Pulmonary Conduit Research Articles

Repair of congenital tricuspid valve abnormalities with artificial chordae tendineae

Background. Congenital abnormalities of the tricuspid valve, including Ebstein’s malformation, dysplasia, straddling, and those found in pulmonary atresia with intact septum and congenitally corrected transposition, are an uncommon cause of tricuspid regurgitation. Congenital tricuspid valve anomalies are found as a spectrum of disease in which both the leaflets and the subvalvar apparatus are often involved. Tricuspid valve repair is complicated in such patients because the chordae tendineae are often abnormally short and thick. Replacement or augmentation of chordae tendineae has proved to be a useful component of mitral valve repair. In the present report, we describe the techniques and results of chordal augmentation in the repair of congenital tricuspid valve abnormalities. Methods. Since July 1992, tricuspid valve repair has been performed in 5 children with severe tricuspid regurgitation secondary to congenital abnormalities of the tricuspid valve with significant chordal pathology. As a component of the repair, chordal replacement or augmentation was performed using expanded polytetrafluoroethylene suture. Results. Intraoperative and postoperative echocardiographic assessment showed good mobility of the tricuspid valve leaflets and trivial to mild tricuspid regurgitation. There were no complications and no early or late mortality. At follow-up of 34 to 60 months (median, 49 months), tricuspid valve function has remained excellent in 4 of the 5 patients. In the remaining patient, progressive regurgitation of the right ventricle to pulmonary artery allograft conduit has led to right ventricular dilatation, with a secondary increase in tricuspid regurgitation from trivial to moderate. Conclusions. Chordal replacement or augmentation with expanded polytetrafluoroethylene suture is a useful technique in the repair of congenitally dysplastic tricuspid valves with abnormal chordal structures.

Mechanical Thrombectomy in Acute and Subacute Thrombosis with Use of the Amplatz Device: Arterial and Venous Applications

To perform a feasibility study of the Amplatz Thrombectomy Device (ATD) in a variety of vascular territories with acute or subacute thrombosis. Thirteen patients (mean age, 44.6 years) with multiple risk factors who had acute/subacute thrombosis of the inferior vena cava (IVC) and iliac veins (n = 3), superior vena cava (SVC) and/or subclavian veins (n = 3), lower extremity polytetrafluoroethylene (PTFE) graft (n = 2), iliac artery (n = 2), portal vein and transjugular intrahepatic portosystemic shunt (TIPS) (n = 2), and an IVC to pulmonary artery Fontan conduit (n = 1), were treated by means of mechanical thrombectomy with use of the ATD. Thrombolysis failed to recanalize the vessels when used before thrombectomy for 12-34 hours in three patients, and was contraindicated in three other patients. Thrombolysis was used as a complement to the ATD procedure in five patients. Technical success was achieved in 11 patients, and procedure success was achieved in 10 patients. Failure was observed in the remaining three patients. One patient with a PTFE graft was successfully declotted but thrombosis occurred 2 weeks later, requiring surgery. The other patient with a PTFE graft did not improve and needed surgery to declot and treat the distal anastomosis and distal circulation. The two patients with an occluded iliac artery underwent successful declotting but rethrombosis occurred in one shortly after the procedure requiring thrombolytic therapy. One patient with TIPS thrombosis improved and another patient with a thrombosed portal vein did not improve after thrombectomy. The ATD is useful for recanalization of acute/subacute clotted native vessels and grafts. The application of the device is broad, and although declotting can be achieved in most cases, long-term success may be limited by anatomical and technical problems of the grafts and multifactorial clinical problems of severely sick patients, as was the case in the series. The use of additional thrombolytic therapy may be necessary in a number of patients.

Moving actuator type total artificial heart with reverse position of the aortic and pulmonary conduits.

Adequate intrathoracic anatomical compatibility is one of the most important considerations in designing a fully implantable total artificial heart (TAH). We have recently developed an innovative concept of reverse positioning of the aortic and pulmonary conduits to facilitate anatomical compatibility of the moving actuator type TAH. The pulmonary conduit of this TAH is designed to be located posterior to the aortic conduit, which results in a substantial reduction in the anteroposterior diameter of this heart, as well as the virtual elimination of the compression of the low pressure pulmonary conduit. In ovine orthotopic implantation experiments with this model of the TAH, we consecutively achieved 3 day survival in 1 sheep and 2 day survival in another. To the best of our knowledge, these were the first significant short-term survival cases in the orthotopic implantation of electric TAHs in sheep.

Use of a bovine jugular vein graft with natural valve for right ventricular outflow tract reconstruction: A one-year animal study

Objective: We evaluated a bovine jugular vein graft with a natural trileaflet valve for right ventricular outflow tract reconstruction in a canine study for an entire year. Methods: Heparinized bovine jugular vein grafts with a natural valve cross-linked with a hydrophilic polyepoxy compound of 18 to 20 mm in internal diameter were implanted in the right ventricular–pulmonary arterial position in eight dogs, and the main natural pulmonary artery was ligated. Anticoagulants were not used after implantation. Five grafts were retrieved on day 182 after implantation and the other three grafts on days 196, 375, and 385, respectively, and were inspected by macroscopic and microscopic observation. Cardiac catheterization, followed by angiography and echocardiography, was done just before graft retrieval. Results: No graft kinking or regurgitation of the valve was observed. Echocardiography showed natural valve motion without thickening of the leaflets. Blood pressure in the conduits ranged from 18/9 to 31/4 mm Hg, in the right ventricle from 18/4 to 40/0 mm Hg, and the gradient varied from 0 to 14 mm Hg. The explanted conduits maintained their original shape, softness, and pliability with good coaptation of valves, without calcification or degenerative changes, except for one leaflet with slight deformation. In microscopic observation, endothelial cells lined the luminal surface of the conduit except for the areas adjacent to the valve. Conclusion: The graft worked perfectly as a right ventricular–pulmonary arterial valved conduit without anticoagulant therapy for a long time. J Thorac Cardiovasc Surg 1997;114:224-33

Extrinsic airway compression secondary to pulmonary arterial conduits: MR findings

Abnormal enlargement or malposition of any vascular structure or mass adjacent to the airway can cause extrinsic airway compression. In children with previous surgery for congenital heart disease, mass effect from prosthetic devices or alteration in the anatomic position of normal structures can lead to extrinsic airway compression. Because many children have complex medical problems after cardiac surgery, wheezing may be attributed to cardiac causes and airway compression may not be investigated. Furthermore, the distal airway compression seen in these children often is not visualized on chest radiographs. MR imaging can be useful in evaluating extrinsic airway compression in these patients. We present the MR imaging of two patients with symptomatic extrinsic airway compression secondary to pulmonary arterial conduits.

Cytosolic Ca2+ and adenylyl cyclase responses in phenotypically distinct pulmonary endothelial cells.

Pulmonary microvascular endothelium forms a tighter barrier than does pulmonary artery endothelium; the mechanism of this important phenotypic difference is uncertain. We examined two regulators of endothelial permeability, cytosolic Ca2+ concentration ([Ca2+]i) and adenosine 3',5'-cyclic monophosphate (cAMP), in microvascular (PMVEC) and pulmonary conduit artery (PAEC) endothelium. Both resting and stimulated [Ca2+]i were lower in PMVEC compared with PAEC (resting [Ca2+]i, 94 +/- 7 vs. 123 +/- 8 nM; ATP-stimulated peak, 1.04 +/- 0.14 vs. 1.98 +/- 0.13 microM). Sustained Ca2+ transients in response to either ATP or thapsigargin were reduced in PMVEC compared with PAEC (ATP, 199 +/- 22 vs. 411 +/- 43 nM; thapsigargin, 195 +/- 13 vs. 527 +/- 65 nM), suggesting reduced Ca2+ influx in PMVEC. Reduced Ca2+ influx in PMVEC was confirmed by Mn2+ quenching and patch-clamp experiments. mRNA for Ca(2+)-inhibitable and protein kinase C-stimulated adenylyl cyclases was detected in both cell types. Whereas ATP caused a [Ca2+]i-mediated decrease in cAMP in PAEC, ATP caused a protein kinase C-mediated increase in cAMP in PMVEC. We conclude that PMVEC express a unique phenotype that favors enhanced barrier function through attenuated Ca2+ influx and preservation of cAMP content.

A new experimental model for simultaneous evaluation of aortic and pulmonary allograft performance in a composite graft.

A model was developed in pigs for simultaneous evaluation of aortic and pulmonary allograft performance in a composite graft. The composite graft consisted of vascular prosthesis and aortic and pulmonary allografts. Following antibiotic preservation, it was anastomosed to the recipient's thoracic descending aorta by an extrapleural approach without using cardiopulmonary bypass. Aortic blood flow was completely diverted into the composite graft. All 12 recipient pigs recovered well, 4 of which were assigned for the initial study to design the suitable experimental schedule. Calcification readily occurred in the aortic allografts and aneurysmal dilatation without calcification developed in the pulmonary allografts. These morphological findings were consistent with those of previous reports. This model has several benefits. First, aortic and pulmonary allograft conduits can be implanted and evaluated simultaneously under the same conditions by making a composite graft. Second, the magnitude of the operation is minimum, and postoperative circulatory and respiratory management is uncomplicated. Third, wound infection rarely occurs, because the skin incision is made on the back. These preliminary studies suggest that this model will allow future study concerning aortic and pulmonary allograft conduits under different conditions.

Common arterial trunk and pulmonary atresia: close developmental cousins? Results from a teratogen induced animal model

To examine morphological similarities between "classically different" congenital heart lesion types induced in fetal rats by the cardiac teratogen N,N'-bis(dichloroacetyl)-1,8-octamethylenediamine (bis-diamine). A single 200 mg oral dose of bis-diamine was given to 50 pregnant rats on the 9th gestational day. Eleven controls were fed an inert vehicle. Experimental and control rats were sacrificed from 15.4 days to term and embryos delivered by caesarean section. Age-matched embryos were processed for histology and sectioned at 7 microns. Cardiac morphology was compared between normal and bis-diamine exposed groups. Hearts from control embryos were morphologically normal. Those from bis-diamine treated embryos exhibited common arterial trunk (32%), overriding aortic valve with valvar pulmonary stenosis (40%) or infundibular atresia (4%), or ventricular septal defect (24%). Development of the outlet septum was affected in all hearts and the arterial duct was absent in 72% of cases. Whilst most hearts demonstrated the anatomy expected for their lesion, some with a common arterial valve demonstrated a pulmonary blood supply similar to that in human cases of pulmonary atresia, where, in the absence of an arterial duct, an essential systemic to pulmonary conduit was provided by a "persistent fifth aortic arch artery". In one such case the proximal part of the aortopulmonary septum was identified above a common valve. The septum was deviated to the left and was not continuous throughout the length of the arterial trunk, causing atresia of the pulmonary component. Others had muscular infundibular atresia but with a pulmonary blood supply arising directly from the solitary trunk as seen in common arterial trunk "type III". Bis-diamine consistently affects development of those structures which partition the arterial segment of the developing heart at one or more levels, often coexistent with agenesis of the sixth aortic arch arteries. Whilst the aortopulmonary and outlet septums were absent in most cases of common arterial trunk, some morphological duality was shared by classically different lesion types in these rat hearts, which may suggest a common aetiology for common arterial trunk "type III" and aortic overriding with absence of the outlet septum and pulmonary atresia.

Size-Reduced Cryopreserved Pulmonary Valve Allograft for an RV-PA Conduit: Technical Modification and Functional Evaluation

Cryopreserved pulmonary allografts harvested from adults at the time of kidney donation were size reduced and used in two children with pulmonary atresia and ventricular septal defect. A technical modification for the creation of size-reduced pulmonary allograft conduits is described. Postoperative ultrasonic and cineangiographic assessments revealed excellent function of the pulmonary bicuspid valved conduit with a minimal pressure gradient and essentially no regurgitation. Although the long-term fate of cryopreserved bicuspid pulmonary valve and conduit is unknown, this conduit provides excellent handling characteristics that render allograft conduits preferable to synthetic conduits. In addition, the remodeled bicuspid pulmonary allograft conduits have exhibited excellent hemodynamic characteristics and are a reasonable alternative to other types of conduits when an appropriate size allograft is not available.

Right ventricular outflow reconstruction with cryopreserved homografts in pediatric patients: Intermediate-term follow-up with serial echocardiographic assessment

Objectives. This study was performed to assess by echocardiography the intermediate-term outcome of cryopreserved homografts employed in pulmonary outflow reconstruction in children and to validate the reliability of Doppler echocardiography in their evaluation.Background. Cryopreserved homografts have become the most widely used pulmonary conduits. Previous reports have shown the occurrence of homograft regurgitation in the immediate postoperative period and the propensity of regurgitation to progress. Although Doppler echocardiography has been useful in assessing extracardiac valved conduit stenosis, its reliability in assessing a large series of cryopreserved homografts has not been documented.Methods. Echocardiograms of 41 patients (43 homografts) who underwent operations between December 1986 and October 1992 were retrospectively reviewed. The median age of patients at operation was 37.5 months (range 3 to 333), and the median duration of follow-up was 28.5 months (range 1 to 68). Homograft regurgitation was classified on a scale of 0 to 4+. Pressure gradients across the homografts measured in 23 catheterizations were correlated with corresponding echocardiographic gradients.Results. Regurgitation: Homograft regurgitation occurred in 100% of patients at follow-up. Progression of severity >2 grades occurred during follow-up in 35% and was associated with operation before age 18 months (p < 0.002) and stenosis progression (p < 0.05) but not with homograft type (aortic or pulmonary). These data predict that 50% of patients operated on before 18 months of age will have severe regurgitation by 15 months postoperatively compared with only 15% operated on after 18 months. Stenosis: At follow-up, 51% of homografts had a stenotic gradient ≥25 mm Hg predominantly at the distal anastomosis, and stenosis progression was related to young age at operation (<18 months, p < 0.005) and small conduit size (p < 0.01). Fifty percent of conduits implanted before age 18 months could be predicted to stenose by 21.8 months compared with only 5% of those implanted after age 18 months. The gradient measured from Doppler echocardiography correlated well with the catheterization gradient (r = 0.86).Conclusions. Cryopreserved homograft dysfunction is frequent and progressive. Young age at operation (<18 months) predicts more rapid deterioration. Doppler echocardiography is reliable in assessing the systolic gradients across homografts. Serial echocardiographic assessment in the follow-up of these patients accurately characterizes these problems.

Effects of atrial natriuretic peptide and nitroprusside on isolated pulmonary resistance and conduit arteries from rats with pulmonary hypertension

1. The relaxant effects of atrial natriuretic peptide (ANP) and nitroprusside were studied on prostaglandin F2 alpha (PGF2 alpha)-contracted preparations of pulmonary resistance vessels (internal diameter 200-500 microns) and main pulmonary arteries taken from rats with pulmonary hypertension induced by monocrotaline (105 mg kg-1, s.c., 4 weeks previously). Control rats received saline. 2. In preparations from monocrotaline-treated rats, the potencies (negative log EC50) of ANP on resistance vessels (8.45) and main pulmonary arteries (8.25) were similar to those obtained in vessels from control rats (8.78 and 8.53 respectively), whereas those of nitroprusside were significantly less than in controls in both resistance vessels (7.13 compared with 7.63 in controls; three fold decrease in potency) and main pulmonary arteries (6.92 compared with 8.17 in controls; 18 fold decrease in potency). 3. On pulmonary resistance vessels from monocrotaline-treated rats, the maximum relaxant responses to ANP and nitroprusside, and also to pinacidil, were increased compared with controls, and reversal of the PGF2 alpha-induced contraction by these drugs was greater than 100%. In contrast, on main pulmonary arteries from monocrotaline-treated rats, the maximum relaxations to ANP and nitroprusside were not increased relative to controls, and reversal of PGF2 alpha was not greater than 100%. 4. Since the high potency of ANP on pulmonary resistance and conduit arteries is retained in vessels from rats with pulmonary hypertension, whether induced by monocrotaline (this study) or by chronic hypoxia (previous findings), it is postulated that elevation of plasma levels of ANP by use of drugs that inhibit the breakdown of this endogenous peptide, may be one approach to the pharmacological treatment of pulmonary hypertension.

Homograft conduit: the superior inexpensive alternative?

Twenty-seven aortic and pulmonary homograft conduits of varying sizes were sterilised in either antibiotics or 0.2% glutaraldehyde and prepared. These were used at six different centres, including ours, for the correction of predominantly complex congenital and some cases of acquired heart disease. Short term follow up indicates satisfactory functioning of the homografts without obstruction or gradients. The added advantage of low cost, better haemostasis and absence of the need of anticoagulant therapy makes them the preferred substitutes when compared with the commercially available synthetic conduits.

Almitrine mimics hypoxic vasoconstriction in isolated rat lungs.

The effect of almitrine bimesylate or the solvent malic acid on pulmonary vascular perfusion pressure was assessed in isolated rat lungs and on the contractile behavior of rat aorta and main pulmonary artery rings. Addition of almitrine to the lung perfusate during normoxia caused a dose-dependent, transient increase in pulmonary artery pressure with no change of the lung microvascular pressure. In systemic or pulmonary conduit arteries, the contractile tension was unaffected by almitrine. This indicates a precapillary locus of drug action. We also examined almitrine's effect on hypoxic pulmonary vasoconstriction (HPVC) in isolated lungs perfused with blood or with physiological salt solution (PSS). Low-dose almitrine potentiated hypoxic vasoconstriction in blood- but not in PSS-perfused lungs. However, a high dose of almitrine reduced hypoxic vasoconstriction dose dependently. When almitrine was added to the lung perfusate during hypoxia- or cyanide-induced (NaCN, 5 x 10(-5) M) pulmonary vasoconstriction, almitrine caused no further vasoconstriction. However, when the pulmonary perfusion pressure was elevated by KCl (20 mM) to the same magnitude as by alveolar hypoxia or cyanide, almitrine elicited a pressor response comparable to that observed during normoxia. Almitrine-induced pulmonary vasoconstriction resembled hypoxic vasoconstriction in that agents known to enhance hypoxic vasoconstriction (phorbol myristate acetate, vanadate, and 4-aminopyridine) enhanced, and known inhibitors of HPVC (the Ca2+ entry blocker nifedipine and hypothermia) inhibited, the almitrine-induced vasoconstriction. These findings lead us to speculate that almitrine also affects the oxygen-sensing limb of the hypoxic pressor response, not simply the effector (contractile apparatus of the vascular muscle cell).

Balloon expandable stent implantation in stenotic right heart valved conduits

Although valved conduits have been used successfully in severe forms of right ventricular-pulmonary artery discontinuity, progressive valved conduit stenosis is an important clinical problem. To determine the feasibility of reducing right heart valved conduit stenosis with a balloon expandable stent, a baboon model was used, in which the pulmonary artery was ligated and a right ventricular to pulmonary artery 14 mm bioprosthetic Dacron valved conduit implanted.In five baboons, at an average of 40 months after valved conduit implantation, fibrointimal stenosis at the valve site resulted in narrowing and a mean transconduit pressure gradient of 49 mm Hg (range 33 to 65). A tubular slotted steel stent (1.2 cm long) was deployed within the valved conduit after inflation of an 8 to 15 mm diameter balloon catheter that was introduced through the femoral vein. A stent was delivered to all valved conduits; however, in two baboons, balloon undersizing resulted in stent dislodgment. In the remaining three baboons, the transconduit gradient was reduced by 59% (49 to 20 mm Hg) and right ventricular systolic pressure decreased acutely by 35% (77 to 50 mm Hg).It is concluded that stent deployment is feasible in right ventricular to pulmonary artery stenotic valved conduits and may result in significant hemodynamic improvement. However, successful stent delivery is critically dependent on the proper selection of stent length and balloon diameter.

Pulmonary allograft conduit repair of tetralogy of Fallot: An alternative to transannular patch repair

Cryopreserved allograft valves and valved conduits have been used in 122 patients during the past 3 years for surgical repair of congenital heart disease. In 55 of these patients, the right ventricular outflow tract was reconstructed with a pulmonary allograft conduit. Although most children requiring a conduit had complex lesions, 12 patients with tetralogy of Fallot without pulmonary atresia or absent valve syndrome have been treated in this manner since April 1985. Patients were selected for conduit therapy because of congenital or iatrogenic pulmonary artery problems (nine patients had 12 prior shunts) or increased pulmonary vascular resistance. Ages ranged from 7 months to 6 years (mean 3.1 years) and weights from 7.4 to 18.5 kg (mean 12.2 kg). Pulmonary artery conduit size ranged from 16 to 24 mm internal diameter (mean 22 mm). Distal pulmonary artery reconstruction beyond the bifurcation was required in nine patients and the proximal connection was completed with a hood-shaped patch. One operative death (8.3%) occurred at 20 days as a result of severe right ventricular dysfunction. Left pulmonary artery thrombosis was discovered postmortem. Eleven survivors observed for 3 to 37 months (mean 17 months) are without cardiac symptoms. A chronologically overlapping group of tetralogy of Fallot repairs accomplished with a transannular patch was also reviewed. Twenty-five patients aged 2 months to 4 years (mean 1.7 years) and weighing 3.6 to 14.8 kg (mean 9.2 kg) underwent this procedure from April 1983 to January 1987 (seven patients had one prior shunt each). The mortality rate in this group was 28% (six operative deaths and one late death). Of 18 survivors observed from 20 to 60 months (mean 41.4 months), five (28%) have required pulmonary artery conduit reconstruction for chronic right ventricular failure. Postrepair right ventricular/left ventricular pressure ratios were available in 19 patients, including five of seven who died and three of five who required reoperation. The ratios averaged 0.54, which indicates adequate relief of obstruction. The operative mortality rate from a number of series for transannular patch repair of tetralogy of Fallot averages 16%, ranging from 3% to 63%. However, when distal pulmonary artery problems are added as a risk factor this rate rises to 21%, and valved conduit insertion increases the mortality rate (Kirklin and Barratt-Boyes, 1986). Although not clearly superior, pulmonary artery conduit repair of tetralogy of Fallot achieves results comparable with those of transannular patch repair and is recommended as an alternative, particularly when distal pulmonary artery anatomy is abnormal or vascular resistance is elevated.

Caveats of balloon dilation of conduits and conduit valves

The results and complications of percutaneous balloon dilation involving 10 patients with a stenotic right ventricle to pulmonary artery prosthetic conduit and 1 patient with an obstructed right atrium to left pulmonary artery Dacron graft (modified Fontan) are reported. For the 10 patients (14.5 ± 5 years) with a right ventricle to pulmonary artery conduit, the mean (±SD) predilation conduit valve gradient was 57 ± 22 mm Hg, right ventricular pressure 104 ± 21 mm Hg and right ventricle to pulmonary artery gradient 75 ± 23 mm Hg; 2 of the patients had additional pulmonary artery stenosis requiring dilation. In one patient, the balloon could not be advanced across the conduit valve.In 9 of 10 patients in whom dilation was successfully performed, the conduit valve gradient decreased by 59 ± 13%, right ventricle to pulmonary artery gradient by 43 ± 22% and right ventricular pressure by 31 ± 11%. After dilation, right ventricular pressure was <65% of systemic pressure in seven patients, although no pressure was <40%. In 8 of the 11 patients, surgery was avoided or postponed. Complications included loss of a balloon fragment after rupture during the unsuccessful dilation of the right atrium to left pulmonary artery graft and circumferential balloon rupture requiring catheter retrieval of the distal portion of the balloon from the femoral vein after successful dilation of the right ventricle to pulmonary artery conduit.Conduit valve dilation by balloon can reduce but rarely eliminate conduit obstruction, and balloon rupture may occur and can result in fragment loss or embolization.

Doppler evaluation of homograft valved conduits in children

To assess the flow characteristics of homograft valved conduits in the immediate postoperative period, 69 children with 71 homograft conduits underwent 2-dimensional and Doppler echocardiographic examination at 1 to 40 days (mean 8) after surgery. Of the 71 conduits studied, 19 were aortic and 52 were pulmonary homograft valved conduits. Two aortic homograft valved conduits were inserted in the aortic position, whereas all remaining homografts were placed in the pulmonary position. On the immediate postoperative echocardiogram, 25 (35%) of the conduit valves had no regurgitation and 44 (62%) had 1+ (mild) regurgitation. Two pulmonary valved conduits (3%) in the pulmonary position had 2+ (moderate) regurgitation and right ventricular dimensions >95% for body surface area. The peak velocity across the homograft valve was normal (<1.3 m/s) in 58 valves (82%). In the remaining 13 valves, peak velocity ranged from 1.4 to 2.6 m/s. No homograft valve had a peak velocity >2.6 m/s in the immediate postoperative period. To assess the fate of homograft valved conduits in the intermediate-term follow-up period, 38 children with 38 conduits had a repeat echocardiogram at 6 to 25 months (mean 15 ± 6) after surgery. Of the 38 conduits examined, 10 (26%) had no regurgitation, 25 (66%) had 1+ regurgitation and 3 (8%) had 2+ regurgitation. Progression of the amount of regurgitation occurred in 11 (29%) patients. At the follow-up examination, peak velocity was ≤1.4 m/s across 34 conduit valves, between 1.4 and 2.6 m/s across 3 valves and >2.6 m/s across 1 valve. This latter patient had a 3.2-m/s jet across the proximal insertion of the conduit and no further increase across the valve itself. Thus, no patient had evidence of conduit valve stenosis. Of the 38 patients, 9 had Doppler evidence of obstruction at the conduit insertion (8 at the distal end and 1 with the aforementioned proximal obstruction). Most obstructions were of mild to moderate severity and only 2 patients (5%) had severe conduit stenosis. Thus, in the immediate postoperative period, normally functioning homograft valved conduits frequently have mild regurgitation (62%) and rarely have moderate or severe regurgitation (3%), with peak velocities reaching <2.6 m/s. In the inpatients, 9 had Doppler evidence of obstruction at the conduit insertion (8 at the distal end and 1 with the aforementioned proximal obstruction). Most obstructions were of mild to moderate severity and only 2 patients (5%) had severe conduit stenosis. Thus, in the immediate postoperative period, normally functioning homograft valved conduits frequently have mild regurgitation (62%) and rarely have moderate or severe regurgitation (3%), with peak velocities reaching <2.6 m/s. In the intermediate follow-up period, homograft valved conduits may develop an additional degree of regurgitation (29%), frequently continue to have conduit peak velocities <2.6 m/s (97%) and uncommonly develop hemodynamically significant obstruction, usually at the ends of the conduit (5%).

Persistent 5th aortic arch — a great pretender: three new covert cases

Although persistence of the embryonic fifth aortic arch is considered a rare congenital malformation, analysis of the records of the cardiopathological collections of the Brompton and Killingbeck Hospitals reveals 6 examples in approximately 2000 specimens, an incidence amongst our material of 1 in 330. Since our review of the literature reveals only a further 13 described cases, we wonder if the condition may go unrecognized rather than being exceedingly rare. This possibility is further supported by the fact that 3 of our cases were incorrectly interpreted when initially described. In this report, we describe the details of 2 of these specimens and one other case that was not included in our earlier descriptions of this malformation. The first case had the persistent fifth arch as a conduit between the pulmonary and systemic circulations in the setting of aortic atresia with interruption of the aortic arch. The second case demonstrated a double lumen aortic arch, the fifth arch in this instance being an accessory systemic-to-systemic conduit. In the final case, the persistent arch was initially considered to represent an aorto-pulmonary window but review revealed an aortic to pulmonary conduit more in keeping with the presence of a fifth arch. We conclude that the powers of mimicry of this enigmatic structure may account for its apparent rarity.

Size and site-dependent heterogeneity of human vascular responses in vitro.

Ring segments of splanchnic, peripheral, coronary, pulmonary and uterine conduit arteries obtained during surgery were studied in tissue baths. Resistance arteries dissected from various sites were studied in a myograph. Both conduit and resistance vessels contracted in response to the alpha 1-agonist phenylephrine (10(-7) to 10(-4) mol/l), an effect that was antagonized by the alpha 1-antagonist doxazosin (10(-8) to 10(-6) mol/l). However, the alpha 2-agonists BHT 933 (10(-7) to 10(-4) mol/l) and UK 14304 (10(-7) to 10(-4) mol/l) only contracted the resistance vessels and not the conduit arteries. The response to BHT 933 was competitively antagonized by the alpha 2-antagonist yohimbine (3.10(-8) to 3.10(-7) mol/l) and the magnitude of the contractile response was inversely related to vessel size. Similarly, neuropeptide Y (10(-9) to 10(-6) mol/l) contracted only the resistance vessels, and induced marked tachyphylaxis. Atrial natriuretic peptide (ANP; 10(-8) to 10(-6) mol/l) produced concentration-dependent relaxation in all conduit arteries studied, being ineffective in resistance arteries from subcutaneous or omental sites, but relaxed those from renal tissue and skeletal muscle. Calcitonin gene-related peptide (10(-8) to 10(-6) mol/l) and vasoactive intestinal peptide (10(-9) to 10(-6) mol/l) relaxed both conduit and resistance arteries. This response was dependent on the integrity of the endothelium in the systemic conduit but not the resistance vessels. These results indicate that the receptors for adrenergic agonists and vasoactive peptides are varyingly distributed throughout the human vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Surgical Management of Patients with Interrupted Aortic Arch and Severe Subaortic Stenosis

Ten patients underwent palliative surgery for interrupted aortic arch and severe subaortic obstruction due to posterior displacement of the conal septum. Their ages ranged between 4 and 28 days (mean, 11.0 ± 7.7 days) and their weights, between 2.1 and 4.2 kg (mean, 2.85 ± 0.6 kg). Preoperative echocardiography and cardiac catheterization were performed on all patients. The ratios of the left ventricular outflow tract diameters and the ascending aortic diameters to the descending aortic diameters were 0.56 ± 0.03 and 0.56 ± 0.06, respectively, compared with 0.81 ± 0.12 and 0.95 ± 0.17, respectively, in 20 patients with interrupted aortic arch but without obstruction ( p < 0.001). Four of the 10 patients underwent pulmonary artery banding and insertion of a bypass graft between the ascending and the descending aorta. All 4 died of low cardiac output soon after operation (100% operative mortality). The remaining 6 patients underwent banding and insertion of a graft between the main pulmonary artery proximal to the band, and the descending aorta. All of these patients survived, and all except 1 are doing well 3 months to 4 years postoperatively. The use of a pulmonary artery-descending aorta conduit and of distal pulmonary artery banding provides good palliation for patients with interrupted aortic arch and major subaortic stenosis.