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Ann Thorac Surg 1998;66:1350-1357
© 1998 The Society of Thoracic Surgeons
a Division of Cardiovascular Surgery, The Montreal Children’s Hospital, McGill University, Montreal, Quebec, Canada
b Division of Cardiology, The Montreal Children’s Hospital, McGill University, Montreal, Quebec, Canada
Address reprint requests to Dr Tchervenkov, Cardiovascular Surgery, The Montreal Children’s Hospital, Room C-827, 2300 Tupper St, Montreal, PQ H3H 1P3, Canada
Presented at the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and methodsResultsCommentReferences |
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Methods. Since late 1988, all 11 neonates seen with hypoplastic left heart complex, which includes aortic arch obstruction, underwent biventricular repair. All patients had antegrade aortic flow and no intrinsic aortic or mitral stenosis. Elimination of the extracardiac afterload was achieved by extensive ascending aorta and aortic arch reconstruction with a pulmonary homograft patch. All intracardiac shunts were eliminated to fully preload the left heart. The median age at first operation was 7 days and the mean weight, 3.59 ± 0.49 kg. The echocardiographic variables used to evaluate the left heart–aorta complex were reviewed, and the preoperative and postoperative measurements were compared.
Results. There were two early deaths. Four patients had six reoperations for left ventricular outflow tract obstruction, 2 of whom have required prosthetic valve replacement (1, aortic and mitral; 1, aortic), and 2 patients had three reoperations for recurrent coarctation. There was one late death at 3 years from pulmonary hypertension. Mean follow-up was 44 ± 35 months. The 8 current survivors are all in New York Heart Association class I or II. The actuarial survival rate at 8 years is 63%, and the freedom from reoperation at 3 years is 25%.
Conclusions. We have successfully achieved biventricular repair in most of the patients with hypoplastic left heart complex, a subset of patients with hypoplastic left heart syndrome. Some growth of the left ventricular structures was already observed at the time of hospital discharge. However, reoperation, particularly for left ventricular outflow tract obstruction, appears likely. Increasing experience will more accurately define predictive criteria for the feasibility of biventricular repair.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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We have identified a subset of patients with hypoplastic left heart syndrome without intrinsic valvular stenosis and use the term hypoplastic left heart complex (HLHC) to describe this subset. We report here our experience since 1988 with primary biventricular repair for these patients.
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Material and methods |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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Hypoplastic left heart complex consists of multiple hypoplastic structures of the left heart–aorta complex including the mitral valve (MV), the left ventricle, the left ventricular outflow tract (LVOT), and the aortic valve (AV). All 11 patients also had a hypoplastic aortic arch and coarctation of the aorta. Measurements were considered significantly small if they were at least two standard deviations away from the mean. All patients had an LVOT diameter and an AV annulus diameter at least four standard deviations from the normal mean and an MV diameter and left ventricular (LV) dimensions at least two standard deviations from the normal mean. However, our criteria for inclusion in the HLHC cohort were not based on specific size discrimination of the left heart–aorta structures alone. Inclusion criteria also required presence of antegrade flow through the left side of the heart and ascending aorta and absence of intrinsic aortic or mitral stenosis. The obstruction at the valvular level was by virtue of hypoplasia. Four patients had a parachute MV apparatus.
Shunting of blood flow in these patients was present at three levels. All patients had left-to-right shunts at the atrial level through either a secundum atrial septal defect (n = 7), a primum atrial septal defect (n = 1), or a patent foramen ovale (n = 3). Four patients had a ventricular septal defect with a left-to-right shunt (n = 3) or bidirectional shunting (n = 1). Nine patients had a patent ductus arteriosus with a right-to-left shunt (n = 5) or bidirectional shunting (n = 4).
Preoperative status
Ductal dependency was present in 9 patients (82%), who required prostaglandin E1 treatment. Preoperative ventilatory support was necessary for 5 patients (45%). Seven patients (64%) were treated for congestive heart failure with cardiac medications.
Echocardiography
Complete echocardiographic studies were done in all patients preoperatively and postoperatively at least once before discharge. Echocardiographic data were systematically obtained using ATL 51D ultrasound equipment in the first 2 years and Acuson 128XP ultrasound equipment thereafter with 5- and 7-MHz mechanical transducers. Aortic measurements were obtained using a combination of parasternal and suprasternal views at end-systole. Mitral valve and tricuspid valve diameters were measured during diastole from the apical four-chamber projection. Aortic valve diameter and LVOT dimensions were obtained during systole from a parasternal long-axis view. Left ventricular diameters at end-diastole and end-systole and LV and right ventricular long-axis lengths during diastole were measured in the four-chamber view. Left ventricular volumes at end-diastole and end-systole were assessed in M-mode four-chamber projection using Simpson’s computer calculation formatted for the Acuson equipment.
The preoperative echocardiographic data are presented in Table 1. Values are given in absolute measurements and indexed to BSA. The z value is the number of standard deviations away from the mean for a normal population of neonates and is often indexed to BSA.
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All patients underwent repair through a median sternotomy with the use of cardiopulmonary bypass for core cooling to deep hypothermia in preparation for circulatory arrest. The diminutive ascending aorta was carefully cannulated on the right side near the base of the innominate artery. Single venous cannulation of the right atrium was used, and during the cooling period, the patent ductus arteriosus was suture ligated. With the patient under deep hypothermic circulatory arrest, the undersurface of the aortic arch was opened longitudinally from the proximal ascending aorta, past the insertion of the ductus, and into the upper descending thoracic aorta for approximately 1.5 cm. The entire opened aorta was then enlarged with an appropriately fashioned pulmonary homograft patch (Fig 1). Through a right atriotomy, any interatrial communication was closed (except to leave a 2- to 3-mm fenestration for the left side of the heart in 3 recent patients). When present, the ventricular septal defect was closed through the right atriotomy.
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The median bypass time was 140 minutes (range, 122 to 457 minutes). The mean duration of circulatory arrest was 53 ± 9 minutes. Delayed sternal closure was necessary in 7 patients.
Follow-up
Mean follow-up for all hospital survivors was 44 ± 35 months (range, 1 to 99 months). All follow-up data were collected by the Divisions of Cardiovascular Surgery and Cardiology. For patients being followed elsewhere, data were collected from parents and referring cardiologists.
Statistical analysis
All echocardiographic data were expressed first as the mean ± the standard deviation. Certain variables were also indexed to BSA. The Z values indexed to BSA were obtained either by calculation using the mean ± the standard deviation for a normal population at that BSA or by established nomograms or both where possible [2, 3]. Actuarial survival and freedom from reoperation were calculated using the Kaplan-Meier formulas. A p value of less than 0.05 was considered significant.
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Results |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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Early survival
The left heart successfully supported the systemic circulation in 10 of the 11 patients (1 patient died intraoperatively). There were 9 hospital survivors (82%). The second early death involved a patient who had junctional ectopic tachycardia for 4 days and required core cooling. On postoperative day 14, cardiac catheterization was performed because the patient was not improving clinically and needed inotropic and ventilatory support. Cardiopulmonary arrest during catheterization could not be reversed.
Of the 9 survivors, only 2 patients required inotropic support for more than 2 weeks postoperatively. The mean ventilatory support time was 12 ± 7 days. The median hospital stay was 22 days. Two patients were discharged on a regimen of digoxin and 5 patients, on a regimen of furosemide.
Late survival
One late death occurred. The patient died in the early postoperative period after reoperation 39 months later. Severe tunnel subaortic stenosis and biventricular failure with pulmonary hypertension necessitated a modified Konno operation. There was difficulty discontinuing cardiopulmonary bypass, and nitric oxide therapy was instituted. Acute deterioration on postoperative day 3 with biventricular failure led to death. Postmortem examination revealed an acute perioperative myocardial infarction of the right ventricle and, to a lesser extent, the left ventricle, with a single right coronary artery system. More importantly, severe primary pulmonary hypertension was present and was likely the cause of the poor outcome. The overall mortality rate for the group is 27%, with an actuarial survival at 8 years of 63%.
All 8 patients currently alive are well from a cardiac point of view. Their functional status is New York Heart Association class I or II at a follow-up ranging from 1 month to 99 months. One patient is on a regimen of digoxin, enalapril maleate, and furosemide and another, furosemide. The remaining 6 patients do not need cardiac medication.
Reoperations
Six of the 9 early survivors have had a total of nine reoperations. The freedom from reoperation at 3 years is 25%.
Four patients underwent six reoperations for LVOT obstruction from 12 to 39 months after the initial operation. One had a modified Konno operation with repair of supravalvar aortic stenosis and mitral valvuloplasty for a cleft MV (severe mitral regurgitation) at 13 months of age. Severe mitral regurgitation caused by double-orifice MV and aortic insufficiency resulting from a perforation in the anterior leaflet developed. When she was 5
years old, the patient underwent MV replacement (25-mm CarboMedics) and AV replacement (16-mm CarboMedics). Also, the aortic root was enlarged with a Dacron patch. The second patient had a Konno operation and AV replacement with an aortic homograft at 14 months of age. She was seen when she was 7 years old with recurrent LVOT obstruction, severe aortic regurgitation, and mitral stenosis with a parachute MV and underwent a redo Konno operation with AV replacement (21-mm prosthetic valve) and MV papillary muscle splitting. The third patient required aortic valvotomy and resection of subaortic stenosis at 15 months of age. She concurrently underwent resection of recoarctation with end-to-end anastomosis. The fourth patient died after a modified Konno operation, as already mentioned.
Two other patients have required three reoperations for recurrent coarctation. The first patient underwent resection with end-to-end anastomosis at 5 months of age and a repeat resection with patch aortoplasty at 21 months. The second patient had resection and end-to-end anastomosis at 4 months of age.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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We have identified a subset of patients with hypoplastic left heart syndrome with hypoplasia of all the structures within the left heart–aorta complex without intrinsic aortic or mitral stenosis. We have adopted the term hypoplastic left heart complex to describe this subset. The main purpose of this term is to isolate this subset from the patients with classic hypoplastic left heart syndrome, who should be considered for biventricular repair. In our opinion, none of the currently existing diagnoses or terms adequately describes patients with HLHC. Critical aortic stenosis or congenital mitral stenosis cannot be used for obvious reasons. The diagnosis of hypoplastic left heart syndrome is not specific enough and implies the impossibility of a two-ventricle repair. The term Shone’s anomaly fails to address the fundamental importance of the hypoplasia of the multiple structures in the left heart–aorta complex, particularly that of the left ventricle [6, 7]. In addition, the diagnosis of HLHC will allow a more accurate comparison of outcomes between different centers for these patients. The following six criteria must be fulfilled for a diagnosis of HLHC: MV hypoplasia without intrinsic stenosis; LV hypoplasia; LVOT obstruction; AV hypoplasia without intrinsic stenosis; aortic arch obstruction; and antegrade flow through the left heart and the ascending aorta into the vessels of the head.
Hypoplastic left heart syndrome has been a difficult structural heart defect to repair and causes a substantial mortality. The debate between heart transplantation and palliation with the Norwood operation followed eventually by a Fontan operation is unresolved [8]. Each approach is lifesaving but not without the cost of lifelong immunosuppression and risk of rejection or infection, or multiple operations with a right ventricle–dependent systemic circulation. A biventricular repair, although preferable, has usually not been possible. Yet there is a large variability in the degree of hypoplasia of the structures in the left heart–aorta complex. How small is too small to support the systemic circulation, and what happens when multiple hypoplastic structures are encountered without intrinsic valvular stenoses? The left ventricle must be of adequate size to function as the systemic pump, but it must also be associated with adequate inflow and outflow orifices and no distal obstruction against which to pump [9]. The functional consequence is likely to be that these abnormalities are additive and that the cumulative impact of small structures is severe [9]. The ability to perform the Norwood operation or neonatal heart transplantation has impeded the accurate determination of the critical sizes required for biventricular repair. Some even refer to the Norwood operation as the "universal operation," as it can be performed in any neonatal heart with a good right ventricle. On the other hand, the two-ventricle approach requires accurate determination of the lowest limits of the left heart structures that can sustain the systemic circulation.
There has been limited success in identifying echocardiographic variable predictive of a successful biventricular repair [10]. Multiple anatomic structures, each with such variability, make this task difficult. This retrospective study used variables previously defined to assess a cohort of patients with HLHC and preoperative anatomic structures smaller than previously published. Most of the previous reports dealt with critical aortic stenosis alone [9, 11, 12]. One issue in this body of literature is which echocardiographic factors should be used, and then, what cutoffs are predictive of survival in biventricular repair of critical aortic stenosis instead of a single-ventricle approach. Rhodes and associates [9] claimed the best accuracy for predicting survival with the indexed MV area, LV long axis relative to total length of the heart, and indexed aortic root size. The critical levels were 4.75 cm2/m2, 0.8, and 3.5 cm/m2, respectively. A careful comparison with our data suggests that we exceeded predicted survival with structural measurements mostly lower than these. This excludes indexed MV area, which we did not measure.
Other investigators [13] have suggested that LV volume determination is important and that survival with a biventricular repair is unlikely with indices less than 20 cm3/m2. We have disproved this observation, but it remains controversial in the literature [14]. Karl and co-workers [11] stated that for critical aortic stenosis, a biventricular repair is not appropriate if the cardiac apex is not formed by the left ventricle or if dimensions of the heart are less than 60% mean for body weight. Leung and colleagues [12] suggested that an unfavorable result can be predicted if the LV inflow dimension is less than 25 mm, the ventriculoaortic junction is smaller than 5 mm, and the MV diameter is less than 9 mm. It is unclear how accurately the data derived from patients with critical aortic stenosis apply to patients with HLHC. The conservative approach of either surgical or balloon valvotomy, to avoid major aortic regurgitation, probably leaves a smaller central orifice than that in the HLHC patients. Furthermore, the pinhole orifice seen in critical aortic stenosis probably stimulates a much greater LV hypertrophy, with consequent decreases in LV compliance and diastolic function. It is perhaps for these reasons that most of the measurements from our patients successfully undergoing biventricular repair fall below these criteria.
This retrospective study reviews the structural components of what we have defined as HLHC and the outcome in a series of patients. Since 1988, 11 patients have fit the criteria preoperatively, and we have attempted biventricular repair in all of them. Each structure in the left heart–aorta complex was consistently hypoplastic. The postoperative hemodynamics can be very worrisome immediately after cardiopulmonary bypass, as depicted by the high LAPs. It is important to be persistent in managing this with inotropic support, as the trend in LAP is downward as early as 6 hours postoperatively. The LAP returns to almost normal by 24 hours after operation. In only 1 patient was the hypoplastic left heart unable to support the systemic circulation, and this patient did not have the smallest left heart structures in this series.
It is difficult to make any predictive comments on the lower limits of the feasibility of biventricular repair because of the small number of patients in our series and the variable contribution of each hypoplastic structure. Other studies have explained that the size of the LV cavity exclusively does not correlate well with prognosis [9, 14, 15]. We agree that as a result of the tremendous variability in this one anatomic structure, it is necessary to look at other factors and structures as previously described. One criticism in measuring LV cavity size has been that it could appear small because of compression and displacement by a dilated right ventricle [16]. This has not been the case in our experience; the ventricular septum was in a neutral position in all patients.
We had three primary surgical objectives that we considered necessary for success: total elimination of the extracardiac afterload, elimination of all intracardiac shunts to fully preload the left heart, and use of a conservative approach for the inflow and outflow obstructions of the left ventricle. The first objective was achieved by extensive enlargement of the ascending aorta and aortic arch to the proximal descending aorta. This was accomplished with a pulmonary homograft patch, as depicted in Figure 1. The second objective was achieved by closing every ventricular septal defect, atrial septal defect, patent foramen ovale, and patent ductus arteriosis. More recently, a 2- to 3-mm interatrial fenestration has been left in place. We think this enables growth and dilatation of the left heart structures to better support the systemic circulation while protecting the left heart from extreme overload and failure. The third objective simplifies the operation and likely contributes to the good early survival.
Our current approach emphasizes noninvasive diagnosis and follow-up in this cohort of patients. All patients underwent at least one postoperative echocardiogram during the hospital stay to reevaluate the left heart structures. These data clearly show some tendency toward normalization of heart structure sizes. The question is whether this is real growth or dilatation secondary to full preloading of the left heart. At late follow-up, the MV and left ventricle both increased to within two standard deviations from the norm. The LVOT, however, does not seem to grow adequately. The subaortic region and aortic annulus remain proportionately small as the patients grow. This is clinically significant, and leads to reoperation for severe LVOT obstruction often within 3 years.
Obstruction of the LVOT is a major late problem and requires reoperation in a substantial number of patients. Using this cohort of patients with HLHC as the standard for measurements, the subaortic area and ventriculoaortic junction are the smallest structures in the left heart–aorta complex. Despite our hypothesis that anatomic afterload reduction would allow the growth of this area, this did not occur consistently. One reason may be that the fibrous annulus restricts early dilatation and eventual accelerated growth. It appears that the LVOT diameter is fixed and grows only proportionately to body growth. This translates into a high probability of reoperation on the LVOT and AV. Four of the 8 patients who have survived longer than a year after initial surgical repair have required reoperation for severe LVOT obstruction.
The hospital survival rate of 82% is significantly higher than the 88% mortality rate reported for similar patients by the Congenital Heart Surgeons Society [5] for coarctation associated with two or more obstructions in the left heart–aorta complex. The actuarial survival at 8 years in our group is 63%. This is comparable to survival statistics for groups with hypoplastic left heart syndrome undergoing heart transplantation (including patients who die while waiting for a donor heart) or stage-one palliation and an eventual Fontan or patients with critical aortic stenosis undergoing univentricular or biventricular repair [8, 17, 18]. The main issue is the size of the left heart–aorta structures, which, in most centers, precludes biventricular repair in patients with small structures, as in this cohort. We believe that biventricular repair will likely result in a better long-term prognosis than a univentricular approach, where the morphologic right ventricle functions as the systemic ventricle.
In conclusion, we have successfully achieved biventricular repair in most patients with HLHC, a subset of patients with hypoplastic left heart syndrome. Some growth of the left heart structures was observed at the time of hospital discharge. However, reoperation, particularly for LVOT obstruction, appears likely. Increasing experience will more accurately define the lower limits for the feasibility of biventricular repair.
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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References |
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TopFootnotesAbstractIntroductionMaterial and methodsResultsCommentReferences |
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