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Biomedical subjects

A M Moran

Publications and source records attributed to A M Moran.

At least 19 recordsLinked to original sources
PubMed2005

Vascular endothelial growth factor delays onset of failure in pressure-overload hypertrophy through matrix metalloproteinase activation and angiogenesis.

OBJECTIVE: Pressure-overload hypertrophy is associated with decreased capillary density in myocardium resulting in impaired substrate delivery. Treatment of hypertrophied hearts with vascular endothelial growth factor (VEGF) induces angiogenesis. Since angiogenesis is associated with extracellular matrix degradation, we sought to determine whether VEGF induced angiogenesis in hypertrophy required matrix metalloproteinases (MMP) activation. METHODS: Newborn rabbits underwent aortic banding. Progression of hypertrophy (mass-to-volume (M/V) ratio) and mid-wall contractility index was monitored by echocardiography. At 4 and 6 weeks, VEGF (2 microg/kg), vehicle or VEGF combined with GM6001 (5 mg/kg), a MMP inhibitor, was administered intrapericardially. CD-31 (indicator of angiogenesis), MMP-2, MT1-MMP and TIMPs (endogenous MMP inhibitors) expression were measured by immunoblotting. MMP-2 activity was determined by gelatin zymography. RESULTS: Untreated hypertrophied hearts progressed to ventricular dilatation at 7 wks (M/V ratio: 0.75 +/- 0.07), but compensatory hypertrophy was maintained with VEGF (0.91 +/- 0.07; p < 0.05). LV contractility declined in untreated hearts from -0.41 +/- 0.9 (5 wks) to -0.73 +/- 0.5 (7 wks; p < 0.05) but remained normal with VEGF (+1.61 +/- 0.6 vs. +0.47 +/- 0.2). MMP-2 expression and activity were significantly elevated in VEGF treated hypertrophied hearts (p < 0.05) and were blocked by concomitant administration of GM6001. VEGF induced neovascularization was inhibited by addition of GM6001. MT1-MMP showed a trend to higher levels in VEGF treated hearts. TIMPs were unchanged in all three groups. CONCLUSIONS: Exogenous VEGF and resultant MMP-2 activation leads to increased capillary formation in severe hypertrophy, preventing progression to ventricular dilation and dysfunction. VEGF and the associated MMP-2 activation play an important and potentially therapeutic role in vascular remodeling of hypertrophied hearts.

Angiogenesis Inducing Agents↗
PubMed2005

Epidemiology of cystic fibrosis-related diabetes.

OBJECTIVES: Cystic fibrosis-related diabetes (CFRD) has emerged as an important complication of CF. To better understand who is at risk of developing CFRD, to gain insight into the impact of CFRD on pulmonary and nutritional status, and to assess the association of CFRD with various practice patterns and comorbid conditions, we characterized the Epidemiologic Study of Cystic Fibrosis (ESCF) patient population. STUDY DESIGN: Analyses were performed on the 8247 adolescents and adults who were evaluated at one of 204 participating sites during 1998. CFRD was defined as the use of insulin or an oral hypoglycemic agent at any time during the year. RESULTS: Previously reported risk factors for CFRD including age, gender (female), and pancreatic insufficiency were confirmed in this study. Patients with CFRD had more severe pulmonary disease, more frequent pulmonary exacerbations, and poorer nutritional status as compared with those without diabetes. CFRD also was associated with liver disease. CONCLUSIONS: CFRD is a common complication in adolescents and adults that is associated with more severe disease.

Adolescent↗
PubMed2003

Haemophilus segnis: a rare cause of endocarditis.

This report presents a case of endocarditis due to Haemophilus segnis, which represents a speciation difficulty for the routine laboratory. In this study, a molecular approach provided speciation, which was confirmed phenotypically by a reference laboratory. The use of molecular genotypic analysis is an additional strategy in the investigation of endocarditis. It has applications not only in isolate identification but also in primary detection of infection, particularly in patients whose blood is culture negative by conventional methodologies.

Base Sequence↗
PubMed2001

Inhibition of tumor necrosis factor-alpha improves postischemic recovery of hypertrophied hearts.

BACKGROUND: Tumor necrosis factor (TNF)-alpha has been implicated in the pathogenesis of heart failure and ischemia-reperfusion injury. Effects of TNF-alpha are initiated by membrane receptors coupled to sphingomyelinase signaling and include altered metabolism and calcium cycling, contractile dysfunction, and cell death. We postulate that pressure-overload hypertrophy results in increased myocardial TNF-alpha expression and that it contributes to decreased contractility in hypertrophied infant hearts subjected to ischemia-reperfusion. METHODS AND RESULTS: Neonatal rabbits underwent aortic banding to induce LV hypertrophy. Myocardial TNF-alpha protein expression increased progressively with LV hypertrophy. Serum TNF-alpha was detected only after the onset of heart failure. Before onset of ventricular dilatation and heart failure (determined by serial echocardiograms), hearts from aortic banded and age-matched control rabbits were perfused in the Langendorff mode and subjected to 45 minutes of ischemia and 30 minutes of reperfusion. Postischemic recovery was impaired in hypertrophied hearts, but addition of neutralizing anti-rabbit TNF-alpha antibody to cardioplegia and perfusate solutions restored postischemic function. This effect was mimicked by treatment with the ceramidase inhibitor N-oleoyl ethanolamine. TNF-alpha inhibition also was associated with faster postischemic recovery of phosphocreatine, ATP, and pH as assessed by (31)P nuclear magnetic resonance spectroscopy. Intracellular calcium handling, measured by Rhod 2 spectrofluorometry, demonstrated lower diastolic calcium levels and higher systolic calcium transients in anti-TNF-alpha treated hearts. CONCLUSIONS: TNF-alpha is expressed in myocardium during compensated pressure-overload hypertrophy and contributes to postischemic myocardial dysfunction. Inhibition of TNF-alpha signaling significantly improves postischemic contractile function, myocardial energetics, and intracellular calcium handling.

Adenosine Triphosphate↗
PubMed2001

Surgical outcome of double-outlet right ventricle with subpulmonary VSD.

BACKGROUND: Optimal management of double-outlet right ventricle with subpulmonary ventricular septal defect remains controversial. We reviewed our 7-year experience with patients who had this anatomic configuration. METHODS: Between January 1992 and January 1999, 20 patients underwent an arterial switch operation (ASO group), and 12 underwent a bidirectional Glenn procedure followed by a modified Fontan in 10 (Glenn/Fontan). Mean follow-up was 23 +/- 18 months. RESULTS: An initial palliative operation was done in 19 patients (9 in the ASO group, 10 in the Glenn/Fontan group). There were no deaths in the Glenn/Fontan group. Four patients in the ASO group died within 33 days postoperatively. Two of them had a single coronary artery, 1 had a straddling mitral valve, 1 had a hypoplastic aortic arch, and 1 had multiple ventricular septal defects. Three patients had reoperation for subaortic stenosis (n = 2) or pulmonary stenosis (n = 1) after the ASO. Four patients (3 in the ASO group, 1 in the Glenn/Fontan) required a pacemaker for postoperative complete atrioventricular block. Actuarial survival at 5 years for the entire group was 87% (70% confidence interval, 81% to 93%). CONCLUSIONS: The ASO remains our preferred treatment for infants with double-outlet right ventricle and subpulmonary ventricular septal defect. However, associated anatomic defects are important risk factors.

Child, Preschool↗
PubMed2001

Congenital supravalvar aortic stenosis: a simple lesion?

The underlying cause of congenital supravalvular aortic stenosis (SVAS) has recently been identified as a loss-of function mutation of the elastin gene on chromosome 7q11.23, resulting in an obstructive arteriopathy of varying severity, which is most prominent at the aortic sinutubular junction. The generalized nature of the disease explains the frequent association with stenoses of systemic and pulmonary arteries. Furthermore, localization of the supravalvular stenosis at the level of the commissures of the aortic valve has important implications for both aortic valve function and coronary circulation. This review summarizes the recent advances with regard to the pathogenesis of SVAS and describes the multitude of clinically relevant pathologic features other that the mere 'supra-aortic' narrowing that have important implications for surgical therapy.

Aorta↗
PubMed2001

Functional small-diameter neovessels created using endothelial progenitor cells expanded ex vivo.

Arterial conduits are increasingly preferred for surgical bypass because of inherent functional properties conferred by arterial endothelial cells, especially nitric oxide production in response to physiologic stimuli. Here we tested whether endothelial progenitor cells (EPCs) can replace arterial endothelial cells and promote patency in tissue-engineered small-diameter blood vessels (4 mm). We isolated EPCs from peripheral blood of sheep, expanded them ex vivo and then seeded them on decellularized porcine iliac vessels. EPC-seeded grafts remained patent for 130 days as a carotid interposition graft in sheep, whereas non-seeded grafts occluded within 15 days. The EPC-explanted grafts exhibited contractile activity and nitric-oxide-mediated vascular relaxation that were similar to native carotid arteries. These results indicate that EPCs can function similarly to arterial endothelial cells and thereby confer longer vascular-graft survival. Due to their unique properties, EPCs might have other general applications for tissue-engineered structures and in treating vascular diseases.

Animals↗
PubMed2001

Long-term results of the lateral tunnel Fontan operation.

OBJECTIVES: Completion of a total cavopulmonary anastomosis with an intra-atrial lateral tunnel is known to yield good early and midterm results. In this study, we sought to determine the long-term outcome (10 years) after a lateral tunnel Fontan procedure. METHODS: Between October 1987 and December 1991, 220 patients (aged 11 months to 32 years) with a wide range of underlying diagnoses underwent a fenestrated or nonfenestrated lateral tunnel Fontan procedure at our institution. Current follow-up information was available for 196 patients (94%, mean follow-up = 10.2 +/- 0.6 years). Risk factor analysis included patient-related and procedure-related variables, with death, failure, and bradyarrhythmia or tachyarrhythmia as outcome parameters. RESULTS: There were 12 early deaths (<30 days or hospital death), 7 late deaths, 4 successful takedown operations, and 4 heart transplantations. Kaplan-Meier estimated survival was 93% at 5 years and 91% at 10 years, and freedom from failure was 90% at 5 years and 87% at 10 years. Freedom from new supraventricular tachyarrhythmia was 96% at 5 years and 91% at 10 years; freedom from new bradyarrhythmia was 88% at 5 years and 79% at 10 years. Three patients had evidence of protein-losing enteropathy. Multivariable risk factors for development of supraventricular tachyarrhythmia included heterotaxy syndrome, atrioventricular valve abnormalities, and preoperative bradyarrhythmia. Risk factors for bradyarrhythmia included systemic venous anomalies. The sole risk factor for late failure was a previous coarctation repair. CONCLUSION: The lateral tunnel Fontan procedure results in excellent long-term outcome even when used in patients with diverse anatomic diagnoses. The incidence of atrial tachyarrhythmia is low and mainly depends on the underlying cardiac morphology and preoperative arrhythmia. The good long-term outcome after an intracardiac lateral tunnel Fontan procedure should serve as a basis for comparison with other surgical alternatives.

Adolescent↗
PubMed2001

Valve-sparing operation for balloon-induced aortic regurgitation in congenital aortic stenosis.

OBJECTIVE: Aortic regurgitation after balloon dilation of congenital aortic stenosis may be treated with valve repair as an alternative to replacement. METHODS: Charts and echocardiograms of all patients undergoing aortic valve operations after balloon dilation of congenital aortic stenosis at our institution between January 1988 and December 1999 were reviewed. RESULTS: Twenty-one patients underwent valvuloplasty for predominant aortic regurgitation 9 months to 15 years (mean, 6.1 years) after balloon dilation. The mean +/- SD age at the time of the operation was 11 +/- 7 years. Aortic regurgitation was caused by a combination of commissural avulsion (10), cusp dehiscence with retraction (9), cusp tear (5), central incompetence (2), perforated cusp (1), or cusp adhesion to the aortic wall (1). Repair techniques included commissural reconstruction with a pericardial patch (8), pericardial patch cusp augmentation (6), primary suture repair (6), raphae release and debridement (4), commissurotomy (4), commissural resuspension with sutures (3), and cusp release (1). There were no deaths. At a mean follow-up of 30.1 months (range, 9 months-8 years), all patients were asymptomatic, and the grade of aortic regurgitation had been significantly reduced (P <.001). Left ventricular end-diastolic dimension z scores and proximal regurgitant jet/aortic anulus diameter ratios were significantly reduced (P <.001) and remained so over time. Freedom from reoperation for late failure was 100%, and overall freedom from reintervention was 80% at 3 years. CONCLUSION: Aortic valve repair for balloon-induced aortic regurgitation is reproducible and durable at medium-term follow-up.

Adolescent↗
PubMed2000

Surgical management of mitral regurgitation after repair of endocardial cushion defects: early and midterm results.

BACKGROUND: Mitral regurgitation (MR) represents the principal indication for reoperation in patients after repair of atrioventricular septal defects (AVSD). Reports of mitral valvuloplasty (MVP) in such patients are few; the alternative, mitral valve replacement (MVR), necessitates commitment to future valve replacement and long-term anticoagulation. We sought to determine the outcome of those patients who underwent either MVP or MVR between January 1, 1988, and December 31, 1998, for significant MR after repair of AVSD. Furthermore, we sought to identify (a) morphological predictors necessitating MVR, and (b) predictors of future reoperation within the MVP group. METHODS AND RESULTS: Retrospective review of clinical, operative, and echocardiographic data were performed. There were 46 patients identified (37 MVP and 9 MVR). The median age at initial AVSD repair was 0.6 years, and the age at subsequent mitral valve operation was 2.8 years. The early postoperative mortality rate was 2.2%, and survival at 1 and 10 years was 89.9% and 86.6%, respectively. A high rate of complete heart block was noted within the MVR group (37.5%). Freedom from later mitral valve reoperation for both groups was similar. No significant morphological predictors necessitating MVR were found. Predictors of reoperation within the MVP group included the presence of moderate or worse MR in the early postoperative period. In both groups New York Heart Association class, degree of MR, growth, and ventricular volumes improved. CONCLUSIONS: Mitral valve surgery significantly improves clinical status, with a sustained improvement in ventricular chamber size. MR can be successfully managed in patients after repair of AVSD independent of morphological type. Overall survival is acceptable, and further reoperation within the MVP group is influenced by early outcome of repair.

Analysis of Variance↗
PubMed2000

Early in vivo experience with tissue-engineered trileaflet heart valves.

BACKGROUND: Tissue engineering is a new approach in which techniques are being developed to transplant autologous cells onto biodegradable scaffolds to ultimately form new functional autologous tissue. Workers at our laboratory have focused on tissue engineering of heart valves. The present study was designed to evaluate the implantation of a whole trileaflet tissue-engineered heart valve in the pulmonary position in a lamb model. METHODS AND RESULTS: We constructed a biodegradable and biocompatible trileaflet heart valve scaffold that was fabricated from a porous polyhydroxyalkanoate (pore size 180 to 240 microm; Tepha Inc). Vascular cells were harvested from ovine carotid arteries, expanded in vitro, and seeded onto our heart valve scaffold. With the use of cardiopulmonary bypass, the native pulmonary leaflets were resected, and 2-cm segments of pulmonary artery were replaced by autologous cell-seeded heart valve constructs (n=4). One animal received an acellular valved conduit. No animal received any anticoagulation therapy. Animals were killed at 1, 5, 13, and 17 weeks. Explanted valves were examined histologically with scanning electron microscopy, biochemically, and biomechanically. All animals survived the procedure. The valves showed minimal regurgitation, and valve gradients were <20 mm Hg on echocardiography. The maximum gradient was 10 mm Hg with direct pressures. Macroscopically, the tissue-engineered constructs were covered with tissue, and there was no thrombus formation on any of the specimens. Scanning electron microscopy showed smooth flow surfaces during the follow-up period. Histological examination demonstrated laminated fibrous tissue with predominant glycosaminoglycans as extracellular matrix. 4-Hydroxyproline assays demonstrated an increase in collagen content as a percentage of native pulmonary artery (1 week 45.8%, 17 weeks 116%). DNA assays showed a comparable number of cells in all explanted samples. There was no tissue formation in the acellular control. CONCLUSIONS: Tissue-engineered heart valve scaffolds fabricated from polyhydroxyalkanoates can be used for implantation in the pulmonary position with an appropriate function for 120 days in lambs.

Absorbable Implants↗
PubMed2000

Functional living trileaflet heart valves grown in vitro.

BACKGROUND: Previous tissue engineering approaches to create heart valves have been limited by the structural immaturity and mechanical properties of the valve constructs. This study used an in vitro pulse duplicator system to provide a biomimetic environment during tissue formation to yield more mature implantable heart valves derived from autologous tissue. METHODS AND RESULTS: Trileaflet heart valves were fabricated from novel bioabsorbable polymers and sequentially seeded with autologous ovine myofibroblasts and endothelial cells. The constructs were grown for 14 days in a pulse duplicator in vitro system under gradually increasing flow and pressure conditions. By use of cardiopulmonary bypass, the native pulmonary leaflets were resected, and the valve constructs were implanted into 6 lambs (weight 19+/-2.8 kg). All animals had uneventful postoperative courses, and the valves were explanted at 1 day and at 4, 6, 8, 16, and 20 weeks. Echocardiography demonstrated mobile functioning leaflets without stenosis, thrombus, or aneurysm up to 20 weeks. Histology (16 and 20 weeks) showed uniform layered cuspal tissue with endothelium. Environmental scanning electron microscopy revealed a confluent smooth valvular surface. Mechanical properties were comparable to those of native tissue at 20 weeks. Complete degradation of the polymers occurred by 8 weeks. Extracellular matrix content (collagen, glycosaminoglycans, and elastin) and DNA content increased to levels of native tissue and higher at 20 weeks. CONCLUSIONS: This study demonstrates in vitro generation of implantable complete living heart valves based on a biomimetic flow culture system. These autologous tissue-engineered valves functioned up to 5 months and resembled normal heart valves in microstructure, mechanical properties, and extracellular matrix formation.

Absorbable Implants↗
PubMed2000

Non-invasive assessment of rejection in pediatric transplant patients: serologic and echocardiographic prediction of biopsy-proven myocardial rejection.

BACKGROUND: Cardiac allograft rejection is a multifocal immune process that is currently assessed using biopsy-guided histologic classification systems (International Society for Heart and Lung Transplantation). Cardiac troponin T and I are established serologic markers of global myocyte damage. The use of load-independent measures of contractility have also been shown to accurately assess the presence of ventricular dysfunction. Little is known about their utility in accurately predicting rejection in the pediatric age group. We undertook the present study to compare rejection grade with echocardiographic and serologic estimates of transplant rejection-related myocardial damage. METHODS: We compared histologic rejection grades (0 to 4) with patient characteristics, echocardiographic measurements, catheterization measurements, and biochemical markers for 86 evaluations in 37 transplant recipients at Children's Hospital. RESULTS: In univariate analyses, biopsy scores correlated (p < 0.05) inversely with left ventricular systolic function (shortening fraction) and contractility (stress velocity index, SVI), and directly with mitral E-wave amplitude. In multivariate analyses, lower contractility and higher mitral E-wave amplitude remained significantly (p < or = 0.01) associated with rejection (SVI, p = 0.002, odds ratio = 0.393; E wave, p = 0.0002, odds ratio = 228). Most rejection episodes were associated with elevation of biochemical markers of myocardial injury. Although troponin I was weakly associated with differences between rejection grades (p = 0.034), troponin T, creatine kinase-MB fraction, and C-reactive protein did not differ with biopsy-rejection scores. Serum markers had a poor predictive capacity for biopsy-detected rejection. Troponin T and I did correlate with increased left ventricular wall thickness and mass. CONCLUSION: Progressively depressed left ventricular contractility and diastolic function are found with worsening pediatric heart transplant rejection-biopsy score; however, sensitive and specific serum markers do not correspond to the degree of active myocardial injury. The use of echocardiographic measures of contractility is associated with a specificity of 91.8% but low sensitivity of 66.7%. Overall we found poor concordance between serum markers and grade of rejection. It is unclear whether myocardial injury as assessed by serum markers, echocardiography, or histologic scoring is more important for assessment of acute rejection or long-term outcome, but it does not appear that serum and tissue markers of rejection can be used interchangeably.

Adolescent↗
PubMed2000

Abnormal myocardial mechanics in Kawasaki disease: rapid response to gamma-globulin.

BACKGROUND: The time course and rate of recovery of myocardial dysfunction in association with Kawasaki disease in response to intravenous gamma-globulin is unknown and may provide mechanistic clues. METHODS AND RESULTS: The acute changes in myocardial contractility in 25 patients with Kawasaki disease were evaluated by noninvasive stress-shortening and stress-velocity analysis. Echocardiograms were performed before and then daily for 4 days during which the patients received gamma-globulin 1.6 to 2 g/kg. Before treatment, contractility was abnormally low (<2 SD) in 14 patients (56%). Contractility increased significantly (2 SD increase) in 17 (68%), including 13 of 14 with depressed contractility and 4 whose initial contractility fell within normal limits. Of the 14 patients with depressed contractility, 8 (57%) normalized within 24 hours and a further 5 (35.7%) normalized within 6 months. A clinical response to treatment (fall in C-reactive protein by 50% and/or resolution of fever within 4 days) was seen in 22 patients (88%). Contractility increased in 17 of the 22 clinical responders and was normal before therapy in the other 5. The 3 patients who did not respond clinically also had no change in contractility with gamma-globulin therapy. Long-term (more than 12 months) follow-up was available in 19 patients. All patients had normal contractility at late follow-up. CONCLUSIONS: More than half the patients with Kawasaki disease have abnormal contractility at presentation. Myocardial response to gamma-globulin therapy is associated with rapid improvement in myocardial mechanics, with a high concordance between the clinical and myocardial response to therapy. The speed of recovery suggests that depressed contractility in patients with Kawasaki disease is caused by a rapidly reversible process such as circulating toxins or activated cytokines. Long-term outcome is good even in those patients with slow recovery of myocardial function.

Child, Preschool↗
PubMed2000

Surgery for bilateral outflow tract obstruction in elastin arteriopathy.

OBJECTIVE: A number of patients with Williams syndrome or other forms of elastin arteriopathy have stenoses of pulmonary arteries in addition to supravalvular aortic stenosis. We sought to investigate the effect of the degree of pulmonary arterial stenosis on the prognosis after an operation for supravalvular aortic stenosis to help define the optimal treatment strategy for patients with severe forms of elastin arteriopathy. METHODS: Between 1960 and 1999, 33 patients underwent operations for supravalvular aortic stenosis while having significant stenoses of the pulmonary arteries. We retrospectively reviewed patient charts, obtained current follow-up information, and determined risk factors for survival and reoperation. RESULTS: Fifteen patients with moderate right-sided obstructions (confirmed by pulmonary artery Z-scores and right ventricular/descending aortic pressure ratio) underwent operations for supravalvular aortic stenosis only. Eighteen patients had more severe right-sided obstructions and underwent surgical relief of pulmonary arterial stenoses or right ventricular outflow tract obstruction in addition to operations for supravalvular aortic stenosis. Eight patients had undergone preoperative balloon dilations of stenotic pulmonary arteries. There were 6 early deaths and 1 late death in our series. Survival at 10 and 20 years was 76% (70% confidence interval, 68%-84%) and freedom from reintervention was 59% (70% confidence interval, 46%-71%) at 10 years and 49% (70% confidence interval, 35%-62%) at 20 years. Multivariate analysis revealed that patients with a right ventricular/descending aortic pressure ratio of 1.0 or more were at higher risk for reintervention but not for death. CONCLUSIONS: Surgical treatment of pulmonary artery obstructions in elastin arteriopathy is palliative but, in conjunction with balloon dilation of peripheral pulmonary arteries, offers good long-term survival to patients with the severest form of elastin arteriopathy.

Adolescent↗
PubMed2000

Patch augmentation of the pulmonary artery with bioabsorbable polymers and autologous cell seeding.

OBJECTIVE: In recent years bioabsorbable synthetic or biologic materials have been used to augment the pulmonary artery or the right ventricular outflow tract. However, each of these polymers has one or more shortcomings. None of these patch materials has been seeded with cells. Thus, we have tested a fast-absorbing biopolymer, poly-4-hydroxybutyric acid, with autologous cell seeding for patch augmentation of the pulmonary artery in a juvenile sheep model. METHODS: Vascular cells were isolated from ovine peripheral veins (n = 6). Bioabsorbable porous poly-4-hydroxybutyric acid patches (porosity > 95%) were seeded on 3 consecutive days with a mixed vascular cell suspension (21.3 +/- 1.3 x 10(6) cells). Forty-five (+/- 2) days after the vessel harvest, 1 unseeded and 6 autologously seeded control patches were implanted into the proximal pulmonary artery. The animals received no postoperative anticoagulation. Follow-up was performed with echocardiography after 1 week and before explantation after 1, 7, and 24 weeks (2 animals each) for the seeded control patches and after 20 weeks for the nonseeded control patch. RESULTS: All animals survived the procedure. Postoperative echocardiography of the seeded patches demonstrated a smooth surface without dilatation or stenosis. Macroscopic appearance showed a smooth internal surface with increasing tissue formation. Histology at 169 days demonstrated a near-complete resorption of the polymer and formation of organized and functional tissue. Biochemical assays revealed increasing cellular and extracellular matrix contents. The control patch showed a slight bulging, indicating a beginning dilatation. CONCLUSION: This experiment showed that poly-4-hydroxybutyric acid is a feasible patch material in the pulmonary circulation.

Absorbable Implants↗