Eur J Cardiothorac Surg 2006;30:910-916
© 2006 Elsevier Science NL
Surgical repair of coarctation of the aorta: up to 40 years of follow-up
Hilde Høimyra,
Thomas D. Christensena,
Kristian Emmertsenb,
Søren P. Johnsenc,
Anders Riisc,
Ole Kromann Hansena,
Vibeke E. Hjortdala,*
a Department of Cardiothoracic and Vascular Surgery and Institute of Clinical Medicine, Skejby Sygehus, Aarhus University Hospital, DK-8200 Aarhus N, Denmark
b Department of Cardiology and Institute of Clinical Medicine, Skejby Sygehus, Aarhus University Hospital, DK-8200 Aarhus N, Denmark
c Department of Clinical Epidemiology and Institute of Clinical Medicine, Aarhus University Hospital, DK-8000 Aarhus C, Denmark
Received 13 July 2006;
received in revised form 1 September 2006;
accepted 17 September 2006.
* Corresponding author. Address: Department of Cardiothoracic and Vascular Surgery and Institute of Clinical Medicine, Skejby Sygehus, Aarhus University Hospital, DK-8200 Aarhus N, Denmark. Tel.: +45 8949 5484; fax: +45 8949 6016. (Email: Vibeke.hjortdal{at}dadlnet.dk).
 |
Abstract
|
|---|
Objective: Coarctation of the aorta (CoA) was previously considered cured after surgical repair. Evidence for excess mortality and late morbidity has later accumulated, although studies with long-term follow-up remain sparse. The aim was to identify patients operated for CoA at Aarhus University Hospital, Denmark between 1965 and 1985 and to assess surgical and late mortality and cardiovascular morbidity in this cohort and possible predictors for an adverse outcome. Methods: Two hundred and twenty nine patients were identified. Baseline characteristics and morbidity and mortality data were obtained from medical records, registries and databases and analysed by Kaplan–Meier graphs and multivariate Cox regression analyses. Results: There were 14 (6%) surgical deaths. The survival in patients who were alive 30 days postoperatively was 95% 10 years after surgery, and 91%, 83% and 69% after 20, 30 and 40 years, respectively. The mortality rate ratio for all long-term survivors compared with an age- and sex-matched reference group was 4.3 (2.9–6.4). In those with no cardiovascular comorbidity at the time of repair, it was 3.4 (1.8–6.4). The causes of late deaths were cardiovascular in 63%. CoA repair in the early decade, age below 1 year at repair and high level of comorbidity were predictors for late mortality. Twenty five percent of current survivors were on antihypertensive medication and further cardiovascular morbidity had occurred in 46 (26%), including cardiovascular surgery and catheter interventions in 35 (19%). Freedom from death, reintervention and cardiovascular complications other than hypertension was 60% 30 years after surgery in the entire study population. Conclusions: Repaired CoA is associated with excess cardiovascular mortality and morbidity and often in need of reintervention. These patients, therefore, need careful follow-up.
Key Words: Aorta • Coarctation • Congenital heart disease (CHD) • Surgery • Outcomes
|
1. Introduction
|
|---|
Untreated coarctation of the aorta (CoA) is associated with premature mortality and morbidity. Campbell [1] described a median age at death of 31 years in autopsy series of patients with CoA reported by Abbott [2] and Reifenstein et al. [3]. These postmortem studies did not include patients below the age of 2 years, underestimating the seriousness of this condition. The first surgical repair of CoA was performed by Crafoord and Nylin [4] in 1944. Initially, surgical mortality was high, and there was a natural selection of patients surviving until the diagnosis was made and repair could be performed [5,6]. Today, neonates and even premature children are operated on with low short-term mortality [7]. Endovascular balloon angioplasty for CoA was introduced in 1982 [8], and supplemented by stent implantation 10 years later [9]. In the early years, repair for CoA was considered curative and no systematic follow-up was done [10]. Later, it became clear that CoA, even after successful repair, is associated with an increased risk of later development of recoarctation (reCoA), systemic hypertension, cerebrovascular disease, premature atherosclerosis and formation of aortic aneurisms [11–13].
At Aarhus University Hospital, Denmark, regular clinical follow-up after surgical treatment of CoA was introduced in the late 80s. Before then, some were seen as outpatients within the first postoperative year, but none were enrolled in longitudinal follow-up unless residual cardiovascular problems had been identified. Some of the patients were later readmitted from local hospitals or by general practitioners for reassessment, but the outcome for the majority of patients who had undergone surgical treatment before 1986 was unknown.
The aim of this study was to identify patients who underwent surgery for CoA during 1965–1985 at Aarhus University Hospital, and to assess surgical and late mortality and morbidity in this cohort, thereby also identifying survivors who could be targeted for systematic clinical follow-up in order to prevent long-term complications. We further wanted to examine the role of possible risk factors for surgical and late mortality.
|
2. Materials and methods
|
|---|
2.1 Study population
We identified the cohort of patients by reviewing the protocols of all cardiothoracic operations performed between January 1, 1965 and December 31, 1985. Patients who underwent surgery after 1971 were registered in the protocols by a national unique 10-digit personal identification (PIN) number, making it possible to link data from different registries and to identify medical records and electronic files in the hospital database. Before 1971, patients were registered only by name and date of birth. Their PIN numbers were sought in the Civil Registration System by name, birth date and private address at time of discharge.
Two hundred and forty six patients underwent surgical repair of CoA (Fig. 1
). Seventeen (7%) had to be excluded from the study due to inability to identify their CPR numbers. Two patients were lost to complete follow-up because of emigration, but due to their long observation time of 24 and 15 years, they were included in the analyses as censored observations. The study population thus, consisted of 229 patients.
2.2 Reference group
Survival and use of antihypertensive medication in the study population were compared with a reference group sampled from the general population. By use of the Civil Registration System, 10 age- (same year of birth) and sex-matched controls for each subject in the study population were selected (n
= 2290). The controls were sampled using the incidence density sampling technique [14].
2.3 Possible predictors of morbidity and mortality
Baseline data were obtained from medical records and in some cases supplemented by the hospital's patient administrative system, which covers all patient contacts to Aarhus University Hospital since 1988. Sex, age at surgery, surgical technique and preoperatively known cardiovascular comorbidity were registered.
2.4 Outcome data
The Civil Registration System provided data on vital status by August 2005 and dates of death or emigration. Causes of death, until 2001 assessed by physicians accorded to the International Classification of diseases (ICD), were obtained from the Causes of Death Registry. Copies of death certificates for those who died later were provided by the National Board of Health. Hospitalisations after CoA repair were sought in the National Hospital Discharge Registry, which covers all non-psychiatric hospitalisations from 1977 and supplemented and cross-checked with information from our institution. The following complications and interventions were retrieved: surgery or balloon angioplasty for reCoA, coronary artery surgery and angioplasty, aortic and mitral valve and aortic surgery. The discharge diagnoses stroke, acute myocardial infarction and acute or subacute infective endocarditis were also recorded.
Hypertension was defined as use of antihypertensive drugs. Patients, who had filled at least one prescription for antihypertensive drugs including beta-blockers, diuretics, calcium antagonists, angiotensin II antagonists or ACE-inhibitors during the year 2004, were classified as hypertensive. This information was only available for residents in four counties where prescriptions for refundable drugs are registered in population-based databases.
2.5 Statistical analyses
Descriptive tables of the main study variables were made for the entire study population. Follow-up began on the date of surgical repair for CoA or the index date for the reference group and ended on the date of death, the date of emigration, or end of follow-up on August 1, 2005, whichever came first. Kaplan–Meier survival curves were constructed to analyse mortality. Mortality was divided into surgical (
30 days after CoA repair) and late mortality and analysed separately. Survival in the study population was compared with survival in the reference group. Kaplan–Meier curves using a combined end point of death, reintervention and cardiovascular complications were also constructed describing freedom from morbidity and mortality. Cox proportional hazards regression analyses were used to estimate mortality rate ratios (MRRs) in order to (1) compare survival in the study population with survival in the reference group and (2) identify possible predictors for mortality. We included age, gender, level of comorbidity at time of surgery, time of CoA repair and surgical technique as possible predictors of mortality in a multivariate analysis. Time of surgery was divided into the early (1965–1975) and late (1976–1985) period, subsequently referred to as early and late decade. Furthermore, sensitivity analyses were performed in order to examine the possible impact of patients with missing data on surgical technique on our findings. In these analyses, all the patients with missing data were assumed to have received an end-to-end anastomosis or a tube prosthesis. The proportional hazard assumptions were tested graphically and were found to be acceptable in all models for Cox regression analyses. Analyses were performed using STATA® software (version 9.0, STATA, College Station, TX, USA).
|
3. Results
|
|---|
3.1 Baseline
3.1.1 Preoperative data
Table 1
shows baseline data and the surgical technique used for CoA repair in the entire study population and divided into the early and late decade. Two out of three patients were males and this distribution remained unchanged between the two decades (p
= 0.48). The age at surgery decreased significantly with more infants (1 year) and relatively fewer adults (>15 years) undergoing repair in the last decade (p
= 0.001). The median age at surgery was 13.8 years in the first and 8.1 years in the latter decade (p
< 0.001).
3.1.2 Cardiovascular comorbidity
Data on cardiovascular comorbidity at baseline were available for the 210 patients where medical records could be found. The aortic valve was tricuspid in 48, bicuspid in 36, and not described in 126 patients. We divided the patients into three classes depending on associated cardiac malformations (Tables 1 and 2
).
3.1.3 Surgical techniques
Table 1 provides data on the surgical techniques performed. The distribution of end-to-end anastomosis and prosthesis, either as an interposition graft or a by-pass, was unchanged comparing the early and late decade (p
= 0.12).
3.2 Mortality
The survival after CoA repair for the study population and reference group are shown in Fig. 2
. Survival for those who lived beyond 30 days of CoA repair was 95% 10 years after surgery, and 91%, 83% and 69% after 20, 30 and 40 years, respectively. The MRR for long-term survivors compared with the reference group was 4.3 (2.9–6.4). Evaluating the survival of exclusively long-term survivors with CoA comorbidity Class I and their reference group, the MRR was 3.4 (1.8–6.4). In patients with CoA Class II, the MRR was 3.6 (0.95–13.5) and in Class III 5.1 (3.5–7.4).
View larger version (26K):
[in this window]
[in a new window]
|
Fig. 2. Crude survival after surgical repair of CoA compared with control group. CI: confidence interval. Comparing survival in the study population with survival in the age-and sex-matched control group. Mortality rate ratio (MRR) comparing late survivors in the study population (n
= 215) with controls: 4.3 (95% CI: 2.9–6.4).
|
|
3.2.1 Surgical mortality
Fourteen patients (6%) died during surgery or within the first 30 postoperative days. Twelve (86%) among these had complex CoA (Class III) and status of comorbidity was not described in the remaining two. Nine (64%) were infants, the remainder were children, giving a surgical mortality for CoA repair of nine among 19 infants (47%), five among 131 children (4%) and none among 79 adults. The overall surgical mortality was 4% in the early and 8% in the late decade (p
= 0.23).
3.2.2 Late mortality
The median follow-up time was 27 years (range: 0.1–40), with a total of 5738 patient-years of observation. There were 35 late deaths (Table 3
) at a median age of 49 years (range: 0.3–87), occurring at a median of 19 years (range: 0.1–38) after CoA repair. Twenty-two patients (63%) died from cardiovascular diseases including three deaths in relation to subsequent cardiothoracic surgery. Three late deaths occurred in 10 patients who survived CoA repair in infancy, eight in 126 repaired in childhood and twenty four in 79 patients who were adults at CoA repaired in adulthood.
Using Cox regression analyses we identified early decade of surgery, age below 1 year and a high level of comorbidity (Class III) as predictors for late mortality (Table 4
). In contrast, surgical technique and sex appeared not to influence the survival. Adjusting the crude MRRs mutually for age group, comorbidity and decade, surgical technique and gender had only a marginal effect on the risk estimates. Sensitivity analyses confirmed that surgical technique did not influence the prognosis even when taking patients with missing data into account.
3.3 Morbidity
A number of cardiovascular interventions and complications occurred in the study population during follow-up (Table 5
). One adult patient had paraplegia immediately after surgery. Subsequent cardiovascular surgery was performed in 42 of the late survivors (19%). Eleven (5%) patients were treated for reCoA by surgery in five and balloon angioplasty in six at a median of 18 years (range: 8–26) after primary repair. Looking exclusively at current survivors, cardiovascular morbidity had occurred in 46 (26%), including cardiovascular surgery and catheter based interventions in 35 (19%).
Information on possible systemic hypertension was available for 87 patients. Twenty two (25%) subjects filled a prescription of antihypertensive medication during 2004, compared with 12% in the reference group, and were classified as suffering from systemic hypertension. The hypertensive patients had a median age of 48 (range: 21–61) and a follow-up time of median 29 years (range: 20–40). Only two (9%) were infants at time of surgery, nine were children and eleven were adults.
3.4 Event-free survival
The probability of avoiding death, reintervention (reCoA, aortic surgery, coronary artery intervention, aortic or mitral valve surgery) and cardiovascular complications (acute myocardial infarction or stroke) in the entire study population was 84%, 74%, 60% and 39% 10, 20, 30 and 40 years after surgery, respectively. Eighty eight (38%) patients experienced one or more of the endpoints during follow-up. Mortality and morbidity risk ratio (MMRR) for event-free survival was 12.8 (6.9–23.7) for patients with complex CoA (Class III) compared with those with CoA Class I comorbidity when adjusting for sex, decade of surgery and age at operation. The adjusted MMRR for patients with CoA Class II was 2.2 (1.0–4.7, p
= 0.043) (Fig. 3
). Excluding patients who died within 30 days after surgery, the adjusted MMRR was still statistically significant comparing patients with CoA Class II (RR: 2.4, 95% CI: 1.1–5.2) and patients with complex CoA Class III (RR: 11.7, 95% CI: 6.1–22.4) with patients with CoA Class I.
View larger version (25K):
[in this window]
[in a new window]
|
Fig. 3. Event-free survival for CoA Class I, II and III. Combined endpoint of death, reintervention (reCoA, aortic surgery, coronary artery intervention, aortic or mitral valve surgery) and cardiovascular complications (acute myocardial infarction or stroke). CI: confidence interval. Class I (n
= 112): isolated CoA, with or without an open arterial duct. Class II (n
= 48): CoA with either a ventricular septal defect without need of treatment, minor aortic valve dysfunction or merely a known bicuspid valve or minor mitral valve abnormality. Class III (n
= 50): complex CoA, with significant associated lesions (Table 2). Mortality and morbidity rate ratio Class III versus Class I: 11.7 (5% CI: 6.1–22.4).
|
|
Twenty years after surgery, the probability for event-free survival was 93%, 87% and 26% for patients with CoA Class I, II, and III, respectively. Nineteen patients had the first complication within the first postoperative year; including 18 deaths in patients with CoA Class III (n
= 15) or not described comorbidity status (n
= 3). Including systemic hypertension in the combined endpoint of failure, there would be another 13 patients experiencing complications during follow-up.
|
4. Discussion
|
|---|
The present cohort of patients who underwent surgery for CoA 20–40 years ago is very different from recent series where neonates and infants predominate and severe cardiovascular comorbidity is very frequent [15,16]. Despite this, some lessons can be learned from the present study, most notably that surgery for CoA is not a curative treatment. Even patients without associated cardiovascular lesions who survived CoA repair experienced a 3.4 times increased long-term mortality and excess morbidity compared with a sex- and age-matched reference group. With associated lesions, the short and long-term prognosis was further impaired.
4.1 Surgical mortality
The surgical mortality in this historical material was high compared with recent series [13,17], but equals what has been reported in other older studies [18]. The surgical deaths occurred mainly in infants with complex associated lesions indicating that surgical treatment of CoA in children and adults in itself was performed with low risk during that period. The not significantly higher surgical mortality in the late decade compared with the early decade reflects more infants with complex associated lesions in the late decade, even though the degree of severity of the associated lesions was minor compared with recent series of CoA patients [17]. Sex and surgical technique had no significant influence on surgical or late mortality.
4.2 Late mortality
The majority of late deaths were due to cardiovascular disease, predominantly ischemic heart disease, aortic lesions, aortic and mitral valve disease and cerebrovascular accidents. This probably reflects the combined effects of associated congenital malformations of the valves and aorta, hypertension and premature atherosclerosis. Most late deaths in absolute numbers occurred in patients who were adults at the time of CoA repair. This probably reflects that after 20–40 years of observation, this patient group had reached a rather high age. However, in multivariate analyses, excess late mortality compared with matched controls was predicted by early decade of surgery, age below 1 year at operation and high level of comorbidity. The present results for long-term survival are similar to those reported in other older series reported by Toro-Salazar et al. [19] and Cohen et al. [12], even though patients with significant cardiovascular malformations were excluded from both these series.
4.3 Morbidity
The pattern of cardiovascular morbidity was similar to the causes of late cardiovascular deaths with prevalent valve and ischemic heart disease, aortic disease and cerebrovascular accidents. ReCoA was detected and treated in 5% of the survivors, compared with 3–23% in other series [12,20]. Even though there is no universally agreed definition of reCoA, the low frequency in the present series probably reflects the lack of systematic clinical follow-up. An additional explanation could be that reCoA is more frequently reported in those treated for CoA in infancy and early childhood than in older children and adults [18], who constitute the great majority of survivors in the present study. The risk of reCoA with end-to-end prosthesis in children is usually considered as high. However, in our series patients treated with this technique were older children and, therefore, it was possible to choose a larger tube preventing reoperation.
Hypertension defined as use of antihypertensive medication was twice as common in the patients compared with this reference group, but probably severely underestimated, undertreated and poorly controlled as shown in other studies [11]. This would contribute significantly to the high cardiovascular mortality and morbidity. Hypertension in some of the patients is supposedly related to undiagnosed reCoA.
A bicuspid aortic valve increases the risk of significant valve dysfunction and dilatation of the aortic root [21]. The prevalence of bicuspid valves in the present series is probably underestimated due to lack of sufficiently sensitive diagnostic methods before two-dimensional echocardiography became widely available in the late 80s.
Endocarditis was diagnosed in approximately one patient per 1000 patient-years of risk, comparable with other series [22,23].
Thus, repaired CoA is associated with a multitude of potential postoperative problems, as also reported by others [5,6,11,12,18,19].
4.4 Limitations
This is a historical study. PIN numbers were used to track patients and their medical history but had to be reconstructed for patients operated on before 1971, which was not possible for all, leading to a possible selection bias. Thus, inability to identify the PIN numbers could reflect no patient contact to the health care system since time of surgical repair, or on the other hand that the patient had died soon after surgery. Ability to identify the patients could reflect reestablished contact to the hospital system due to complications. Systemic hypertension increases the risk of cardiovascular death; assessing its prevalence in survivors, therefore, underestimates the true frequency of postoperative hypertension. On the other hand, antihypertensive drugs are also used in treatment of cardiac insufficiency, which is likely to be more frequent in survivors than in the reference group. Information on postoperative mortality and morbidity were retrieved from two different registries using different and changing codes for diagnoses and surgical procedures during the years. By cross-checking all missing values and different codes, we sought to minimize this source of error. Finally, even though data were missing on some of the patients, sensitivity analyses indicated that this had only minor influence on the results.
|
5. Conclusions
|
|---|
CoA after surgical repair is associated with excess long-term mortality compared with population controls, due to ischemic heart disease and morbidity, due to anomalies of the ascending aorta and aortic arch, hypertension, premature atherosclerosis, valve abnormalities and other associated cardiac malformations. Careful follow-up should be carried out and would probably identify many patients in whom medical, surgical or catheter intervention would improve the long-term outcome.
|
References
|
|---|
- Campbell M. Natural history of coarctation of the aorta. Br Heart J 1970;32(5):633-640.[Abstract/Free Full Text]
- Abbott ME. A statistical study and historical retrospect of 200 recorded cases with autopsy, of stenosis or obliteration of the descending arch in subjects above the age of two years. Am Heart J 1928;3(4):381-421.
- Reifenstein GH, Levine SA, Gross RE. Coarctation of the aorta: a review of 104 autopsied cases of the ‘adult-type’, 2 years of age or older. Am Heart J 1947;33:146-168.[CrossRef]
- Crafoord C, Nylin G. Congenital coarctation of the aorta and its surgical treatment. J Thorac Surg 1945;14:347-361.
- Maron BJ, Humphries JO, Rowe RD, Mellits ED. Prognosis of surgically corrected coarctation of the aorta. A 20-year postoperative appraisal. Circulation 1973;47(1):119-126.[Abstract/Free Full Text]
- Presbitero P, Demarie D, Villani M, Perinetto EA, Riva G, Orzan F, Bobbio M, Morea M, Brusca A. Long term results (15–30 years) of surgical repair of aortic coarctation. Br Heart J 1987;57(5):462-467.[Abstract/Free Full Text]
- Bacha EA, Almodovar M, Wessel DL, Zurakowski D, Mayer Jr. JE, Jonas RA, del Nido PJ. Surgery for coarctation of the aorta in infants weighing less than 2 kg. Ann Thorac Surg 2001;71(4):1260-1264.[Abstract/Free Full Text]
- Lock JE, Niemi T, Burke BA, Einzig S, Castaneda-Zuniga WR. Transcutaneous angioplasty of experimental aortic coarctation. Circulation 1982;66(6):1280-1286.[Abstract/Free Full Text]
- Suarez de LJ, Pan M, Romero M, Medina A, Segura J, Pavlovic D, Martinez C, Tejero I, Perez Navero J, Torres F. Balloon-expandable stent repair of severe coarctation of aorta. Am Heart J 1995;129:1002-1008.[CrossRef][Medline]
- Schuster S, Gross RE. Surgery for coarctation of the aorta: a review of 500 cases. J Thorac Cardiovasc Surg 1962;43:54-70.[Medline]
- de BJ, Freeman LJ. Aortic coarctation repair—lost and found: the role of local long term specialised care. Int J Cardiol 2005;104(2):176-183.[CrossRef][Medline]
- Cohen M, Fuster V, Steele PM, Driscoll D, McGoon DC. Coarctation of the aorta. Long-term follow-up and prediction of outcome after surgical correction. Circulation 1989;80(4):840-845.[Abstract/Free Full Text]
- Celermajer DS, Greaves K. Survivors of coarctation repair: fixed but not cured. Heart 2002;88(2):113-114.[Free Full Text]
- Wacholder S, McLaughlin JK, Silverman DT, Mandel JS. Selection of controls in case-control studies. I. Principles. Am J Epidemiol 1992;135(9):1019-1028.[Abstract/Free Full Text]
- Head CE, Jowett VC, Sharland GK, Simpson JM. Timing of presentation and postnatal outcome of infants suspected of having coarctation of the aorta during fetal life. Heart 2005;91(8):1070-1074.[Abstract/Free Full Text]
- O'Sullivan JJ, Derrick G, Darnell R. Prevalence of hypertension in children after early repair of coarctation of the aorta: a cohort study using casual and 24 h blood pressure measurement. Heart 2002;88(2):163-166.[Abstract/Free Full Text]
- Walhout RJ, Lekkerkerker JC, Oron GH, Bennink GB, Meijboom EJ. Comparison of surgical repair with balloon angioplasty for native coarctation in patients from 3 months to 16 years of age. Eur J Cardiothorac Surg 2004;25(5):722-727.[Abstract/Free Full Text]
- Koller M, Rothlin M, Senning A. Coarctation of the aorta: review of 362 operated patients. Long-term follow-up and assessment of prognostic variables. Eur Heart J 1987;8(7):670-679.[Abstract/Free Full Text]
- Toro-Salazar OH, Steinberger J, Thomas W, Rocchini AP, Carpenter B, Moller JH. Long-term follow-up of patients after coarctation of the aorta repair. Am J Cardiol 2002;89(5):541-547.[CrossRef][Medline]
- Roos-Hesselink JW, Scholzel BE, Heijdra RJ, Spitaels SE, Meijboom FJ, Boersma E, Bogers AJ, Simoons ML. Aortic valve and aortic arch pathology after coarctation repair. Heart 2003;89(9):1074-1077.[Abstract/Free Full Text]
- Warnes CA. Bicuspid aortic valve and coarctation: two villains part of a diffuse problem. Heart 2003;89(9):965-966.[Free Full Text]
- Moller JH, Anderson RC. 1000 consecutive children with a cardiac malformation with 26- to 37-year follow-up. Am J Cardiol 1992;70(6):661-667.[CrossRef][Medline]
- Morris CD, Reller, MD, Menashe VD. Thirty-year incidence of infective endocarditis after surgery for congenital heart defect. J Am Med Assoc 1998;279(8):599-603.[Abstract/Free Full Text]
This article has been cited by other articles:
|
|
|
|
 
E. Troost, M. Gewillig, W. Daenen, B. Meyns, J. Bogaert, K. Van Deyk, and W. Budts
Behaviour of polyester grafts in adult patients with repaired coarctation of the aorta
Eur. Heart J.,
May 1, 2009;
30(9):
1136 - 1141.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Vijayalakshmi, A. Griffiths, A. Hasan, and J. O'Sullivan
Late hazards after repair of coarctation of the aorta
BMJ,
April 5, 2008;
336(7647):
772 - 773.
[Full Text]
[PDF]
|
|
|
Top
Abstract
1. Introduction
