| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Thorac Cardiovasc Surg 1996;112:672-680
© 1996 Mosby, Inc.
SURGERY FOR CONGENITAL HEART DISEASE |
Received for publication Oct. 24, 1995 Revisions requested Jan. 5, 1996; revisions received Jan. 29, 1996 Accepted for publication Feb. 2, 1996. Address for reprints: Robert H. Feldt, MD, Mayo Clinic, 200 First St. SW, Rochester, MN 55905.
Abstract
Patients were observed after the Fontan operation to determine the frequency and severity of protein-losing enteropathy. A total of 427 patients who survived for 30 days after the Fontan operation, performed between 1973 and January 1987, were analyzed and, thus far, protein-losing enteropathy has developed in 47 of 427. The cumulative risk for the development of protein-losing enteropathy by 10 years was 13.4% among 30-day survivors, and 5-year survival after the diagnosis was 46%. Hemodynamic studies done coincident with the diagnosis of protein-losing enteropathy have shown increased systemic venous pressure, decreased cardiac index, increased pulmonary vascular resistance, and increased ventricular end-diastolic pressure. Medical management of protein-losing enteropathy was only partially successful. Statistical analysis has shown that factors related to protein-losing enteropathy were ventricular anatomy, increased preoperative ventricular end-diastolic pressure, longer operative bypass time, increased length of hospital stay, and postoperative renal failure. This study suggests that scrupulous selection of cases for the Fontan operation is mandatory and that certain perioperative factors may predispose to this serious complication of the Fontan procedure. (J THORACCARDIOVASCSURG1996;112:672-80)
Protein-losing enteropathy (PLE) associated with cardiovascular disease was first noted in patients in whom constrictive pericarditis developed
1 or those who had long-standing congestive heart failure. 2 PLE also has been reported in patients who have had the Mustard procedure for complete transposition of the great arteries and in whom obstruction of the intraatrial baffle had developed. 3 It has been theorized that PLE results from increased systemic venous pressure that subsequently causes lymphangiectasis, which has been documented by jejunal biopsy. PLE associated with the Fontan operation was reported in 1980 and again in 1984. 4,5 A preliminary review of the experience at the Mayo Clinic was reported and the frequency of PLE after the Fontan operation was approximately 10%. For another recent series 6 a 24% frequency of PLE was reported after the Fontan operation.
The purpose of this study was to estimate the probability of PLE developing among 30-day survivors of the Fontan operation. In addition, the clinical course of patients with PLE was analyzed to determine survivability and to describe the effects of different options for management. Various preoperative and perioperative risk factors for the development of PLE were also assessed. An understanding of the occurrence and severity of this important complication of the Fontan operation, as well as a knowledge of certain risk factors that may be associated with PLE, can enhance the ability to select optimal candidates for the Fontan operation.
Methods
This report is based on patients who had the Fontan operation between 1973 and January 1987 at the Mayo Clinic and who were alive 30 days after the operation. A database for these patients has been used for previous publications. 7-10 This database was updated by data from recent return visits, reports from local physicians, and information obtained from recent written questionnaires or telephone interviews. Recent follow-up information was available for all 30-day survivors except for five patients who were known to be alive 3 to 5 years after their Fontan operation. Excluded were patients whose Fontan repair was taken down in the first 30 days after the operation.
Current data included vital status, cardiovascular symptoms or signs, medications and other management regimens, date of onset of PLE if present, clinical course, and results of pertinent echocardiographic or hemodynamic studies. PLE was considered present when increased enteric loss of 
1-antitrypsin was documented or the clinical syndrome of PLE was present (persistent or intermittent edema with hypoproteinemia without evidence for deficient protein production or excessive protein loss from organ systems other than the gastrointestinal tract).
To identify factors associated with development of PLE, we analyzed several preoperative, perioperative, and postoperative factors. Preoperative factors included calendar year of operation, age at operation, type of anatomic defect, ventricular anatomy, presence of preoperative arrhythmia, estimate of ventricular systolic function by echocardiographic or angiographic methods, measured ventricular end-diastolic pressure, total pulmonary resistance, and pulmonary arteriolar resistance. Perioperative and postoperative factors analyzed included length of cardiopulmonary bypass, need for atrioventricular valve surgery at the time of the Fontan operation, need for early reoperation for any reason, right and left atrial pressures at the end of the operation, postoperative arrhythmias, postoperative renal failure, and length of stay in the hospital after the operation. For survival analysis, time zero was the thirtieth postoperative day, whether or not the patient was still hospitalized.
These factors were analyzed among all 30-day survivors. In addition, we assessed survival subsequent to the development of PLE by standard univariate and multivariate analyses previously described by Driscoll and associates. 10 Two-tailed p values 
0.05 were taken as evidence of findings not attributable to chance.
Results
A total of 427 patients were identified as eligible 30-day survivors. These included 260 male and 167 female patients. Basic cardiac anatomic types were distributed as follows: tricuspid atresia, 148 patients; univentricular heart, 138; and other complex cyanotic lesions, 141. The survival curve for all 30-day survivors shows that the 10-year survival of these patients was 77% (Fig. 1).
|
Current status of patients with PLE
The 5-year survival after diagnosis of PLE was 46% (Fig. 2). Survivorship was not related to length of time between operation and onset of PLE. Among the 20 current survivors, four patients are in remission. One patient had transient PLE coincident with a Salmonella intestinal infection. Another has been in remission for 3 years after cardiac transplantation. One patient is currently in remission coincident with the placement of a sequential atrioventricular pacemaker for intermittent bradycardia. Another patient currently is in remission after having had PLE from 1979 until 1991. This patient derived significant clinical benefit after moving from high altitude (Denver) to sea level (San Diego).
|
Laboratory data from current PLE survivors includes total serum protein values ranging from 3.0 to 5.9 gm/dl (mean 4.3 gm/dl) and serum albumin values ranging from 1.3 to 4.0 gm/dl (mean 2.6 gm/dl). Serum calcium values range from 4.5 to 9.5 mg/dl. The patient with the lowest calcium value manifested tetany. Six patients had 24-hour 1-antitrypsin clearances ranging from 46.4 to 584.0 ml/day (mean 265 ml/day). Normal clearance has been determined to be less than 27 ml/day. Lymphocytopenia is common (range 2% to 46% lymphocytes, with a mean of 15% lymphocytes in the peripheral smear).
Hemodynamic findings
In an effort to better understand the hemodynamic derangement associated with PLE, we tabulated the results of cardiac catheterization or echocardiographic studies (or both) (Table I). Included were data from postoperative studies coincident with the development of PLE, irrespective of current vital status. The factors measured show wide ranges of variability, with the tendency for increased right-sided filling pressures, decreased cardiac index, increased pulmonary resistance, and increased ventricular end-diastolic pressure. Estimated ventricular ejection fractions were decreased (mean 53%). Patients underwent cardiac catheterization during hospitalization for treatment of edema, fluid accumulation, and congestive heart failure. They were considered to be in reasonably stable cardiopulmonary states at the time of their catheterization.
|
11,12 has been tried on four patients but none continued these dietary measures on a long-term basis. Nineteen of 20 survivors of PLE (95%) are receiving digoxin and diuretics. Although the reinstitution of these anticongestive measures had a significant clinical effect and often was associated with a dramatic decrease in enteric protein loss, the patients continue to have PLE. Twelve of 20 patients (60%) are being treated with afterload-reducing agents in their regimen, with similar partial benefit.
Nine of 20 patients (45%) have required periodic albumin infusion that is often given before intravenous administration of furosemide therapy. For the patient with marked edema and hypoproteinemia, the benefits can be dramatic. The duration of benefit is variable and not predictable. Three patients have had courses of corticosteroid therapy given in therapeutic doses for adequate trial periods. None of these patients derived any benefit from such therapy.
Death and PLE
Of the 96 30-day survivors who have subsequently died during follow-up, 27 (28%) were patients in whom PLE had developed. Reoperation during follow-up for whatever reason is associated with high perioperative mortality among patients with PLE. Nine of 12 patients with PLE died in connection with their reoperation. Two of the deaths at reoperation occurred in patients undergoing transplantation. These two patients were believed to have long-standing congestive heart failure and had marked nutritional debilitation. All other deaths were attributed to deteriorating ventricular function and congestive heart failure.
Univariate analysis of factors associated with development of PLE
Factors not associated with development of PLE included calendar year of the Fontan procedure, sex of the patient, preoperative ejection fraction (echocardiography or angiography), presence of preoperative arrhythmia, preoperative mean pulmonary artery pressure, and preoperative total pulmonary resistance or pulmonary arteriolar resistance (Table II). Factors associated with development of PLE included ventricular anatomy other than dominant left ventricle and increased preoperative ventricular end-diastolic pressure. Patients with tricuspid atresia were less likely to have PLE develop than patients with other types of defects (Table II).
|
(Table II) included longer cardiopulmonary bypass time, increased left atrial pressure after the operation, longer length of hospital stay, and presence of postoperative renal failure. Postoperative renal failure was considered present when the patient needed renal or peritoneal dialysis. Early reoperation for any reason was also associated with later development of PLE.
From analysis of continuous variables (Pc in Table II), higher total pulmonary resistance, higher preoperative ventricular end-diastolic pressure, higher mean left atrial pressure after the Fontan operation, longer cardiopulmonary bypass time, and longer hospital stay were associated with the development of PLE.
Multivariate analysis
From Cox proportional-hazards modeling, the sole preoperative variable associated with later development of PLE was ventricular anatomy other than dominant left ventricle (Pm in Table II). Of perioperative variables similarly analyzed, length of hospital stay also predicted PLE development. The most significant factor predictive of PLE was the presence of renal failure in the postoperative period. PLE ultimately developed in nine of 39 such patients. A curve of probability of remaining free of PLE for those who had renal failure (Fig. 3) demonstrates that PLE often developed early in the postoperative course and the rate may level off after 5 postoperative years.
|
|
This report is the largest and most comprehensive study of PLE cases after the Fontan operation. The chance of PLE developing among 30-day survivors was approximately 13.4% by 10 years. Other reports in the literature have been limited by the small number of patients or the brevity of the follow-up. 4,5 The data reported in this article show that PLE can be a late complication; therefore continued and careful follow-up of all patients who have had the Fontan operation is considered necessary to identify those in whom PLE may develop in the late follow-up period.
Diagnosis and clinical manifestations of PLE
The diagnosis of PLE is reasonably certain for these patients. Data in the literature 13-15 suggest that 1-antitrypsin studies accurately detect excessive loss of enteric protein and, therefore, this test remains the standard for documenting PLE. In this retrospective review involving patients operated on between 1973 and 1987, 1-antitrypsin data were not available for all patients. With reasonable certainty, a retrospective review could identify patients who fit the clinical syndrome of PLE. Two points are worth emphasizing. Most frequently, the onset of PLE is heralded by a new onset of pleural effusion, ascites, or peripheral edema. In the presence of hypoproteinemia and no other cause for protein loss, the diagnosis of PLE is reasonable. Changes in gastrointestinal signs and symptoms are relatively uncommon. This is in contrast to other diseases associated with PLE resulting from primary gastrointestinal disease. 11,16-18 The effect of protein loss on maturation has been documented in patients whose growth has been delayed as well as in one instance of delay in the onset of puberty. Similar problems have been identified for noncardiac causes of PLE. 18
PLE is represented by a spectrum of severity, with a patient mortality rate of 54% by 5 years after the diagnosis. The mortality rate noted for patients with PLE has not been reported previously. The survival data for all 30-day survivors is similar to findings reported by Fontan and associates 19 in 1990.
The fact that PLE can be transient suggests that other phenomena may have an effect, such as an intercurrent bacterial intestinal infection that occurred in one patient. The adverse effect of living at high altitude after a Fontan operation is suggested by the finding that the condition of one patient improved after he moved from high altitude to sea level. The improvement in the condition of one patient coincident with the use of atrioventricular sequential pacing is of interest, but this modality is still untested. PLE has developed in patients who had pacemakers placed at the time of their Fontan operation.
The laboratory manifestations of PLE (hypoproteinemia, hypoalbuminemia, hypocalcemia, and lymphocytopenia) have been observed in other forms of PLE. Despite low levels of lymphocytes, a severe infection or a septic catastrophe did not develop in any of these patients. Although periodic albumin infusions have been used, gamma globulin infusions have not been considered necessary.
Management
The fact that anticongestive measures are not curative should not discourage the physician from vigorously initiating this therapy. A tendency toward improvement in the amount of enteric protein loss has been associated with the diuresis that comes with reinstituting digoxin, furosemide, and afterload-reduction agents. Unfortunately, there is usually still excessive enteric protein loss despite initiation of therapy. A clinical management strategy of periodic albumin infusions with intravenous administration of furosemide has been judged clinically effective for some patients and, in those who have stable ventricular function and other hemodynamic factors, has been used for extended periods without negative sequelae. The long-term use of dietary changes other than sodium restriction has not been successful for this group of patients. Part of management should include frequent follow-up visits with serial measures of serum proteins and 1-antitrypsin stool concentrations. Serial echocardiographic studies to monitor ventricular function have also been done.
Hemodynamic findings for patients with PLE
The hemodynamic findings in patients who had cardiac catheterization coincident with development of PLE demonstrate increased right-sided pressures, decreased cardiac output, decreased ventricular systolic function, and abnormal ventricular diastolic function as measured by end-diastolic pressure or mean wedge pressures. Comparisons between hemodynamic findings for this group of patients and for other patients who are 30-day survivors without PLE would be distorted by the fact that the only patients having catheterization were those in whom hemodynamic derangement was suspected. Furthermore, these patients represented a clinical spectrum of severity, and protocols such as fluid challenge were not used during this period.
These data do describe the hemodynamic abnormalities seen for the first time in patients with PLE, however. The relative importance of one hemodynamic variable and PLE could not be identified.
The experience at the Mayo Clinic with use of corticosteroids in patients with PLE has not been favorable. Barber (Barber G, New York University Medical Center, personal communication) has noted a subgroup of patients with PLE after the Fontan operation who, at cardiac catheterization, have relatively normal right-sided pressures. He believes that these patients should have an intestinal biopsy and, if a cellular infiltrate is noted on biopsy, may respond favorably to corticosteroid therapy. In the patients in the present study, low right-sided pressures were infrequent and none had received corticosteroid therapy.
Although cardiac transplantation has been used infrequently in the past, it is the option that may be considered for patients who have PLE associated with deteriorating hemodynamic variables and poor response to anticongestive measures. If transplantation is considered, it should be undertaken before nutritional debilitation is manifest. The role of creating a right-to-left shunt at the atrial level as a method of treating PLE has been used on too few patients to reach a conclusion about this strategy. However, a recent report has suggested benefit from that approach. 20 Theoretically, lowering right atrial pressure might result in clinical improvement of PLE provided that other measures of cardiac function are adequate and stable.
Factors associated with development of PLE
The finding of significant preoperative and perioperative factors associated with later development of PLE resulted from statistical methods similar to the one reported by Driscoll and associates. 10 This series looked only at 30-day survivors and included a longer operative experience. Similarities in mortality risk noted by Driscoll's group 10 and results in this report are not surprising. Unfavorable preoperative factors included defect other than tricuspid atresia, ventricular anatomy other than dominant left ventricle, increased ventricular end-diastolic pressure, and increased total pulmonary resistance. These findings clearly emphasize the need to be scrupulous in selecting patients for the Fontan operation. Unfavorable perioperative factors included prolonged duration of cardiopulmonary bypass, increased postoperative left atrial pressure, postoperative renal failure, and increased duration of postoperative hospital stay. It was not possible to analyze other potential postoperative risk factors for PLE, such as duration of pleural effusions, because of the aggressive and highly effective use of chemical and mechanical pleurodesis during this period. The presence of one or more of those unfavorable variables should help alert the clinician to the possible increased risk of PLE occurring later in the patient's postoperative course.
This retrospective review includes patients operated on with techniques for the Fontan operation used before February 1, 1987. Since that time direct cava–pulmonary artery connections, lateral atrial tunnel, and similar techniques have been introduced. Short-term mortality rates after the Fontan operation have declined steadily since 1987. 21 This improvement may well result from a combination of better case selection and improved surgical techniques. It remains to be seen whether experience since 1987 is associated with a lower rate for PLE development during the postoperative course. Because PLE may be a late complication, follow-up of at least 5 years is needed to assess the effects of newer operative techniques on incidence of this complication.
Footnotes
From the Section of Pediatric Cardiology,a Section of Biostatistics,b Division of Gastroenterology and Internal Medicine,c and Section of Cardiovascular Surgery,d Mayo Clinic and Mayo Foundation, Rochester, Minn. 
References
This article has been cited by other articles:
|
|
 |
|
  J. Simmonds, M. Burch, H. Dawkins, and V. Tsang Heart transplantation after congenital heart surgery: improving results and future goals. Eur. J. Cardiothorac. Surg., August 1, 2008; 34(2): 313 - 317. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Haddad, R. Doyle, D. J. Murphy, and S. A. Hunt Right Ventricular Function in Cardiovascular Disease, Part II: Pathophysiology, Clinical Importance, and Management of Right Ventricular Failure Circulation, April 1, 2008; 117(13): 1717 - 1731. [Full Text] [PDF]
|
|
|
|
 |
|
 K. M. Bhagirath and J. W. Tam Resolution of Protein-Losing Enteropathy With Low-Molecular Weight Heparin in an Adult Patient With Fontan Palliation Ann. Thorac. Surg., December 1, 2007; 84(6): 2110 - 2112. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. H Kiesewetter, N. Sheron, J. J Vettukattill, N. Hacking, B. Stedman, H. Millward-Sadler, M. Haw, R. Cope, A. P Salmon, M. C Sivaprakasam, et al. Hepatic changes in the failing Fontan circulation Heart, May 1, 2007; 93(5): 579 - 584. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. E. Canter, R. E. Shaddy, D. Bernstein, D. T. Hsu, M. R.K. Chrisant, J. K. Kirklin, K. R. Kanter, R. S.D. Higgins, E. D. Blume, D. N. Rosenthal, et al. Indications for Heart Transplantation in Pediatric Heart Disease: A Scientific Statement From the American Heart Association Council on Cardiovascular Disease in the Young; the Councils on Clinical Cardiology, Cardiovascular Nursing, and Cardiovascular Surgery and Anesthesia; and the Quality of Care and Outcomes Research Interdisciplinary Working Group Circulation, February 6, 2007; 115(5): 658 - 676. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Fernandez, A. Ashraf, and L. S. Dure Nutritional Vitamin D Deficiency Presenting as Hemichorea J Child Neurol, January 1, 2007; 22(1): 74 - 76. [Abstract] [PDF]
|
|
|
|
|
|
O. Uzun, J. K. Wong, V. Bhole, and O. Stumper Resolution of Protein-Losing Enteropathy and Normalization of Mesenteric Doppler Flow With Sildenafil After Fontan Ann. Thorac. Surg., December 1, 2006; 82(6): e39 - e40. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Ostrow, H. Freeze, and J. Rychik Protein-Losing Enteropathy After Fontan Operation: Investigations Into Possible Pathophysiologic Mechanisms Ann. Thorac. Surg., August 1, 2006; 82(2): 695 - 700. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Dodge-Khatami, M. Rahn, R. Pretre, and U. Bauersfeld Dual Chamber Epicardial Pacing for the Failing Atriopulmonary Fontan Patient Ann. Thorac. Surg., October 1, 2005; 80(4): 1440 - 1444. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R Kaulitz and M Hofbeck Current treatment and prognosis in children with functionally univentricular hearts Arch. Dis. Child., July 1, 2005; 90(7): 757 - 762. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W.-H. Kim, H. G. Lim, J. R. Lee, J. R. Rho, E. J. Bae, C. I. Noh, Y. S. Yoon, and Y. J. Kim Fontan conversion with arrhythmia surgery Eur. J. Cardiothorac. Surg., February 1, 2005; 27(2): 250 - 257. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Gamba, M. Merlo, R. Fiocchi, A. Terzi, C. Mammana, R. Sebastiani, and P. Ferrazzi Heart transplantation in patients with previous Fontan operations J. Thorac. Cardiovasc. Surg., February 1, 2004; 127(2): 555 - 562. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S Chakrabarti, B R Keeton, A P Salmon, and J J Vettukattil Acquired combined immunodeficiency associated with protein losing enteropathy complicating Fontan operation Heart, October 1, 2003; 89(10): 1130 - 1131. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. L. Connor, S. Angelides, M. Gibson, D. W. Larden, M. R. Roman, O. Jones, B. G. Currie, A. S. Day, and T. D. Bohane Successful Resection of Localized Intestinal Lymphangiectasia Post-Fontan: Role of 99mTechnetium-Dextran Scintigraphy Pediatrics, September 1, 2003; 112(3): e242 - 247. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. D. Coon, J. Rychik, R. T. Novello, P. S. Ro, J. W. Gaynor, and T. L. Spray Thrombus formation after the Fontan operation Ann. Thorac. Surg., June 1, 2001; 71(6): 1990 - 1994. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. D. Mair, F. J. Puga, and G. K. Danielson The Fontan procedure for tricuspid atresia: early and late results of a 25-year experience with 216 patients J. Am. Coll. Cardiol., March 1, 2001; 37(3): 933 - 939. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H B Ravn, V E Hjortdal, E V Stenbog, K Emmertsen, O Kromann, J Pedersen, and K E Sorensen Increased platelet reactivity and significant changes in coagulation markers after cavopulmonary connection Heart, January 1, 2001; 85(1): 61 - 65. [Abstract] [Full Text]
|
|
|
|
|
|
G. Balling, M. Vogt, H. Kaemmerer, A. Eicken, H. Meisner, and J. Hess INTRACARDIAC THROMBUS FORMATION AFTER THE FONTAN OPERATION J. Thorac. Cardiovasc. Surg., April 1, 2000; 119(4): 745 - 751. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J Therrien, G D Webb, and M A Gatzoulis Reversal of protein losing enteropathy with prednisone in adults with modified Fontan operations: long term palliation or bridge to cardiac transplantation? Heart, August 1, 1999; 82(2): 241 - 243. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R C van Nieuwenhuizen, M Peters, L J Lubbers, M D Trip, J G P Tijssen, and B J M Mulder Abnormalities in liver function and coagulation profile following the Fontan procedure Heart, July 1, 1999; 82(1): 40 - 46. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Petrossian, V. M. Reddy, D. B. McElhinney, G. P. Akkersdijk, P. Moore, A. J. Parry, L. D. Thompson, and F. L. Hanley EARLY RESULTS OF THE EXTRACARDIAC CONDUIT FONTAN OPERATION J. Thorac. Cardiovasc. Surg., April 1, 1999; 117(4): 688 - 696. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.A.M. van Son, F.W. Mohr, J. Hambsch, P. Schneider, H. Hess, and G.S. Haas Conversion of atriopulmonary or lateral atrial tunnel cavopulmonary anastomosis to extracardiac conduit Fontan modification Eur. J. Cardiothorac. Surg., February 1, 1999; 15(2): 150 - 158. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Masetti, S. M. Marianeschi, A. Cipriani, F. S. Iorio, and C. F. Marcelletti Reversal of protein-losing enteropathy after ligation of systemic-pulmonary shunt Ann. Thorac. Surg., January 1, 1999; 67(1): 235 - 236. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Y. Sze, R. C. Robbins, C. P. Semba, M. K. Razavi, and M. D. Dake Superior vena cava syndrome after heart transplantation: percutaneous treatment of a complication of bicaval anastomoses J. Thorac. Cardiovasc. Surg., August 1, 1998; 116(2): 253 - 257. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Mertens, D. J. Hagler, U. Sauer, J. Somerville, and M. Gewillig Protein-losing enteropathy after the Fontan operation: An international multicenter study J. Thorac. Cardiovasc. Surg., May 1, 1998; 115(5): 1063 - 1073. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Mavroudis, C. L. Backer, B. J. Deal, and C. L. Johnsrude Fontan Conversion To Cavopulmonary Connection And Arrhythmia Circuit Cryoablation J. Thorac. Cardiovasc. Surg., March 1, 1998; 115(3): 547 - 556. [Abstract] [Full Text]
|
|
|
|
|
|
K. BULL The Fontan procedure: lessons from the past Heart, March 1, 1998; 79(3): 213 - 214. [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
