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Ann Thorac Surg 1996;62:161-168
© 1996 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Spontaneous Acquisition of Discontinuous Pulmonary Arteries

Congenital Heart Registry aand the Sections of Pediatric Cardiologyd, Cardiovascular Pathologye and Cardiovascular Surgeryb, University of Chicago, Chicago, Illinois USA and Faculty of Medicine, Department of Anatomy, University of Leidenc, Leiden, the Netherlands

Accepted for publication March 6, 1996.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Background. Discontinuous pulmonary arteries have been considered a rare complication of systemic-to-pulmonary shunt operations. We report a series of children who spontaneously acquired pulmonary artery discontinuity.

Methods. All children from 1989 through 1995 with congenital pulmonary atresia were reviewed.

Results. Pulmonary artery discontinuity developed in 29% (15 patients), none related to shunt operation. In 6 of 15 patients, the neonatal angiogram showed a pattern that seemed to predict subsequent discontinuity; in 9 of 15, pulmonary arteriography was normal at birth. Two clinical patterns were identified: an early rapid acquisition of discontinuity within hours to days, and a delayed, more subtle development that occurred over months. Eight of 15 have died. Pathologic studies in 6 children showed ductal tissue extending along and into the pulmonary artery wall as well as intimal hypertrophic reaction and maladaptive remodeling.

Conclusions. Children with congenital pulmonary atresia may experience spontaneous acquisition of pulmonary artery discontinuity. Ductal tissue is responsible for local pulmonary artery distortion and discontinuity; this may be exacerbated by previous prostaglandin E₁ administration. Clinical algorithms are suggested for patients with pulmonary atresia.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
In the past, discontinuity of the pulmonary arteries has been considered either a congenital anomaly [1, 2] or a postsurgical complication. Recently, we have experience with a number of children who acquired discontinuity of their pulmonary arteries, not related to operation. Pathologic studies in our patients have shown that tissue identified as ductus arteriosus is involved directly in the obstructive process. When correlated with clinical experience, a pathophysiologic construct and clinical algorithms are suggested.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Patient Selection
All children with pulmonary atresia seen as neonates at the University of Chicago from 1989 through 1995 were considered for this study. These children were reviewed for the development of acquired discontinuity of the pulmonary arteries. Echocardiograms, cineangiograms, catheterization, clinical, surgical, and pathologic studies were reviewed. When pulmonary artery discontinuity was found at catheterization, pulmonary vein wedge angiography was performed to assess the existence of both pulmonary artery branches. When available, pulmonary artery specimens were sectioned serially across the long axis of the pulmonary arterial system (from left to right pulmonary artery) and stained with hematoxylin and eosin as well as two complimentary connective tissue methods (Weigert von Giesen and Gomori trichrome with aldehyde-fuchsin) to distinguish cells, collagen, and elastin. These specimens were compared to the specimens reported by Elzenga and colleagues [3] as ``coarctation of the pulmonary artery."

Patient Population
Fifteen of 52 children (29%) met the selection criterion: initial echocardiographic or angiographic studies, or both, that showed continuous pulmonary arteries and subsequently pulmonary arteriography that demonstrated discontinuity of the pulmonary arteries or critical stenosis of a branch pulmonary artery.

In addition to pulmonary atresia, the 15 patients (Table 1) had (1) tetralogy of Fallot (6 patients); (2) tricuspid atresia (5); (3) intact ventricular septum (3); or (4) asplenia syndrome (1 patient). As neonates, each had a single left-sided patent ductus arteriosus and each was given prostaglandin E₁ at 0.05 to 0.1 µg • kg^-1 • min^-1 until operation. Each had a neonatal systemic-to-pulmonary Gore-Tex (W. L. Gore & Assoc, Flagstaff, AZ) tube graft shunt procedure (12 right, 2 "central," and 1 left).

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
The median age at which discontinuity of the pulmonary arteries was recognized was 6.5 months (range, 4 days to 17 months); 13 of 15 patients were less than 1 year of age. Figures 1A, 1C, and 1E show normal pulmonary artery images before operation with an infusion of prostaglandin E₁, and Figures 1B, 1D, and 1F were taken long after shunt operation. In every patient, the atresia/stenosis was found at the origin of the left pulmonary artery. Figures 2B and 2CAu: OK? show abnormal pulmonary artery images before operation with an infusion of prostaglandin E₁, and Figures 2A and 2C show follow-up angiograms long after shunt operation. The initial clinical course was similar in all patients: (1) diagnosis of pulmonary atresia with confluent pulmonary arteries by echocardiography or angiography; (2) administration of prostaglandin E₁ from admission through operation; (3) performance of a systemic-to-pulmonary shunt (usually right-sided) and prostaglandin E₁ discontinued in the operating suite; (4) good immediate course with arterial oxygen saturation more than 80% for 6 to 24 hours. At this point, one of two different patterns emerged: (1) progressive decrease noted in oxygen saturation and sometimes left lung oligemia on chest roentgenogram (Fig 3A); (2) trial of prostaglandin E₁ with variable clinical response; (3) urgent angiography done to assess adequacy of shunt; (4) shunt found to be well patent but left pulmonary artery stenosis/atresia now identified; or (1) after neonatal shunt, hospital discharge with adequate oxygen saturation; (2) gradual decrease in oxygen saturation over months considered secondary to somatic growth; (3) repeat cardiac catheterization with angiography at 3 to 9 months of age showing discontinuous pulmonary arteries. Very rarely, this diagnosis was made on "routine" repeat angiography at 9 to 15 months of age.

View larger version (42K): [in this window] [in a new window]   Fig 1. . Images of acquired discontinuity of the pulmonary arteries: (A, B) patient 1, (C, D) patient 9, (E, F) patient 12. (A) Note the large patent ductus arteriosus ( dashed lines) and filling of both branch pulmonary arteries. (B) Ten months after right modified Blalock-Taussig shunt (shunt) there is no filling of the left pulmonary artery. (C) Echocardiogram at 3 days of age shows no stenosis between the main pulmonary artery and left pulmonary artery. (D) Angiography into the right-sided shunt shows severe circumferential constriction (white arrow) at the origin of the left pulmonary artery and relative oligemia of the left lung. (E) On the first day of life there is no obstruction in either the right (R) or left (L) pulmonary artery. (F) Four months after shunt there is spontaneously acquired stenosis of the left pulmonary artery; see text for details. (DAo = Descending aorta; L = left; M = main; PA = pulmonary artery; PDA = patent ductus arteriosus; R = right; Shunt = systemic-to-pulmonary anastomosis using a Gore-Tex tube graft.)

View larger version (47K): [in this window] [in a new window]   Fig 2. . Angiographic harbinger of discontinuity of the pulmonary arteries. (A) Note filling of both pulmonary arteries with a line of continuity (dashed white line) between the patent ductus arteriosus and left pulmonary artery, but not equal contrast density at the right pulmonary artery–left pulmonary artery junction. (B) The corresponding lateral view to A shows an indentation (white arrow) between the right pulmonary artery and left pulmonary artery not in the immediate proximity to the ductal insertion into the pulmonary artery system. (C) Neonatal angiogram shows obstruction between the two branch pulmonary arteries where the patent ductus arteriosus inserts. (D) Obliquely angulated angiogram at 3 days of age demonstrates the patent ductus arteriosus–pulmonary artery confluence. It is unclear from the picture whether the section of vessel identified by ? is stenotic right pulmonary artery, stenotic left pulmonary artery, or ductal tissue. (L = Left; PA = pulmonary artery; PDA = patent ductus arteriosus; R = right.)

View larger version (50K): [in this window] [in a new window]   Fig 3. . Angulated angiography best defines discontinuous pulmonary arteries. (A) Note that pulmonary vascular markings are increased on the right and diminished on the left 3 days after right shunt and discontinuation of prostaglandin E1. (B) Oblique pulmonary arteriography demonstrates severe stenosis at the ductal insertion into the pulmonary arteries 10 days after shunt. (C, D) True lateral (C) and anteroposterior (D) angiograms taken at the same cathAu: spell out as B fail to demonstrate the stenosis because of overlap interference. (DAo = Descending aorta; LPA = left pulmonary artery; PDA = patent ductus arteriosus; RPA = right pulmonary artery.)

In those patients where prostaglandin E₁ was restarted shortly after shunt insertion, there was a partial response. The oxygen saturation consistently improved but angiography always showed a patent shunt and severe left pulmonary artery narrowing. Prostaglandin E₁ seemed to restore flow into the left lung but did not fully redilate the ductus.

In one patient (patient 10), during dissection of the ductus arteriosus–left pulmonary artery junction in preparation for patch arterioplasty, a circumferential band phenomenon (Fig 1E) was released and the stenotic area "snapped" open. No further procedures were done on the pulmonary artery in that patient.

Eight children have died; autopsy permission was granted in 5 patients. Patient 7 died 2 days after the initial right modified Blalock-Taussig shunt without adequate explanation. Patients 1, 4, 14, and 15 died at a second operation required for the pulmonary artery discontinuity. Three patient deaths were unrelated to the pulmonary arteries: patient 2 died 8 months after cavopulmonary anastomosis of lung disease secondary to extreme prematurity (28 weeks' gestation); patient 11 died 3 months after neonatal shunt of dehydration during gastroenteritis; patient 9 died of postoperative cardiac herniation and strangulation [4].

Histopathologic studies of the ductus–pulmonary artery junction and the adjacent pulmonary artery wall demonstrate various degrees of extension of ductal tissue into the pulmonary artery wall (Figs 4 and 5) with disruption of left pulmonary artery-to-main pulmonary artery continuity of elastic fibers. The ductal tissue often seemed to penetrate among the elastic lamellae of the pulmonary artery wall (Fig 5B,C). Within the vessel lumen, an intimal hypertrophic reaction was found with evidence of both chronicity and adaptive remodeling. The cellular and matrix components demonstrated neoformation of an internal elastic lamina beneath the intact endothelium (Fig 4D).

View larger version (66K): [in this window] [in a new window]   Fig 4. . Pathology of acquired discontinuity of the pulmonary arteries. (A) Insertion of the ductus arteriosus into the left pulmonary artery is seen as well as the pericardial patch (P) used to relieve the obstruction in patient 9 (see Fig 1D). (B) The pulmonary artery wall seen in A is reflected cephalad to demonstrate where ductal tissue is present. Notice the irregular ductal tissue in comparison to the normal pulmonary artery wall. (C) Surgical specimen (patient 1) of the ductus arteriosus–left pulmonary artery junction shows muscular ductal tissue involved in at least 50% of the arterial wall. The elastic pulmonary artery wall is distinguishable from ductal tissue on gross inspection. (Elastic stain; magnification, x15.) (D) Increased magnification (x40) of C shows the elastic lamellae (EL) of the pulmonary artery wall and two internal elastic laminae. There is the normal layer (IEL-1) furthest from the lumen (L) that forms the border between intima and media of the ductus (a muscular artery). In addition, there is a new lamina (IEL-2) with a zone of fibrocellular hypertrophy between the two internal elastic laminae. (AAo = Ascending aorta; C = calcium deposit; DA = ductus arteriosus; DT = ductal tissue; EL = elastic lamellae (of the pulmonary artery wall); IEL = internal elastic lamina; L = lumen; LPA = left pulmonary artery; MPA = main pulmonary artery; P = pericardial patch; PA = pulmonary artery.)

View larger version (72K): [in this window] [in a new window]   Fig 5. . Penetration of the pulmonary artery wall by ductal tissue. All panels were taken from the surgically resected section of pulmonary artery in patient 14 and prepared with elastic stain. (A) Section across the junction of the ductus arteriosus and the left pulmonary artery demonstrates ductal tissue from 11 to 3 o'clock with extension (arrows) into the pulmonary artery wall. (Magnification, x19.8.) (B) Close-up of A shows a tongue of muscular ductal tissue penetrating between elastic lamellae (E). (Magnification, x39.6.) (C) Section of the left pulmonary artery closer to the right pulmonary artery than in B shows muscular ductal tissue extensively interdigitated with elastic lamellae. (Magnification, x60.) (DT = ductal tissue; E = elastic lamellae of pulmonary artery wall; L = lumen.) (All magnifications are before 10% reduction.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment References

Although our report is largely descriptive, some conclusions can be reached. First, the presence of a nonstenotic pulmonary artery confluence in a neonate, especially during prostaglandin E₁ infusion, provides no assurance that the patient will remain free of stenosis or even atresia of the pulmonary artery confluence. Second, local deformation by ductal tissue appears to be the consistent factor associated with the stenosis. Thus, wherever ductal tissue extends beyond the ductus itself, there is the potential for acquired obstruction.

The presence of ductal tissue in both the aorta [6–8] and the pulmonary arteries has been previously noted [3, 9–12]. Our experience shows that this muscular tissue can involve the antiductal pulmonary artery wall, can extend for some length within the pulmonary artery, and can be interspersed between the elastic lamellae of the pulmonary artery wall.

There are at least two important pathophysiologic factors involved in the development of discontinuous pulmonary arteries: abnormal extension of ductal tissue along and within the pulmonary artery wall, and damage to ductal tissue (wherever it is present) by prostaglandin E₁. (It is of note that only 1 of more than 50 pulmonary artery specimens obtained before the prostaglandin E₁ era showed the findings noted in the present study: AC Gittenberger-de Groot, unpublished observation.) The phenomenon of early postshunt left pulmonary artery occlusion seems more related to the presence and active contraction of ductal tissue within the pulmonary artery wall. Delayed acquisition of discontinuity is due to progressive edema, fibrosis, and calcification of the ductal tissue [13] with intimal proliferation (Fig 4D) leading to fibrocellular hypertrophy [14]. Whether the vessel marked by the question mark in Figure 2D is narrowed because ductal tissue has "invaded" the pulmonary artery wall or because ductal tissue has produced a long segment intimal hyperplastic reaction is not known. The anatomic consequences of ductal tissue within the pulmonary artery wall are summarized in Figure 6.

View larger version (43K): [in this window] [in a new window]   Fig 6. . Consequences of ductal tissue In the pulmonary artery. (Top) The aorta–ductus arteriosus–pulmonary artery area with the ductus–left pulmonary artery segment cutaway for detailed examination. Ductal tissue is signified by cross-hatching and pulmonary artery wall indicated by dots. (A) Ductal tissue involving part of the pulmonary artery wall and (A') the effect of ductal closure causing vascular constriction and producing a ridge of tissue within the vessel lumen. (B) Ductal tissue throughout the pulmonary artery wall that produces (B') complete occlusion/discontinuity after ductal closure. (C) In 1 patient ductal tissue seemed to be around but not within the pulmonary artery wall; this produced a "band" (C') around the left pulmonary artery (Fig 1E) that was released by surgical dissection. Condition C is unconfirmed as no pathologic specimens have been encountered where ductal tissue was found exclusively on the outside of the pulmonary artery.

In view of the temporal and morphologic findings seen in these neonates, it is likely that stenosis at the ductus arteriosus-to-pulmonary artery junction represents an aberration of the remodeling process that takes place when the ductus closes. However, it is not presently known whether abnormal local hemodynamics or extension of ductal tissue is the primary event. Changes in both wall tensile stress and wall shear stress may induce the excessive penetration of ductal tissue into the pulmonary artery wall. The associated (postnatal) intimal proliferative response would reflect an attempted adjustment of the local vessel effective radius to reestablish baseline wall shear stress. This phenomenon is often noted at anastomoses and at other sites where wall shear stress is reduced [14]. The converse might also be true, that is, abnormal extension of ductal tissue into the pulmonary artery wall in pulmonary atresia could be the primary problem, leading to altered local hemodynamic conditions that change the tensile strength/shear stress relations so that maladaptive remodeling takes place.

Before a systemic-to-pulmonary shunt procedure in a patient being treated with prostaglandin E₁, pulmonary angiography may be helpful in identifying the pattern (present in 40% of our patients) predictive of discontinuous pulmonary arteries. However, unless one plans to approach this surgically at the first procedure, preshunt catheterization will not alter the treatment plan. Therefore, we have generally chosen not to do a preshunt diagnostic cardiac catheterization unless there are other indications.

The clinical use of prostaglandin E₁ in those with pulmonary atresia requires clarification. Although the neonatal administration of prostaglandin E₁ is a likely factor in the development of discontinuous pulmonary arteries, it is not suggested that prostaglandin E₁ usage be curtailed. The advantages of a stable, nonacidotic newborn for catheterization or operation outweigh the potential complication of pulmonary artery obstruction.

It was considered that a central shunt providing flow equally to both pulmonary arteries or a left-sided shunt with preferential flow ipsilateral to the ductus arteriosus might prevent the development of discontinuous pulmonary arteries. This was not our experience as 3 of our 15 patients had such shunts but still developed discontinuous pulmonary arteries. It is now clear that the mechanism is closure and fibrosis of ductal tissue probably independent of shunt-altered hemodynamic/flow considerations. Therefore, there seems no advantage of one type of shunt over another with regard to the acquisition of discontinuous pulmonary arteries.

The signs of early development of pulmonary artery discontinuity include decreasing oxygen saturation or, less commonly, oligemia on the chest roentgenogram contralateral to the shunt (Fig 3A). We believe that urgent pulmonary arteriography is indicated when such signs are present postoperatively to rule out obstruction related to the shunt and to evaluate the pulmonary artery confluence. These angiograms usually require angulated views, such as +25 degrees coronal and +25 degrees cephalad (Fig 3B), to define clearly the ductus–left pulmonary artery junction. Because we have encountered several children without low saturation or pulmonary vascular asymmetry who developed discontinuous pulmonary arteries, our current policy is to follow all shunted patients closely with echocardiography, especially Doppler flow studies in the left pulmonary artery. We "routinely" do pulmonary arteriography in all children with pulmonary atresia 6 to 10 weeks after shunt operation.

The therapeutic response to discontinuous pulmonary arteries depends in part on the future repair. When a two-ventricle approach is possible, a right ventricle-to-pulmonary artery homograft conduit is generally used. As there usually is sufficient room on the left pulmonary artery between the atretic segment and the upper lobe branch for conduit anastomosis, early complete relief of pulmonary artery discontinuity is less critical. Therefore, when discontinuity is found early in such patients, a small additional shunt on the oligemic side may be reasonable palliation. When found after 4 months of age, repair with a conduit is the best choice.

When a Fontan-type approach is planned (9 of 15 patients in our series), early restoration of unobstructed pulmonary artery confluence is important. We have favored resection and end-to-end anastomosis, analogous to repair of coarctation of the aorta, when a 5-mm shunt has been previously inserted. If the initial shunt was 4 or 3.5 mm, a small additional shunt might be added to the pulmonary arterioplasty. If right pulmonary artery stenosis is found (usually by angiography as in Fig 1B), this should be repaired at the time of any subsequent operation. If the patient is more than 3 months of age and has low pulmonary vascular resistance, a cavopulmonary anastomosis with shunt take-down and left pulmonary arterioplasty is our preferred approach. Insertion of endovascular stents within the pulmonary artery may be a viable option [15] but placement may be technically difficult because of angulation of structures or inability to traverse the obstruction in patients with atresia rather than stenosis.

The high mortality in this group of patients is disturbing. It may reflect the less-than-optimal treatment outcomes seen in right heart atresia syndromes and single ventricle circulations. On the other hand, the tendency to develop discontinuous pulmonary arteries may be an independent risk factor.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Address reprint requests to Dr Waldman, Division of Pediatric Cardiology, Department of Pediatrics, University of New Mexico, 2211 Lomas Blvd NE, Albuquerque, NM 87131-5311.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Robert B. Karp Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Waldman, J. D. Articles by Glagov, S. Search for Related Content PubMed PubMed Citation Articles by Waldman, J. D. Articles by Glagov, S.