ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Meena Nathan
Pedro J. del Nido
John E. Mayer
Emile A. Bacha
Rodrigo Gonzalez
Frank Pigula
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nathan, M.
Right arrow Articles by Pigula, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nathan, M.
Right arrow Articles by Pigula, F.
Related Collections
Right arrow Congenital - acyanotic

Ann Thorac Surg 2006;82:2227-2232
© 2006 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Aortic Atresia or Severe Left Ventricular Outflow Tract Obstruction with Ventricular Septal Defect: Results of Primary Biventricular Repair in Neonates

Meena Nathan, MDa, David Rimmer, MSa, Pedro J. del Nido, MDa, John E. Mayer, MDa, Emile A. Bacha, MDa, Andrew Shin, MDb, William Regan, MSa, Rodrigo Gonzalez, MDa, Frank Pigula, MDa,*

a Department of Cardiac Surgery, Harvard Medical School, Children’s Hospital Boston, Boston, Massachusetts
b Department of Cardiology, Harvard Medical School, Children’s Hospital Boston, Boston, Massachusetts

Accepted for publication May 18, 2006.

* Address correspondence to Dr Pigula, Department of Cardiac Surgery, Children’s Hospital, Bader 273, 300, Longwood Ave, Boston, MA 02115 (Email: frank.pigula{at}childrens.harvard.edu).

Presented at the Poster Session of the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Aortic atresia or severe aortic stenosis and left ventricular outflow tract obstruction is a frequent component of complex congenital heart disease. Aortic atresia or severe aortic stenosis and left ventricular outflow tract obstruction with two adequate ventricles is sometimes treated by Norwood palliation followed by late biventricular repair. We reviewed our experience with primary biventricular repair in this group of neonates.

METHODS: Retrospective review identified 17 neonates (10 males) with aortic atresia or severe left ventricular outflow tract obstruction with ventricular septal defect and an adequate left ventricle undergoing primary biventricular repair between 1986 and 2002. Mean age was 7.7 ± 2.9 days, weight 3.3 ± 0.7 kg, and body surface area 0.21 ± 0.04 kg/m2. Associated anomalies included arch hypoplasia, 7 (41%); aortic atresia, 7 (41%); and coarctation, 5 (29%). Results are reported as mean ± standard deviation.

RESULTS: Median follow-up was 6 years (range, 1 to 17.7 years). Three of the 17 (18%) died within 30 days. There were no deaths in this series since 1992. Nine patients (38.9%) required one reoperation, 7 of which were for conduit stenosis, 1 for left ventricular outflow tract obstruction, and 1 for residual ventricular septal defect with left ventricle–to–right atrium shunt. Freedom from death at 10 years was 82% by Kaplan–Meier estimate.

CONCLUSIONS: Excellent long-term survival can be achieved by primary biventricular repair as corroborated by our survival rate of 82%. Primary biventricular repair is an effective operation for aortic atresia and severe left ventricular outflow tract obstruction with adequate sized left ventricle that avoids interstage attrition associated with Norwood palliation and is our procedure of choice.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Hypoplastic left heart syndrome includes a wide spectrum of cardiac malformations with varying degrees of underdevelopment of the structures of the left heart and aorta. At one end of the spectrum is complete atresia of aortic and mitral valves and a diminutive left ventricle (LV) incapable of supporting the systemic circulation. At the other end of the spectrum are milder forms of aortic stenosis and mitral stenosis with a reasonable sized LV. Depending on the severity of the obstructive lesions, surgical management of neonates with hypoplastic left heart structures [1] involves one of three options: (1) Norwood palliation, (2) cardiac transplantation, or (3) biventricular repair (BVR).

Aortic atresia (AA) or severe LV outflow tract obstruction (LVOTO) with an associated ventricular septal defect (VSD) in the presence of an adequate LV is an infrequent combination. The management strategy for this rare group of lesions clearly depends on the adequacy of the LV inflow, ie, the mitral valve dimensions, as well as the adequacy of the LV chamber dimensions. The treatment options for this group of lesions involve one of the following:

(1) Staged approach: initial Norwood followed by delayed BVR. The second stage in this approach consists of baffling of the LV to the Stansel connection (main pulmonary artery [PA] to aortic anastomosis), establishment of right ventricular (RV) to PA connection, closure of the atrial septal defect, and takedown of the systemic to PA shunt. The disadvantages of this staged procedure is the existence of a parallel circulation with its resultant volume overload, and the assumption of risks associated with the shunted single ventricle circulation that results in interstage attrition of 4% to 16% [2, 3].
(2) Primary BVR: This approach consists of a Stansel anastomosis with arch augmentation as necessary. The VSD baffles LV output through both the aortic and pulmonary valves into the systemic circulation. An RV to PA homograft completes the repair. This approach was first described by Yasui [4]. The clear advantage of neonatal BVR is the early establishment of circulation in series. Subjecting a hypoplastic LV to normal or near normal preload allows for postnatal growth toward normal [5–7].

Decision-making involves careful assessment of preoperative studies including echocardiogram or catheterization data with special attention paid to the size of the mitral valve, LV dimensions, the position of the VSD, and likely path of the LV to pulmonary valve baffle and its effect on the ventricular outflow tracts. We reviewed our experience with primary BVR in this group of neonates.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
We undertook a retrospective chart review, which revealed 17 neonates (10 males) with AA or severe LVOTO and VSD who had undergone primary BVR between 1986 and 2002 at Children’s Hospital, Boston. This retrospective chart review was approved by the Institutional Review Board at Children’s Hospital, and parental consent was waived. All data were procured according to guidelines established by the committee on clinical investigation.

All patients’ preoperative studies including echocardiograms and catheterization studies were reviewed. The following data were obtained from the preoperative echocardiograms: mitral valve diameter (anteroposterior and lateral), aortic valve diameter, aortic root diameter, aortic arch (transverse arch) diameter, LV and RV length in the four-chamber view, and corresponding calculated z scores. Special attention was paid to mitral valve and LV dimensions as these were considered the primary determinants of suitability for BVR. The VSD size and location was also documented.

All charts were reviewed for operative variables. Variables of interest included patient survival, procedure performed, cardiopulmonary bypass times, aortic cross-clamp times, circulatory arrest times, and homograft size. Postoperative variables of interest were length of intensive care unit stay, length of hospital stay, duration of ventilatory support, surgical and catheter reinterventions, surgical complications, and length of follow-up.

Follow-up data were obtained by review of hospital and clinic charts and databases. Details of follow-up clinic visits, echocardiograms and catheterization, and reoperations were obtained and reviewed.

Results are reported as mean ± standard deviation. Probabilities of survival and freedom from reoperation were estimated using the Kaplan–Meier method.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
Patient demographics and diagnoses are outlined in Tables 1 and 2. Go There were 10 males and 7 females. Mean age at operation was 7.7 ± 2.9 days, mean weight was 3.3 ± 0.7 kg, and mean body surface area was 0.21 ± 0.04 kg/m2. All 17 patients had a VSD and some form of LVOTO. Seven (41%) had AA and 10 (59%) had aortic stenosis or sub–aortic stenosis. Associated anomalies included arch hypoplasia in 7 (41%), coarctation in 7 (41%), and interrupted aortic arch in 5 (29%).


View this table:
[in this window]
[in a new window]

  		Table 1. Diagnosis
 

View this table:
[in this window]
[in a new window]

  		Table 2. Preoperative Echocardiographic Data
 
All patients had preoperative echocardiograms. Four patients had preoperative cardiac catheterization to further delineate anatomy. The average LV long-axis dimension was 29.5 ± 3.8 mm with a mean z score of –0.09. Similarly the average mitral valve diameter was 9.79 ± 3.5 mm with a mean z score of +1.26,, all indicative of adequacy of LV inflow and chamber to support a BVR. Figures 1 and 2 Go depict representative preoperative images. Preoperative echocardiographic data are presented in Table 2.


Figure 1
View larger version (122K):
[in this window]
[in a new window]

  		Fig 1. Preoperative cardiac catheterization of atretic ascending aorta with coronary arteries well outlined.

 

Figure 2
View larger version (127K):
[in this window]
[in a new window]

  		Fig 2. Preoperative cardiac catheterization depicting ventricular septal defect (VSD).

 
All of the patients had a Yasui operation [4] as described above (Fig 3). Aortic cross-clamp time was 96 minutes (range, 65 to 134 minutes), circulatory arrest time was 65 minutes (range, 13 to 135 minutes), and cardiopulmonary bypass time was 211 minutes (range, 144 to 365 minutes). Homograft size was 10.96 ± 2.67 mm (range, 7 to 17 mm). Duration of mechanical ventilation was 7 days (range, 1 to 20 days), average intensive care unit stay was 13 days (range, 2 to 33 days), and total hospital stay was 20 days (range, 6 to 57 days). Median follow-up was 6 years (range, 1 to 17.7 years). Nine patients (53%) required one reoperation, 7 of which were for conduit stenosis. There was only one reoperation for LVOTO and one for a residual VSD resulting in an LV to right atrial shunt. In addition 3 patients in this group of 9 had arch narrowing that required surgical intervention at the time of their first reoperation. One patient had a residual VSD closed at the time of conduit change. In this group of 9 patients, 4 required a second reoperation for conduit stenosis, 1 required a third reoperation for conduit replacement, and 1 required a fourth reoperation for conduit revision. The diagnoses at reoperation are represented in Table 3, and complications in Table 4.


Figure 3
View larger version (98K):
[in this window]
[in a new window]

  		Fig 3. Yasui procedure consisting of a Stansel connection and arch augmentation, ventricular septal defect baffle of left ventricle to pulmonary artery, and right ventricle to pulmonary artery valved conduit.

 

View this table:
[in this window]
[in a new window]

  		Table 3. Reoperations
 

View this table:
[in this window]
[in a new window]

  		Table 4. Complications
 
There were 3 early deaths, all secondary to biventricular failure. All patients had AA and hypoplastic aortic arch with normal z score for mitral valve and LV dimensions. The first patient died within 24 hours of biventricular failure and pseudomonas bacteremia. The second patient died 28 days postoperatively of biventricular failure leading to multisystem organ failure. Of note, the postoperative course was complicated by Enterobacter spp sepsis. The third patient died on postoperative day 2 of biventricular failure. All 3 patients had autopsies, which revealed no evidence of obstruction to coronary flow, no residual VSD, no obstruction in the LV to neoaortic pathway, and no evidence of arch obstruction. All deaths occurred in the first 6 years of the study period.

Nine patients had follow-up catheterization and interventions, which included dilatation of coarctation (8 interventions), conduit dilatation or stenting (11 interventions), and branch PA dilatation or stenting (8 interventions). Only 3 of the 14 survivors have had no catheter or surgical reintervention (18%) with a mean follow-up of 8.5 years in the survivors. Freedom from death by Kaplan–Meier estimate at 10 years was 82% (Fig 4).


Figure 4
View larger version (13K):
[in this window]
[in a new window]

  		Fig 4. Kaplan–Meier curves of freedom from death and reoperation at 10 years; the number at risk at each time interval is depicted above the x-axis. The top row of numbers indicates risk for death and bottom row the risk for reoperation at each time interval.

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
Hypoplasia of the left heart falls along an anatomic spectrum that may include hypoplasia of the mitral valve, LV, aortic valve, and aorta. In its most severe form, hypoplastic left heart syndrome, severe hypoplasia of these structures renders the left heart incapable of supporting the systemic circulation, and requires staged palliation. In less severe forms, in which aortic valve or aortic hypoplasia exists in the presence of adequate LV and mitral valve dimensions [8–10], the left heart may be suitable for inclusion into the systemic circulation.

Two surgical strategies are pursued in the treatment of these patients. One strategy favors a staged approach in which initial palliation is provided by a stage I operation, followed by subsequent consideration of a BVR. The alternate approach is primary BVR as a neonate.

The potential advantages of primary BVR include early normalization of physiology, without assumption of risk associated with the palliated single ventricle. Although in general these patients do not have significant hypoplasia of the LV, and possess more cardiovascular reserve than patients with classic hypoplastic left heart syndrome, the shunted circulation remains unstable relative to a biventricular circulation.

The operative approach to primary BVR was first published by Yasui and colleagues [4]. The VSD is patched to both semilunar valves, the arch is enlarged as necessary, and a homograft is placed between the RV and the PAs. Although some authors have suggested an REV modification [11] to this procedure, thus avoiding the placement of a homograft between the RV and the PAs, it is our opinion that a valved conduit is important, especially in the early postoperative period.

The decision to proceed to neonatal BVR depends on accurate and precise preoperative anatomic information. The ability of a hypoplastic LV to support the systemic circulation in the presence of critical aortic stenosis requires that the mitral valve dimensions and LV end-diastolic dimensions be near normal.

Schwartz and associates [12] found that the presence of a moderate to large VSD, unicommissural aortic valves, hypoplastic mitral valve (z scores < –2), and hypoplastic LV with low LV end-diastolic volume (z scores < –2) were risk factors for failure of BVR in multiple left heart obstructive lesions. Although the patients in the current report had very abnormal aortic valves, the mitral valve and LV dimensions fell within the normal range (–2 < z scores < 2). Even in the setting of modest LV hypoplasia, there appears to be the potential for LV growth [5–7, 13]. McElhinney and colleagues [5] in their review of 113 neonates who had undergone balloon valvuloplasty were able to demonstrate that LV end-diastolic dimensions normalized within the first 1 to 2 years of life. It has been shown that as complete relief as possible of LVOTO at all levels should be the goal of intervention [13–15]. These principles and observations underlie the ongoing efforts related to aggressive recruitment of the LV into the systemic circulation, even during the fetal period [6, 7].

If, after anatomic evaluation, the patient is deemed suitable for BVR, the choice between primary or staged repair must be made. Pearl and associates [16] reported their series of 8 neonates undergoing staged repair to a biventricular circulation. Six of 8 underwent successful BVR at an average age of 7 months, with 1 awaiting repair and 1 palliated to a Glenn shunt.

In a series of 28 neonates with interrupted aortic arch reported by Erez and coworkers [17], 13 had severe LVOTO and were palliated with a stage I procedure, with no operative deaths. However 2 patients required arteriopulmonary shunt revision within 1 month of initial palliation, and 2 patients with DiGeorge syndrome died of infection. Six of the survivors went on to undergo BVR (3 after bidirectional Glenn operation). One patient had a Fontan operation, and 5 patients are awaiting definitive surgery with a bidirectional Glenn.

Ohye and colleagues [18] compared staged versus primary BVR in a cohort of 20 patients with AA and VSD and showed no statistical difference, with an actuarial survival at 5 years of 89% for the staged repair and 73% for the BVR. The authors recommended BVR as the preferred approach. Our current report, documenting 82% survival at 10 years, supports a calculation even more favorable to primary BVR.

Interstage period of the shunted single-ventricle circulation remains a vulnerable time for the child. Although interstage mortality for patients with true hypoplastic left heart syndrome has been reported to be as high as 15%, patients presenting with a normal or near normal LV are not immune. Daebritz and associates [19] compared their results of traditional Norwood procedure for hypoplastic left heart syndrome versus primary BVR in a second group with left-side obstructions at different levels but with near normal LV (LV long axis was 80% of the long axis of the heart) prospectively. They had 10 patients who underwent staged palliation with 1 early death and 2 interstage deaths. All 3 patients in the primary BVR group did well at 1 year of follow-up. This experience provides an additional motivation to pursue primary repair, avoiding the potential disadvantages associated with the palliated single-ventricle circulation [20–22].

The 3 deaths in this series occurred early as a result of biventricular failure. All of these patients had a very small ascending aorta, and coronary ischemia must be considered a likely factor. It should be noted that since 1992, there have been no deaths in patients undergoing primary neonatal repair, and the long-term survival is gratifying. Although reoperation is unavoidable when pursuing either approach, homograft replacement is relatively straightforward and low risk.

In summary, primary BVR of neonates with AA or severe LVOTO results in excellent 10-year survival. This approach avoids a vulnerable period associated with the shunted single ventricle. When the anatomy allows, this is our preferred approach to the surgical management of these patients.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
We would like to thank Kimberley Gauvreau, ScD, for assistance with statistics.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Morell VO, Quintessenza JA, Jacobs JP. Biventricular repair in the management of hypoplastic left heart syndrome Cardiol Young 2004;14(Suppl 1):101-104.[Medline]
  2. Daebritz SH, Nollert GD, Zurakowski D, et al. Results of Norwood stage I operation: comparison of hypoplastic left heart syndrome with other malformations J Thorac Cardiovasc Surg 2000;119:358-367.[Abstract/Free Full Text]
  3. Mahle WT, Spray TL, Gaynor JW, Clark 3rd BJ. Unexpected death after reconstructive surgery for hypoplastic left heart syndrome Ann Thorac Surg 2001;71:61-65.[Abstract/Free Full Text]
  4. Yasui H, Kado H, Nakano E, et al. Primary repair of interrupted aortic arch and severe aortic stenosis in neonates J Thorac Cardiovasc Surg 1987;93:539-545.[Abstract]
  5. McElhinney DB, Lock JE, Keane JF, Moran AM, Colan SD. Left heart growth, function, and reintervention after balloon aortic valvuloplasty for neonatal aortic stenosis Circulation 2005;111:451-458.[Abstract/Free Full Text]
  6. Marshall AC, Tworetzky W, Bergersen L, et al. Aortic valvuloplasty in the fetus: technical characteristics of successful balloon dilation J Pediatr 2005;147:535-539.[Medline]
  7. Tworetzky W, Wilkins-Haug L, Jennings RW, et al. Balloon dilation of severe aortic stenosis in the fetus: potential for prevention of hypoplastic left heart syndrome: candidate selection, technique, and results of successful intervention Circulation 2004;110:2125-2131.[Abstract/Free Full Text]
  8. Tchervenkov CI, Tahta SA, Jutras LC, Beland MJ. Biventricular repair in neonates with hypoplastic left heart complex Ann Thorac Surg 1998;66:1350-1357.[Abstract/Free Full Text]
  9. Tchervenkov CI. Two-ventricle repair for hypoplastic left heart syndrome Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 2001;4:83-93.[Medline]
  10. Tchervenkov CI. Indications, criterions, and principles for biventricular repair Cardiol Young 2004;14(Suppl 1):97-100.[Medline]
  11. Black MD, Smallhorn JF, Freedom RM. Aortic atresia with a ventricular septal defect: modified single-stage neonatal biventricular repair Ann Thorac Surg 1999;67:751-755.[Abstract/Free Full Text]
  12. Schwartz ML, Gauvreau K, Geva T. Predictors of outcome of biventricular repair in infants with multiple left heart obstructive lesions Circulation 2001;104:682-687.[Abstract/Free Full Text]
  13. Alboliras ET, Mavroudis C, Pahl E, Gidding SS, Backer CL, Rocchini AP. Left ventricular growth in selected hypoplastic left ventricles: outcome after repair of coarctation of aorta Ann Thorac Surg 1999;68:549-555.[Abstract/Free Full Text]
  14. Minich LL, Tani LY, Hawkins JA, Shaddy RE. Possibility of postnatal left ventricular growth in selected infants with non-apex-forming left ventricles Am Heart J 1997;133:570-574.[Medline]
  15. Serraf A, Piot JD, Bonnet N, et al. Biventricular repair approach in ducto-dependent neonates with hypoplastic but morphologically normal left ventricle J Am Coll Cardiol 1999;33:827-834.[Abstract/Free Full Text]
  16. Pearl JM, Cripe LW, Manning PB. Biventricular repair after Norwood palliation Ann Thorac Surg 2003;75:132-137.[Abstract/Free Full Text]
  17. Erez E, Tam VK, Kanter KR, Fyfe DA. Successful biventricular repair after initial Norwood operation for interrupted aortic arch with severe left ventricular outflow tract obstruction Ann Thorac Surg 2001;71:1974-1977.[Abstract/Free Full Text]
  18. Ohye RG, Kagisaki K, Lee LA, Mosca RS, Goldberg CS, Bove EL. Biventricular repair for aortic atresia or hypoplasia and ventricular septal defect J Thorac Cardiovasc Surg 1999;118:648-653.[Abstract/Free Full Text]
  19. Daebritz SH, Tiete AR, Rassoulian D, et al. Borderline hypoplastic left heart malformations: Norwood palliation or two-ventricle repair? Thorac Cardiovasc Surg 2002;50:266-270.[Medline]
  20. Bartram U, Grunenfelder J, Van Praagh R. Causes of death after the modified Norwood procedure: a study of 122 postmortem cases Ann Thorac Surg 1997;64:1795-1802.[Abstract/Free Full Text]
  21. Krasemann T, Fenge H, Kehl HG, et al. A decade of staged Norwood palliation in hypoplastic left heart syndrome in a midsized cardiosurgical center Pediatr Cardiol 2005;26:751-755.[Medline]
  22. Ashburn DA, McCrindle BW, Tchervenkov CI, et al. Outcomes after the Norwood operation in neonates with critical aortic stenosis or aortic valve atresia J Thorac Cardiovasc Surg 2003;125:1070-1082.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 J. Thorac. Cardiovasc. Surg.Home page
P. B. Blasco, J. G. Comas, A. G. Estella, Q. F. Menduna, M. C. C. Dominguez, J. B. Ramirez, B. M. Garcia, and F. G. Ipina
Hybrid approach as a bridging procedure to biventricular repair for aortic hypoplasia with ventricular septal defect in a 1720-g premature infant
J. Thorac. Cardiovasc. Surg., August 1, 2007; 134(2): 516 - 518.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Meena Nathan
Pedro J. del Nido
John E. Mayer
Emile A. Bacha
Rodrigo Gonzalez
Frank Pigula
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nathan, M.
Right arrow Articles by Pigula, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nathan, M.
Right arrow Articles by Pigula, F.
Related Collections
Right arrow Congenital - acyanotic

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