| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Thorac Cardiovasc Surg 1994;108:841-854
© 1994 Mosby, Inc.
SURGERY FOR CONGENITAL HEART DISEASE |
New York, N.Y., Boston, Mass., and Birmingham, Ala.
Address for reprints: John W. Kirklin, MD, University of Alabama at Birmingham, University Station, Birmingham, AL 35294.
Abstract
Among 326 severely symptomatic neonates with coarctation with or without ventricular septal defect, four died before an initial procedure was performed. Among the 322 undergoing an initial procedure, survival for at least 24 months was 84%; the hazard function for death was lower initially but more prolonged in patients without than in those with ventricular septal defect. Important mitral valve anomalies coexisted in 5% of patients, left ventricular hypoplasia in 5% (more commonly in patients without ventricular septal defect), narrowing of the left ventricular outflow tract in 9% (more common in patients without ventricular septal defect), and narrowing of the proximal arch in 1%; one or more of these anomalies was present in most patients without ventricular septal defect who died. Five percent of the 322 patients had more than one of these coexisting anomalies, and 8% had just one. The most commonly used technique of repair of the coarctation was resection and end-to-end anastomosis, but no technique was a risk factor for death by multivariable analysis. Extension of the area of resection so that the end-to-end anastomosis was proximal to the left subclavian artery but distal to the left common carotid artery did not increase risk; extensions beyond this, and in the case of patch graft repair, extensions proximal to the left subclavian artery, did increase risk. Patch graft repair was associated with the highest prevalence (21%) of reintervention to the coarctation repair. Among patients with coexisting moderate-sized or large ventricular septal defects, repair of the coarctation, pulmonary trunk banding, and subsequent repair of the defect were associated with the highest 2-year survival, 97% in those with single ventricular septal defect. The risk-adjusted outcomes in two institutions were less good than in all others. (J THORACCARDIOVASCSURG1994;108:841-54)
About 10% of persons born with coarctation without or with ventricular septal defect (VSD) have heart failure and require treatment in the first month of life.
1 Most of those in whom repair is not promptly accomplished die. The therapeutic problem in neonates presenting in this fashion is more complex and less well understood than in older patients.
For these reasons, a prospective multiinstitutional study was undertaken; management was directed by the physicians caring for the patients, and not assigned randomly. All patients were systematically observed after hospital dismissal. The data were extensively explored, with the purpose of understanding the nature of the condition and its response to treatment and providing information relevant to therapy.
PATIENTS AND METHODS
Patients
This study addresses the 326 neonates with coarctation without (n = 171) or with (n = 155) VSD, who are among the 435 neonates with coarctation entering the 27 institutions between January 1, 1990, and January 1, 1992. The remainder (n = 109) were neonates in whom coarctation coexisted with other major congenital cardiac anomalies (Appendix Table I).
|
Management
Most patients entered critically ill, and treatment was begun immediately with prostaglandin E1, intubation and ventilation, and catecholamines when indicated. 2 Diagnosis was established quickly, usually by two-dimensional echocardiography but at times by cardiac catheterization and cineangiography. Management was a joint effort of the pediatric cardiology and pediatric cardiac surgery departments and involved other groups of physicians as well. Generally, a procedure was accomplished as soon as good hemodynamic and ventilatory states were achieved; in some patients, however, treatment could not achieve this, and a procedure was undertaken with the neonate in an unstable and unsatisfactory condition.
Follow-up
A cross-sectional follow-up of all patients in the study was undertaken annually between March 1 and May 1, and the last follow-up period from which data for this study were taken was in 1992. Eighty percent of the patients were followed by the Data and Analysis Center, and the remainder were followed by the treatment institution, at the institution's request.
The median follow-up time for survivors was 13.3 months, and the range was 3 days to 32.4 months; the mean follow-up time was 14.0 ± 7.50 months (standard deviation). Ninety percent of the patients were observed for 5.2 months or longer, 75% for 7.8 months or longer, 50% for 13.3 months or longer, 25% for 20.3 months or longer, and 10% for 24.3 months or longer. Nine patients have been untraceable since the time of hospital discharge.
Database
Copies of the relevant parts of the hospital records were provided to the Data and Analysis Center in the Division of Cardiothoracic Surgery at the University of Alabama at Birmingham. The patient-specific information was entered into a computer database and rechecked and upgraded on numerous occasions. Both noncomputerized and computerized files were treated in a private and confidential manner.
Analysis
A dataset for analysis was created from the computer database, using SAS System software (SAS Institute, Inc., Cary, N.C.) and an IBM RISC 6000 computer. Numerous explorations were made using Kaplan-Meier time-related nonparametric estimations, 3 cumulative frequency distribution plots, and contingency tables. P values were estimated, and the method (model) is given wherever these are shown. Seventy percent confidence intervals were computed for most proportions, including time-related proportions, using these rather than 95% intervals to avoid overlooking possibly important differences in this rather small sample of 322 patients. Survival and hazard functions were also estimated parametrically, by means of the hazard function regression model. 4
Numerous multivariable analyses of time-related determined outcomes (hazard function regression domain), many more than are presented in this publication, were performed with a P value of less than 0.1 used as the criterion for retaining a variable in the final equation, with the same reasoning as for 70% confidence intervals. However, the P values for most retained variables were considerably smaller than this. Potential risk factors (Appendix Table 2) were entered sequentially in groups (groups of patient-specific, procedural, and institutional variables). Echocardiographic measurements were transformed to Z-values (standard deviation units) for the analyses. 5 Numerous transformations and interactions were explored, as well as various combinations of the groups of potential risk factors.
|
2) value. In the other method, the time-related freedom from the event was determined by the Kaplan-Meier method. This was compared with the percent freedom from the event obtained by averaging the individual time-related freedoms of each patient; the comparison was considered satisfactory when the 70% confidence limits of the estimates were overlapping.
Definitions
The presence, size (small, moderate-sized, or large, aggregate size in the case of multiple VSDs unless stated otherwise), multiplicity, and location of VSDs was judged from echocardiographic, angiographic, and operative reports. Coexisting lesions in the left heart–aorta complex (listed in Appendix Table 2) were subjectively graded as to the severity of their obstructiveness from 0 to 5 (5 being the most severe) on the basis of these documents and any available echocardiographic measurements; grade 2 or more was considered to represent a functionally important degree of obstruction. This method was used because of the paucity of echocardiographic measurements made by the institutions and because of the inappropriateness of inferences about obstruction based on gradients across these areas in neonates with patency of the ductus arteriosus and/or a VSD.
"Classic" coarctation repair is defined in this study as one (end-to-end anastomosis, subclavian flap, or patch graft) that does not extend proximal to the left subclavian artery. Even though hypoplasia of that portion of the distal arch between the left common carotid artery and the left subclavian artery is not considered a coexisting obstructive anomaly because of clear evidence of its reversibility, 6 the repair was considered to augment the diameter of the arch when it extended proximal to the left subclavian artery.
Hospital deaths are included, as well as deaths at any time in the follow-up period. Time zero was usually the time of initial repair. The 30-day mortality is evident in all the time-related depictions.
Non-risk-adjusted prevalences and percents of death (or survival) and other events are those that were obtained by simply counting and dividing, or by actuarial (Kaplan-Meier) analysis. Risk-adjusted prevalences and percents are those in which the values for all variables except the one(s) under consideration are kept constant; that is, the effect of the variable(s) under consideration is isolated from the effect of any other variables and thus the risk associated with it per se is more clearly evident. Risk-adjusted prevalences are valuable in drawing inferences, but there is a degree of uncertainty (quantified by confidence intervals and P values) in their values.
RESULTS
Prevalences
The median birth weight at entry was 2.97 kg (90% between 1.61 and 4.04 kg). The median age at entry was 6 days (90% were between 0 and 23 days old). The median interval between entry and the first procedure was 3 days (90% were between 0 and 17 days).
Obstruction was present at levels in the left heart–aorta complex other than at the coarctation in 13% of the patients (Table I). The subaortic area (median Z for diameter -6.5), the "anulus" (median Z -4.2), and the ascending aorta (median Z -3.0) were abnormally small by echocardiographic measurement in most patients in whom these measurements were available (Fig. 1).
|
|
Table II). Most commonly (74 of the 115 single VSDs) the VSD was conoventricular in type, and multiple VSDs were most commonly all muscular.
|
|
Table II, Appendix Fig. 1) and believably decreased the risk-adjusted survival (Table III). Multiplicity of VSDs was associated with a considerably decreased non-risk-adjusted and risk-adjusted survival when the aggregate size of the VSD was moderate or large. The location of a single VSD had little effect on non-risk-adjusted or risk-adjusted survival.
|
|
Table I) and the risk-adjusted (see Table III, Fig. 3) survival.
|
Table IV) nor the risk-adjusted (see Table III) survival so long as the repair was not extended proximal to the left subclavian artery. When an end-to-end repair was extended proximal to the left subclavian artery but only to the left common carotid artery, the non-risk-adjusted (see Table IV) and risk-adjusted (see Table III, Fig. 4) survivals were not believably different from those when end-to-end anastomosis was used in the "classic" fashion. When patch grafting was used as the technique of repair and was similarly extended proximally (that is, only as far up as the level of the left common carotid artery), the non-risk-adjusted survival was not believably decreased compared with that of patch graft repair limited to the upper descending thoracic aorta (29%; 70% C1* 10% to 55% versus 13%; 70% CL 4%-29%, P(Fisher) = 0.4, see Table IV); the risk-adjusted survival was decreased by this extension of the patch graft technique (see Table III, Fig. 4). No matter what the technique, extensions proximal to the left common carotid artery were associated with decreased survival. Only eight patients (one death) had a reverse subclavian flap used as part of the initial repair of coarctation, so generalizations about survival with this technique are not possible.
|
|
Among those with moderate-sized or large VSD, repair of the coarctation alone at the initial repair of the coarctation was associated with a non-risk-adjusted survival that was less, but only possibly believably so, than that after repair of the coarctation and pulmonary trunk banding (Table V, Fig. 5). Repair of the coarctation plus pulmonary trunk banding was associated with the highest non-risk-adjusted and risk-adjusted (see Table IV) survivals; the risk-adjusted survival was 97% for at least 24 months when there was no coexisting obstruction elsewhere in the left heart–aorta complex (see Fig. 4). One-stage repair was associated with the lowest non-risk-adjusted survival, but the P value for these differences in survival between one-stage repair and coarctation repair alone and coarctation plus pulmonary trunk band were all greater than about 0.1 (see Table V and Fig. 5). The risk-adjusted disadvantage of one-stage repair, in terms of time-related survival, had a P value of 0.02 (see Table III).
|
|
Table VI). Survival was not better in more recent cases than in earlier cases (Table VI).
|
|
Subsequent procedures and events related to a VSD
Among the 47 patients with moderate-sized or large VSDs who initially underwent coarctation repair alone, five (in one of whom the VSD had spontaneously narrowed, but the patient died after three operations directed against coexisting obstructive lesions at other levels) died before the VSD was repaired, four received a pulmonary trunk banding as the next procedure (of whom two died), and 17 received VSD repair as the next procedure (three of whom died). In this and the group with concomitant banding of the pulmonary trunk, all deaths after subsequent procedures are accounted for in the total deaths after the initial procedure.
Among the 34 patients who initially underwent coarctation repair plus banding of the pulmonary trunk, 12 (no deaths) underwent repair of the VSD and debanding (or the leaving of a band that was loose), one (who lived) underwent debanding alone (because the VSD had become smaller), 18 had as yet no additional procedure but were living, and three died without any subsequent procedure.
One patient, who had a one-stage repair, underwent rerepair of the VSD and died.
Spontaneous narrowing of the VSD to at least small size, in the patients with moderate-sized or large VSDs that were not closed at the initial procedure, occurred within 24 months in only 19% of patients (Fig. 6). Muscular VSDs were the most likely type to spontaneously narrow in size.
|
|
Table VII).
|
Reliability and validity of the data
The source of the information in this article was photostatic copies of the original hospital documents. Values for most variables were contained in multiple places in the record. In the case of each patient these were studied by a single expert reviewer, who used professional judgment to evaluate disparate values from several sources and to fuse them into the single most reasonable, reliable, and valid value. When desired values or information could not be found in the available copies of the medical record, renewed efforts were made to obtain the missing documents. When this was not possible, the value or variable was entered as "missing." Thus, overall, the information in this study is considered as reliable and valid as that contained in the various parts of the hospital and outpatient medical record.
Implications for treatment
This study suggests that seriously ill neonates, who have coarctation without or with a single VSD, who are without other obstructive lesion in the left heart–aorta complex, and who undergo a repair of the coarctation that is "classic," or, in the case of end-to-end anastomosis, is extended proximally only as far as the left common carotid artery, can have about a 97% survival for at least 24 months after repair (see Figs. 3 and 4). In those with moderate-sized or large VSD, this high proportion of survivors is dependent on the initial procedure being repair of the coarctation and banding of the pulmonary trunk; debanding and repair of the VSD should be done as soon as the patients' condition becomes good, and ideally should be done during the initial hospitalization (Williams W: personal communication, 1993).
However, there are potential advantages to one-stage repair in patients with coarctation and single, moderate-sized, or large VSD. This, and the lack of certainty (P values were generally greater than 0.05) that the initial procedure of coarctation repair plus pulmonary trunk banding provides better outcomes, is a strong indication for continuing this study. If uncertainty remains with additional patients and longer follow-up, a prospective randomized trial would be indicated.
The results have been less good in the 13% of patients with particularly narrow subaortic channels, aortic valve "anuli," and ascending aortas; principles of management in this group may be the same as in patients with interrupted aortic arch. 7 This implies that no concomitant procedure other than arch augmentation should be done at the initial repair; close follow-up with echocardiographic monitoring may indicate the need or lack thereof for a subsequent procedure. This suggestion is based on the probability that the pathways enlarge rather promptly in most patients after repair without concomitant procedures. This enlargement has been clearly documented in the case of that portion of the distal arch that is between the left common carotid and left subclavian arteries. 6 However, good results from concomitant procedures at the time of initial repair in small numbers of cases have been reported by others. 8,9
We express our appreciation for the work of the pediatric cardiologists, cardiac surgeons, nurses, and coordinators in the institutions participating in this study of the Congenital Heart Surgeons Society. The institutions, in random order, are Mott Children's Hospital at the University of Michigan Medical Center; University of Alabama Medical Center; The Boston Children's Hospital; The Children's Hospital in Buffalo, N.Y.; University of Chicago; Children's Memorial Hospital in Chicago; Children's Hospital of Michigan in Detroit; The Pennsylvania State College of Medicine (The Milton S. Hershey Medical Center); University of Iowa Hospital and Clinics; Children's Hospital of Los Angeles; Miami Children's Hospital; University of Miami (and Jackson Memorial Hospital) in Miami; The Montreal Children's Hospital; Columbia-Presbyterian Medical Center in New York; Children's Hospital of Philadelphia; University of California San Francisco; University of Utah Medical Center (and Primary Children's Medical Center); All Children's Hospital in St. Petersburg, Fla.; Hospital for Sick Children in Toronto; University of California Los Angeles; University of São Paulo; Children's Hospital Medical Center, Cincinnati; Tulane University Medical Center Hospital, New Orleans; Children's Memorial Hospital, Omaha, Neb.; Children's Hospital of Pittsburgh; Medical University of South Carolina; Children's Hospital and Health Center, San Diego; St. Christopher's Hospital for Children, Philadelphia. We are deeply indebted to Mary Lynne Clark, Phyllis Newsom, and Gail Mertz for their management of the follow-up, to Rob Brown for the data management and some of the analyses, and to Debbie Nuby for her skill in developing the graphics and the manuscript.
Appendix: DISCUSSION
Dr. William G. Williams (Toronto, Ontario, Canada).
Were the four infants who died prior to surgery all in the group of infants with intact ventricular septum?
Dr. Blackstone.
There were two in each group. Death was either from intractable acidosis or from severe, uncorrectable noncardiac congenital anomalies.
Sir Brian Barratt-Boyes (Auckland, New Zealand).
You have analyzed the data relative to the type of operation performed and also to the degree of associated left ventricular outflow obstruction. I would wonder whether the type of operation performed was not related to additional factors that you have not analyzed, for example, the fact that the anastomosis is at a high level or that a patch was used. Was this a routine type of management in the particular institutions or did it vary according to the anatomy? What effect does that variable have on this analysis? I suspect it might not be appropriate to assume that these data reflect only the type of operation performed.
Dr. Blackstone.
Sir Brian, what you are really asking is the confounding between the morphology and the repair done. I tried desperately to separate those. First of all, none of the morphologic details fell out of the analysis when these details of the repair came in. My inference from that, from a statistical point of view, is that these modifications and various types of repair are not just related to the morphology or I should have seen more interactions between these.
Many patients in whom there is no evidence of more than the usual hypoplasia got rather extensive operations, and those that had multiple levels of additional obstruction often had the simplest repairs. I could find no good correlation between the morphology and what was done, and it perhaps more reflected the repair that the institutions were used to doing or to their perceptions of what the morphology might have been.
Dr. Tjark Ebels (Groningen, The Netherlands).
You have looked at survival, but can you give us any data on recoarctation? That, of course, is another matter of concern. We have recently finished a study together with our colleagues from Rotterdam in which recoarctation necessitating further procedures was more prevalent in patients having single-stage repair. Can you give us any information on the prevalence of that complication?
Dr. Blackstone.
Yes. At 24 months 88% of the patients with subclavian flap repairs are free of recoarctation or reintervention, 94% of the patients with an end-to-end repair are free of reintervention, but only 70% of patients having patch graft repairs are free of reintervention. The staging of the repair did not seem to be related; rather, the type of coarctation repair was related.
Dr. John W. Brown. (Indianapolis, Ind.).
For one-stage repair of a VSD and coarctation, I presume that the coarctation is repaired with homograft tissue or pericardium. Is that correct, or is there a mixture of materials? May I assume that the repair is not end to end?
Dr. Blackstone.
It was a mixture. Many were end-to-end repairs, some were subclavian flap, and some were patch graft repairs.
Appendix: APPENDIX
Management of variables with a small number of events
The small numbers of patients and/or events associated with some institutions, and a few other variables, posed special problems in the multivariable analyses, which were handled as follows. As the multivariable equation was being finalized, work was begun using the Q statistic to develop further an equation containing the already identified risk factors and, for example, all "institutions." The Q statistic was determined noniteratively as an estimate of the strength and believability (statistical significance) of each institution as a risk factor. Then all "institutions" with a noniterative P value of <0.1 and a reasonably small coefficient were subjected, along with the other variables, to an iterative estimation. Very occasionally neither a coefficient nor a P value could be estimated iteratively for one of these; in other words the variable(s) "institution X," let us say, was computationally intractable. All institutions behaving in this manner had only one, two, or three patients and a similarly small number of events. The question as to whether such institutions, or other variables behaving in this fashion, were risk factors could not be pursued further in a formal (iterative) fashion, and they were not included in the final equation; however, they were considered to be possibly risk factors.
|
10 The basic theorem of the method was proved by Turner (Turner ME: personal communication; 1985), which allowed its adaptation to the hazard function regression method. 11,12 The validations consisted of P values for comparisons between the actual and predicted (by the parametric method) total deaths in each group in a stratification and of visual comparisons of the confidence intervals of Kaplan-Meier actuarial estimates of time-related survival for each group with the parametric predictions of time-related survival, the latter obtained by averaging the parametrically (hazard function method) predicted probability of time-related survival of each individual in the stratified group.
Footnotes
From the Division of Cardiothoracic Surgery, College of Physician's & Surgeons of Columbia University, New York, N.Y. a; the Department of Cardiac Surgery, The Children's Hospital, Boston, Mass. b; and the Division of Cardiothoracic Surgery, the Department of Surgery, The University of Alabama at Birmingham Medical Center, Birmingham, Ala. c 
Read at the Seventy-fourth Annual Meeting of The American Association for Thoracic Surgery, New York, N.Y., April 24-27, 1994.
References
This article has been cited by other articles:
|
|
 |
|
  P. T. Burch, C. G. Cowley, R. Holubkov, D. Null, L. M. Lambert, P. C. Kouretas, and J. A. Hawkins Coarctation repair in neonates and young infants: Is small size or low weight still a risk factor? J. Thorac. Cardiovasc. Surg., September 1, 2009; 138(3): 547 - 552. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Karamlou, A. Bernasconi, E. Jaeggi, F. Alhabshan, W. G. Williams, G. S. Van Arsdell, J. G. Coles, and C. A. Caldarone Factors associated with arch reintervention and growth of the aortic arch after coarctation repair in neonates weighing less than 2.5 kg. J. Thorac. Cardiovasc. Surg., May 1, 2009; 137(5): 1163 - 1167. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. L. Walters III, C. E. Ionan, R. L. Thomas, and R. E. Delius Single-stage versus 2-stage repair of coarctation of the aorta with ventricular septal defect. J. Thorac. Cardiovasc. Surg., April 1, 2008; 135(4): 754 - 761. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Alsoufi, S. Cai, J. G. Coles, W. G. Williams, G. S. Van Arsdell, and C. A. Caldarone Outcomes of Different Surgical Strategies in the Treatment of Neonates with Aortic Coarctation and Associated Ventricular Septal Defects Ann. Thorac. Surg., October 1, 2007; 84(4): 1331 - 1337. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. R. Kanter, W. T. Mahle, B. E. Kogon, and P. M. Kirshbom What is the Optimal Management of Infants With Coarctation and Ventricular Septal Defect? Ann. Thorac. Surg., August 1, 2007; 84(2): 612 - 618. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R. Kaltman, G. P. Jarvik, J. Bernbaum, G. Wernovsky, M. Gerdes, E. Zackai, R. R. Clancy, S. C. Nicolson, T. L. Spray, and J. W. Gaynor Neurodevelopmental outcome after early repair of a ventricular septal defect with or without aortic arch obstruction J. Thorac. Cardiovasc. Surg., April 1, 2006; 131(4): 792 - 798. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. C. Fiore, L. K. Fischer, T. Schwartz, S. Jureidini, I. Balfour, D. Carpenter, D. Demello, K. S. Virgo, D. G. Pennington, and R. G. Johnson Comparison of Angioplasty and Surgery for Neonatal Aortic Coarctation Ann. Thorac. Surg., November 1, 2005; 80(5): 1659 - 1665. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. K. Fesseha, B. W. Eidem, D. J. Dibardino, S. G. Cron, E. D. McKenzie, C. D. Fraser Jr, J. F. Price, A. C. Chang, and A. R. Mott Neonates With Aortic Coarctation and Cardiogenic Shock: Presentation and Outcomes Ann. Thorac. Surg., May 1, 2005; 79(5): 1650 - 1655. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Ma, Y. Deng, and X. Li Bilateral Minithoractomy Repair of Aortic Coarctation With Ventricular Septal Defect and Persistent Ductus Arteriosus Ann. Thorac. Surg., March 1, 2005; 79(3): 1049 - 1050. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. D. Puchalski, R. V. Williams, J. A. Hawkins, L. L. Minich, and L. Y. Tani Follow-up of aortic coarctation repair in neonates J. Am. Coll. Cardiol., July 7, 2004; 44(1): 188 - 191. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Azakie and I. A. Russell Gender differences in pediatric cardiac surgery: The surgeon's perspective J. Thorac. Cardiovasc. Surg., July 1, 2004; 128(1): 4 - 6. [Full Text] [PDF]
|
|
|
|
 |
|
 K. S. Murthy, R. Coelho, C. Roy, S. Kulkarni, B. Ninan, and K. M. Cherian One-Stage Repair of Cardiac and Arch Anomalies Without Circulatory Arrest Asian Cardiovasc Thorac Ann, September 1, 2003; 11(3): 250 - 254. [Abstract] [Full Text]
|
|
|
|
|
|
R. J. Walhout, J. C. Lekkerkerker, G. H. Oron, F. J. Hitchcock, E. J. Meijboom, and G. B.W.E. Bennink Comparison of polytetrafluoroethylene patch aortoplasty and end-to-end anastomosis for coarctation of the aorta J. Thorac. Cardiovasc. Surg., August 1, 2003; 126(2): 521 - 528. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. W. Gaynor Management strategies for infants with coarctation and an associated ventricular septal defect J. Thorac. Cardiovasc. Surg., March 1, 2003; 125(90030): S87 - 89. [Full Text] [PDF]
|
|
|
|
|
|
P. Narasinga Rao, R. N. S. Kumar, D. Anil Kumar, H. M. Mohmoud, S. Chandran, A. K. Dhir, D. K. Saxena, S. P. Azhagappan, V. R. Pillai, C. G. Venkitachalam, et al. Coarctation of the Aorta in Neonates And Young Infants: Surgical Experience Asian Cardiovasc Thorac Ann, December 1, 2002; 10(4): 310 - 313. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. K. Younoszai, V. M. Reddy, F. L. Hanley, and M. M. Brook Intermediate term follow-up of the end-to-side aortic anastomosis for coarctation of the aorta Ann. Thorac. Surg., November 1, 2002; 74(5): 1631 - 1634. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J J O'Sullivan, G Derrick, and R Darnell Prevalence of hypertension in children after early repair of coarctation of the aorta: a cohort study using casual and 24 hour blood pressure measurement Heart, August 1, 2002; 88(2): 163 - 166. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. B. McElhinney, S.-G. Yang, A. N. Hogarty, J. Rychik, M. M. Gleason, C. H. Zachary, J. J. Rome, T. R. Karl, W. M. DeCampli, T. L. Spray, et al. Recurrent arch obstruction after repair of isolated coarctation of the aorta in neonates and young infants: Is low weight a risk factor? J. Thorac. Cardiovasc. Surg., November 1, 2001; 122(5): 883 - 890. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. W. Gaynor Management strategies for infants with coarctation and an associated ventricular septal defect J. Thorac. Cardiovasc. Surg., September 1, 2001; 122(3): 424 - 426. [Full Text] [PDF]
|
|
|
|
|
|
Y. Isomatsu, Y. Imai, T. Shin'oka, M. Aoki, and K. Sato Coarctation of the aorta and ventricular septal defect: Should we perform a single-stage repair? J. Thorac. Cardiovasc. Surg., September 1, 2001; 122(3): 524 - 528. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. I. Tchervenkov, D. Shum-Tim, M. J. Beland, L. Jutras, and R. Platt Single ventricle with systemic obstruction in early life: comparison of initial pulmonary artery banding versus the Norwood operation Eur. J. Cardiothorac. Surg., May 1, 2001; 19(5): 671 - 677. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. A. Bacha, M. Almodovar, D. L. Wessel, D. Zurakowski, J. E. Mayer Jr, R. A. Jonas, and P. J. del Nido Surgery for coarctation of the aorta in infants weighing less than 2 kg Ann. Thorac. Surg., April 1, 2001; 71(4): 1260 - 1264. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. S. Landsman and P. J. Davis Aortic Coarctation: Anesthetic Considerations Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2001; 5(1): 91 - 97. [Abstract] [PDF]
|
|
|
|
|
|
M. Jahangiri, E. A. Shinebourne, D. Zurakowski, M. L. Rigby, A. N. Redington, and C. Lincoln Subclavian flap angioplasty: Does the arch look after itself? J. Thorac. Cardiovasc. Surg., August 1, 2000; 120(2): 224 - 229. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. W. Gaynor, G. Wernovsky, J. Rychik, J. J. Rome, W. M. DeCampli, and T. L. Spray Outcome following single-stage repair of coarctation with ventricular septal defect Eur. J. Cardiothorac. Surg., July 1, 2000; 18(1): 62 - 67. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Haas, C. S. Goldberg, R. G. Ohye, R. S. Mosca, and E. L. Bove Primary repair of aortic arch obstruction with ventricular septal defect in preterm and low birth weight infants Eur. J. Cardiothorac. Surg., June 1, 2000; 17(6): 643 - 647. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Ishino, M. Kawada, H. Irie, K. Kino, and S. Sano Single-stage repair of aortic coarctation with ventricular septal defect using isolated cerebral and myocardial perfusion Eur. J. Cardiothorac. Surg., May 1, 2000; 17(5): 538 - 542. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Cobanoglu, G. K. Thyagarajan, and J. L. Dobbs Surgery for coarctation of the aorta in infants younger than 3 months: end-to-end repair versus subclavian flap angioplasty: is either operation better? Eur. J. Cardiothorac. Surg., July 1, 1999; 14(1): 19 - 26. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Y. Tani, L. L. Minich, L. T. Pagotto, R. E. Shaddy, E. C. McGough, and J. A. Hawkins LEFT HEART HYPOPLASIA AND NEONATAL AORTIC ARCH OBSTRUCTION: IS THERHODES LEFT VENTRICULAR ADEQUACY SCORE APPLICABLE? J. Thorac. Cardiovasc. Surg., July 1, 1999; 118(1): 81 - 86. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Ad and B. A. Vidne Coarctation of the aorta with right aortic arch: surgical technique and new classification Ann. Thorac. Surg., April 1, 1999; 67(4): 1125 - 1129. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. A. Vitullo, S. Y. DeLeon, L. C. Graham, B. W. Eidem, P. T. Roughneen, J. J. Javorski, and F. Cetta Extended end-to-end repair and enlargement of the entire arch in complex coarctation Ann. Thorac. Surg., February 1, 1999; 67(2): 528 - 531. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. I. Tchervenkov, S. A. Tahta, L. Jutras, and M. J. Beland SINGLE-STAGE REPAIR OF AORTIC ARCH OBSTRUCTION AND ASSOCIATED INTRACARDIAC DEFECTS WITH PULMONARY HOMOGRAFT PATCH AORTOPLASTY J. Thorac. Cardiovasc. Surg., December 1, 1998; 116(6): 897 - 904. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. I. Tchervenkov, S. A. Tahta, L. C. Jutras, and M. J. Beland Biventricular repair in neonates with hypoplastic left heart complex Ann. Thorac. Surg., October 1, 1998; 66(4): 1350 - 1357. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. L. Backer, C. Mavroudis, E. A. Zias, Z. Amin, and T. J. Weigel Repair of coarctation with resection and extended end-to-end anastomosis Ann. Thorac. Surg., October 1, 1998; 66(4): 1365 - 1370. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. A. Seirafi, K. G. Warner, R. L. Geggel, D. D. Payne, and R. J. Cleveland Repair of coarctation of the aorta during infancy minimizes the risk of late hypertension Ann. Thorac. Surg., October 1, 1998; 66(4): 1378 - 1382. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Shiokawa and A. E. Becker The Surgical Anatomy of the Left Ventricular Outflow Tract in Hearts With Ventricular Septal Defect and Aortic Arch Obstruction Ann. Thorac. Surg., May 1, 1998; 65(5): 1381 - 1387. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. I. Tchervenkov, S. A. Tahta, R. Cecere, and M. J. Beland Single-Stage Arterial Switch With Aortic Arch Enlargement for Transposition Complexes With Aortic Arch Obstruction Ann. Thorac. Surg., December 1, 1997; 64(6): 1776 - 1781. [Abstract] [Full Text]
|
|
|
|
|
|
J.-P. Pfammatter, G. Ziemer, R. Kaulitz, M. K. Heinemann, I. Luhmer, and H. C. Kallfelz Isolated Aortic Coarctation in Neonates and Infants: Results of Resection and End-to-End Anastomosis Ann. Thorac. Surg., September 1, 1996; 62(3): 778 - 782. [Abstract] [Full Text]
|
|
|
|
|
|
H. A. Rajasinghe, V. M. Reddy, J. A. M. van Son, M. D. Black, D. B. McElhinney, M. M. Brook, and F. L. Hanley Coarctation Repair Using End-to-Side Anastomosis of Descending Aorta to Proximal Aortic Arch Ann. Thorac. Surg., March 1, 1996; 61(3): 840 - 844. [Abstract] [Full Text]
|
|
|
|
|
|
G. B. Luciani, R. J. Ackerman, A. C. Chang, W. J. Wells, and V. A. Starnes ONE-STAGE REPAIR OF INTERRUPTED AORTIC ARCH, VENTRICULAR SEPTAL DEFECT, AND SUBAORTIC OBSTRUCTION IN THE NEONATE: A NOVEL APPROACH J. Thorac. Cardiovasc. Surg., February 1, 1996; 111(2): 348 - 358. [Abstract] [Full Text]
|
|
|
|
 |
|
 C. L. Backer, K. Paape, V. R. Zales, T. J. Weigel, and C. Mavroudis Coarctation of the Aorta : Repair With Polytetrafluoroethylene Patch Aortoplasty Circulation, November 1, 1995; 92(9): 132 - 136. [Abstract] [Full Text]
|
|
|
|
|
|
C. J. Knott-Craig, R. C. Elkins, K. Ramakrishnan, D. A. Hartnett, M. M. Lane, E. D. Overholt, K. E. Ward, and J. R. Razook Associated Atrial Septal Defects Increase Perioperative Morbidity After Ventricular Septal Defect Repair in Infancy Ann. Thorac. Surg., March 1, 1995; 59(3): 573 - 578. [Abstract] [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 |
grade 2 in severity) lesions in the left heart–aorta complex, other than coarctation, in neonates with coarctation, without or with VSD
