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Ann Thorac Surg 1998;66:649-652
© 1998 The Society of Thoracic Surgeons

Supplement

Subaortic obstruction and the fontan operation

Robert M. Freedom, MDa

a Division of Cardiology, Department of Pediatrics, The Hospital for Sick Children, University of Toronto Faculty of Medicine, Toronto, Ontario, Canada

Address reprint requests to Dr Freedom, The Hospital for Sick Children, Rm 1503C, 555 University Ave, Toronto, ON, Canada M5G 1X8

Presented at the Workshop on "One and One-Half Ventricle Repairs," Gubbio, Italy, Dec 6–7, 1996.

Abstract

Systemic outflow tract obstruction in the heart with a functional single ventricle promotes myocardial hypertrophy, and this has been shown to be an unequivocal risk factor for poor outcome at Fontan procedure. Such systemic outflow tract obstruction may be congenital or acquired. Those factors contributing to acquired systemic outflow tract obstruction in those patients with a double-inlet left ventricle, a rudimentary right ventricle, and a discordant ventriculoarterial connection include the size of the ventricular septal defect, previous pulmonary artery banding, and other volume unloading surgical procedures. Staging with a bidirectional cavopulmonary connection and construction of a proximal pulmonary artery-aortic connection or ventricular septal defect enlargement has neutralized this factor.

Since the introduction a quarter of a century ago of the Fontan procedure to effectively separate the systemic from the pulmonary venous circulations without a pumping chamber in the pulmonary circulation [1], a number of risk factors have been identified that forecast a poor outcome, including early death or Fontan takedown [2, 3]. One such risk factor is profound myocardial hypertrophy [4–9]. The causes of myocardial hypertrophy are complex, and methodologies to accurately quantitate this risk factor are indirect. Nonetheless, a number of studies have now stratified ventricular wall mass against Fontan outcome, providing evidence that myocardial hypertrophy is an important risk factor, requiring preoperative assessment [4–9]. Among those causes promoting myocardial hypertrophy is subaortic stenosis. How myocardial hypertrophy leads to an adverse outcome is unclear. But certainly it must alter ventricular filling and disadvantage ventricular compliance, with preservation of systolic function. This article will focus on the clinical recognition of subaortic stenosis in the context of the Fontan algorithm and surgical maneuvers to address this risk factor.

The morphologic substrate

The morphologic bases for subaortic stenosis in those hearts amenable only to a one-ventricle repair are diverse, and are clearly related to the cardiac template [10–13]. For those hearts with either double-inlet left ventricle with a rudimentary right ventricle and discordant ventriculoarterial connections; tricuspid atresia with discordant ventriculoarterial connections; or absent left atrioventricular connection with a dominant left ventricle, a rudimentary right ventricle, and discordant ventriculoarterial connections, it is the ventricular septal defect (VSD) that effectively guards the systemic outlet. Thus if the VSD is intrinsically small, becomes progressively smaller with time, or is crowded by contiguous atrioventricular valve tissue or tissue tags, subaortic stenosis or systemic outflow tract obstruction is the inevitable result or sequel. The mechanism of subaortic stenosis in those hearts of right ventricular morphology is similar to that seen in patients with the Taussig-Bing form of double-outlet right ventricle. The subaortic outflow tract in this situation is related to right ventricular structures. The subaortic right ventricular outflow tract is elongated and narrowed and indeed wedged between the right-sided ventriculoinfundibular fold and the infundibular septum [14–16].

Systemic outflow tract obstruction is a well-known finding in those hearts with tricuspid atresia or severe stenosis and so-called anatomically corrected malposition of the great arteries [17–19]. Despite ventriculoarterial concordance, the aorta is supported by an obstructive subaortic infundibulum [17–22]. The aorta is usually levo-malpositioned, but despite the abnormal spatial relationship between the great arteries, the atrioventricular and ventriculoarterial connections are not discordant [23, 24].

Clinical recognition of subaortic obstruction in double-inlet ventricle

In the clinical assessment of patients with a double-inlet ventricle and increased pulmonary blood flow with pulmonary artery hypertension, one must always be cognizant of the reality or potential for systemic outflow tract obstruction. This suspicion should be heightened if there is a coexisting obstructive anomaly of the aortic arch [11, 14–16, 25–27]. In hearts characterized by a dominant left ventricle, a rudimentary right ventricle, and discordant ventriculoarterial connections, the VSD must be carefully scrutinized. In the neonate or young infant with this cardiac template, in heart failure with pulmonary artery hypertension and a borderline cardiac output, it is unlikely that a pressure gradient across the VSD will be recorded by intracardiac hemodynamic measurements. Thus, it is the echocardiographic or angiocardiographic appearance of the VSD that will guide therapy [12, 14–16, 26–28].

We and others have provided clinical evidence that administration of intravenous isoprenaline may unmask latent subaortic obstruction, especially in those patients with dominant left ventricle, a rudimentary right ventricle, and discordant ventriculoarterial connections subjected to previous pulmonary arterial banding, by provoking a pressure gradiant between the left ventricle and aorta [14, 15, 29, 30]. Although this maneuver has been helpful in ascertaining latent subaortic obstruction, we have not defined the sensitivity or the specificity of this particular finding. The angiocardiographic findings of the restrictive VSD in this setting have been amply recorded [12, 14–16, 30, 31]. The VSD is usually not oval or circular, but rather is elliptic, much like a buttonhole. It can be profiled by selective injection into either the dominant left ventricle or the rudimentary chamber supporting the aorta. The precise axial projection will be determined by the ventricular organization. When the ventricular relationship conforms to a D-ventricular loop (as in classic tricuspid atresia) the VSD is best profiled in a long axial oblique projection. Angiocardiography performed in the frontal or shallow right axial oblique projection should profile the VSD when the rudimentary right ventricle supporting the aorta is left-sided (so-called L-loop). For those patients with a double-inlet right ventricle, right ventricular angiocardiography performed in the frontal projection, with or without cranial angulation, should define the character of the right ventricular subaortic outflow tract [12, 14–16, 30, 31].

Pulmonary artery banding and the development of subaortic stenosis

The particular relationship between pulmonary artery banding and the development of subaortic obstruction in hearts with double-inlet left ventricle, rudimentary right ventricle, and discordant ventriculoarterial connections is complex. There is little doubt that subaortic stenosis reflecting a restrictive VSD occurs after pulmonary artery banding [9, 14, 25, 30, 32], and that with both arterial outlets obstructed (the pulmonary artery by the pulmonary artery band and the systemic outlet by the restrictive VSD), myocardial hypertrophy is inevitable. What remains contentious is the specific role of the pulmonary artery band in the genesis or causality of the restrictive VSD. Rao [33] takes the position that it is the natural tendency for the moderate-sized VSD in these patients to become smaller that results in subaortic stenosis. Others take the position that reduction of left ventricular end-diastolic volume and remodeling of the left ventricle causes VSD restriction [34]. We have taken the position for many years that pulmonary artery banding causes VSD restriction, subaortic stenosis, and then myocardial hypertrophy [6, 8–10, 14–16, 25, 30, 32]. But it is likely that pulmonary artery banding by promoting both ventricular hypertrophy and some reduction of left ventricular end-diastolic volume accelerates the natural history of the moderate-sized muscular VSD to become smaller. Furthermore, because systemic outflow tract obstruction has been documented after the Fontan operation [35], it is too simplistic to suggest that only one factor is responsible for the change in form and function of the VSD in these hearts.

Surgical inferences

The improving results in Fontan surgery reflect not just a better appreciation of Fontan’s criteria [36] but the reality that better results can be obtained by adhering strictly to these criteria [37]. Better myocardial protection and enhanced postoperative care also contribute in a generic way to improved results. But as more and more patients with difficult and challenging anatomy and hemodynamics were referred for consideration of a Fontan operation or any of its surgical variations, various maneuvers were introduced to reduce morbidity and mortality including atrial fenestration and staging to the Fontan operation with the bidirectional cavopulmonary connection [38–40]. In addition, there have been an increasing number of reports addressing the surgical approach to relieving subaortic stenosis [40–51]. These surgical procedures include direct enlargement of the VSD, construction of a proximal pulmonary artery–ascending aortic anastomosis, or in some patients a palliative arterial switch procedure. Data from the Mayo Clinic indicate that patients with subaortic stenosis do better if they are staged to the Fontan operation with the subaortic obstruction addressed at the staging operation with later completion of the Fontan operation [52, 53]. We have had an experience similar to that of the Mayo Clinic and have also dramatically improved our Fontan results by a combination of staging to the Fontan and fenestration, and by addressing the subaortic stenosis at the hemi-Fontan. Our overall institutional mortality for nearly 500 Fontan procedures has dropped from 8.6% to only one death in the last 100 consecutive Fontan operations. But these improving Fontan results are germane only to patients undergoing a Fontan operation, and these statistics do not address attrition before the Fontan procedure [54, 55]. Indeed, for patients with tricuspid atresia, a substantial number will die before they become candidates for the Fontan operation or will be excluded from consideration because they do not meet contemporary criteria. Finally, the ability to perform an early bidirectional cavopulmonary connection has led to a renewed interest in pulmonary artery banding as the initial palliation for some babies with double-inlet ventricle [56, 57], although this perspective is not universally held [58].

References

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