of elastin were demonstrated histologically only in patients with PA/IVS who had ventriculocoronary fistulae.
In conclusion, precise definition of coronary arterial anatomy remains imperative to the management of neonates with PA-IVS. Early mortality among such patients appears to be related to coronary ischemia at or around the time of BTS. In patients surviving initial BTS, single-ventricle palliation yields excellent mid- to long-term survival with well-preserved LV systolic function. Neonates with aortocoronary atresia—the most extreme form of RVDCC—represent a unique population in whom cardiac transplantation should be performed, whereas most other patients with PA/IVS and RVDCC can be successfully managed by a single-ventricle approach. Longer term follow-up will be necessary to assess whether these patients will be at risk either for sudden death due to ventricular dysrhythmias or for ventricular dysfunction as a result of coronary perfusion with subnormal saturated blood.
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DR GULESERIAN: Thank you, Dr Backer. To answer your second question first, yes, we are recommending transplantation for this particular subgroup of patients with complete aortocoronary atresia—in other words, the most extreme form of RV-dependent coronary circulation. We believe that since there has been 100% mortality in our experience with such patients, a finding supported in review of the literature where there has not been a single survivor reported with this anatomy, that transplantation is probably the best approach.
In response to your first question, yes, we actually did go back to take a look at all of these patients' follow-up angiograms and compared them to their initial studies when available. Of the survivors, there were 20 patients who had adequate studies available for review and 3 patients who are still awaiting their pre-Glenn catheterization.
There were 5 patients in whom we noted regression in these fistulae and 1 patient in whom there was regression of coronary stenosis, but there were no situations in which we could confidently say that patients had transitioned from an RV-dependent to a non–RV-dependent coronary circulation.
DR GLEN S. VAN ARSDELL (Toronto, Ontario, Canada): That was a beautiful presentation and I think very nice outcomes in a very difficult group of patients.
I think there are two issues. One is, are these patients really stable enough to be on a transplant list? In other words, are they going to succumb before ever getting a heart, which may take 2 or 3 months.
The second issue is that for years we have now learned, based on a Norwood population, that the best way to manage a balanced circulation is to use afterload reduction. And data are emerging that the pulmonary component of the manipulation is relatively unimportant.
Based on the data you have, is there some question that maybe in this particular subset of patients we should be take a vasoconstriction mode of treatment strategy that isn't inotropic? In other words, should we be using vasopressin? Because, obviously, if we use norepinephrine or epinephrine we're going to increase myocardial O2 consumption. So have you looked at that specifically? Are there signs of coronary ischemia? Should we be using a different perioperative management strategy?
DR GULESERIAN: We haven't looked at that strategy specifically, but I do believe that all of the deaths in this group have been related in some way to coronary ischemia. It seems that once these patients undergo some sort of hemodynamic insult, whether they experience just a brief episode of hypotension or become volume depleted or perhaps even develop tachycardia from a fever at home, they start heading along a downward spiral and don't seem to have the capacity or the reserve to recover from it. I think that your suggestion would be an interesting strategy.
As far as the transplantation issue goes, I think that it presents the next challenge: how do you optimally maintain these patients on a waiting list? You are absolutely correct, we are not going to have donors immediately available.
I do think that given the promising early results with ABO-incompatible cardiac transplantation these patients may be ideal candidates for that sort of approach and perhaps such a strategy could decrease the waiting time.
DR VAN ARSDELL: Since I come from one of those ABO institutions, we still sometimes have to wait 2 or 3 months.
DR RALPH S. MOSCA (New York, NY): This is a very interesting study in a very heterogenous group of patients.
I'm having some difficulty trying to determine what you think the etiology of the perioperative mortality is. I can understand the patients with aortocoronary atresia being a high-risk group at the initial palliation as a result of coronary ischemia, but can you explain why they're not at just as high a risk at the Glenn stage when you decompress the RV? Can you describe what your technique is for the shunt? Is it done through a sternotomy? Do you tie the ductus? How do you perform the second stage procedure? All these technical details could impact on the incidence of coronary ischemia.
DR GULESERIAN: First of all, there were no patients with aortocoronary atresia who survived to second-stage palliation, so I don't really have any data about the comparative risk at the Glenn stage.
As far as our operative approach goes, we do attempt to perform all of these BT shunts without the use of cardiopulmonary bypass to keep the right heart full, and we do ligate the ductus after completion of the shunt. I don't know whether other institutions follow the same strategy, but that has been our approach.
DR JOHN E. MAYER, JR (Boston, MA): Can I just make one other comment. I think the important concept here is, obviously, you have to keep the right ventricle filled and contracting in order to prevent coronary ischemia. I think that's why the experience with trying to use ECMO to resuscitate these kids who have had an arrest is a hopelessly flawed strategy, because you can't keep the right heart filled; and if you can't fill the right heart, you can't perfuse the coronaries. I mean, it's a hopelessly bad situation when you get into that. So the critical issue is to try to make sure they don't arrest or they don't get hypotensive.[27,30
One of the interesting things that Kris didn't really have time to say, but I'm going to take a minute now to say, is we've had some interesting experiences trying to do the Glenn and the Fontans on bypass. And even then I think you can make the argument that you have to be very careful with your technique of bypass because if you empty the heart out too much, you can see the ECG going crazy right in front of you. And you have to tell the guys who are sitting behind you running the pump to fill the heart back up because you'll get coronary ischemia. So I think that's an important concept about how you translate the RV dependence of the coronary circulation into your management techniques.
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