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| CONGENITAL HEART DISEASE |
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| Year : 2002 | Volume
: 3
| Issue : 2 | Page : 6 |
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Congenital heart disease - B: Surgical management of the atrial septal defects
Roxane McKay
Division of Cardiothoracic Surgery, Department of Cardiology & Cardiovascular Surgery, Hamad Medical Corporation, Doha, Qatar
| Date of Web Publication | 22-Jun-2010 |
Correspondence Address:
Roxane McKay
Department of Cardiology & Cardiovascular Surgery, Hamad Medical Corporation, P.O. Box 3050, Doha; Consultant Congenital Heart Surgeon, Hamad Medical Corporation Doha
Qatar
 Source of Support: None, Conflict of Interest: None  | Check |
 Abstract | | |
The first cardiac malformation to benefit from open-heart surgery was atrial septal defect. It is of particular interest, both as a reflection of past achievements in congenital heart surgery and as an example of present refinements in surgical management. This article reviews the surgical anatomy of atrial septal defects, the indications for closure, surgical techniques and results as well as the impact of closure on survival, functional status and quality of life.
How to cite this article:
McKay R. Congenital heart disease - B: Surgical management of the atrial septal defects. Heart Views 2002;3:6 |
| Introduction and Historical Background | |  |
Although Leonardo da Vinci illustrated an atrial septal defect postmortem [1] , it was not until the twentieth century that this malformation was diagnosed during life [2],[3] . The first successful surgical closure is attributed to Murray, who used an external suture technique in 1948 [4] . Thereafter, a number of procedures followed which achieved, to a variable degree, obliteration of interatrial communications without actually opening the heart [5],[6] . These were subsequently supplanted by methods of "open" closure under hypothermia with inflow occlusion [7] , or working by touch beneath a pool of blood [8] . The advent of the pump oxygenator, however, made possible precise repair under direct visualization, and it was, in fact, this operation with which Gibbon initiated the modern era of true open-heart surgery in 1953 [9] . Since then, refinements in surgical management have evolved from improved methods of anesthesia and cardiopulmonary support, better knowledge of detailed surgical anatomy, and the development of instruments and sutures specifically designed for delicate cardiovascular tissues.
With the introduction of devices, which could be placed percutaneously to close interatrial communications in 1976 [10] , the focus of subsequent surgical innovations has been limited or minimal access procedures [11],[12],[13],[14],[15],[16],[17] , culminating recently in robotic closure of atrial septal defects [18] . There has been also, not surprisingly, a new need for operations to deal with complications arising from transcatheter closure [19],[20],[21],[22],[23].
| Surgical Anatomy of Atrial Septal Defects | | |
For the cardiac surgeon, there are six types of isolated atrial septal defects [Figure 1], some of which merge into other malformations at the extreme ends of the spectrum. The commonest interatrial communication is found within the oval fossa, the so-called "secundum" or "fossa ovalis" atrial septal defect. This usually results from fenestration or deficiency of the septum primum, which forms the normal flap valve or floor of the oval fossa. But, rarely, there is, instead, hypoplasia of the surrounding limbus, producing a defect high in the right atrium or closer to the atrioventricular valves. When the septum primum is completely absent, the interatrial communication reaches the junction of the right atrium with the inferior caval vein. In this situation, there may be preferential streaming of systemic venous blood into the left atrium, causing cyanosis without Eisenmenger's Syndrome. It is also in this situation that the surgeon may mistake the Eustachian valve for the inferior rim of the defect, approximation of which to the limbus causes the inferior caval vein to drain to the left atrium postoperatively. If there is not actually a deficiency of either the flap valve or the limbus, a small interatrial communication may result nonetheless when these two structures fail to meet. This is properly called a "stretched" or patent foramen ovale rather than an atrial septal defect. At the other extreme, effacement of the limbus with complete absence of the septum secundum produces a very large communication, which resembles a common atrium both anatomically and physiologically. It is differentiated from the latter, however, by the presence of a normal atrioventricular septum and absence of a "cleft" in the mitral valve. While the anatomical boundaries of the fossa ovalis defect are defined at birth, recent studies have confirmed that the size of these defects usually changes with the passage of time [24] . Strictly speaking in developmental terms, sinus venosus defects include any interatrial communication involving the right horn of the embryological sinus venosus. In general usage however, this name has been used to designate communications lying immediately below the entrance of the superior caval vein and above the limbic tissue. These are also called "subcaval," "inlet," or "superior sinus venosus" atrial septal defects or, because of the nearly inevitable association of partial anomalous pulmonary venous connection [25] , "sinus venosus syndrome." The lower margin of the defect is the upper rim of the limbic tissue. There is no upper margin, because the superior caval vein lies immediately above the defect. Usually, pulmonary veins from the right upper and middle lobes are connected to the superior caval vein and/or its junction with the right atrium. If a patent foramen ovale or secundum atrial septal defect is also present, it will be separated from the sinus venosus defect by the limbus. The converse of a sinus venosus atrial septal defect is the much less common "inferior caval" defect, which occurs at the junction of the inferior caval vein and the right atrium. It may or may not have associated anomalies of pulmonary venous drainage and is separated from the oval fossa (in which there may be a separate defect) by the lower part of the septum primum. The third type of interatrial communication related to the right horn of the sinus venosus is the "posterior" atrial septal defect. This lies behind the limbus of the oval fossa and extends to the entrance of the right pulmonary veins. While internally the pulmonary veins may appear to drain to the right atrium, external inspection of the heart generally confirms their normal connection to the left atrium. By virtue of a common wall shared with the left atrium, a hole in the coronary sinus will connect its orifice in the right atrium with the left atrium, resulting in a "coronary sinus" atrial septal defect.
Developmentally, this anomaly derives from the left horn of the sinus venosus. If there is an associated left superior caval vein draining to the coronary sinus, deoxygenated blood returns directly to the left atrium, causing mild cyanosis. This situation, however, as well as complete or more extensive deficiencies of the partition between the left atrium and coronary sinus, is generally regarded as part of the unroofed coronary sinus syndrome rather than an isolated atrial septal defect. "Confluent" atrial septal defects consist of a combination of the above malformations, usually resulting in particularly large interatrial communications. The most common associations are oval fossa and posterior defects, or oval fossa and coronary sinus defects. In the case of a very large oval fossa with multiple fenestrations, it may be impossible to differentiate a confluent inferior caval-secundum defect from a complete absence of the septum primum. "Primum" atrial septal defects, in which the communication between the atria extends to the atrioventricular valves, are now recognized to be part of the spectrum of malformations involving the atrioventricular septal structures and hence, more complex both anatomically and surgically. They should, therefore, be considered atrioventricular septal defects rather than atrial septal defects, despite their physiological similarity of left-to-right shunting at atrial level.
| Indications for Closure | | |
Elective closure has been advised routinely for all atrial septal defects with a significant left to right shunt. This is generally regarded as a Qp:Qs > 1.5:1, or signs of right ventricular volume overload on echocardiography. With increasing experience of open-heart surgery in neonates and infants, there is now little reason to wait until the traditional age of 4 to 5 years for operation, and it could be argued that earlier normalization of the systemic and pulmonary circulations may facilitate regression of right ventricular dilatation. While most children with an atrial septal defect are asymptomatic, those who experience paradoxical embolus or heart failure should be offered closure at any age without delay. Recent publications also support early closure in asymptomatic children who have poor somatic growth [26] . Severe pulmonary vascular disease is the only clear contraindication to closure of an atrial septal defect, but up to a total pulmonary resistance of about 14 units·m2 at rest (or more than about 7 units·m2 with administration of pulmonary vasodilators), overall outcome is still improved by closure of the defect [27] . These limits must be reconsidered in the presence of associated mitral valve regurgitation, which may add a venous component to the pulmonary hypertension. Such patients may still have a favorable outcome, despite a preoperative pulmonary vascular resistance in excess of 14 units · m2. While elderly patients suffer more perioperative complications and a higher operative mortality, old age, of itself, is not a contraindication to surgery. Those who survive operation have normalization of life expectancy [28] as well as relief of symptoms, improved hemodynamics [29] and reduction of adverse cardiovascular events [30] . The association of mitral and/or tricuspid valve regurgitation, which tends to occur in older patients, is an important consideration in planning treatment but does not preclude atrial septal defect closure. Because decompression of the mitral regurgitation through the right atrium is no longer possible, its effects are exacerbated, potentially resulting in acute pulmonary oedema. Repair of valvar regurgitation is thus done routinely at the time of septal defect closure, and, when it can be anticipated that this may not be successful, closure of the atrial septal defect may be postponed until the onset of symptoms to delay mitral valve replacement.
| Surgical Technique | | |
A variety of incisions have been used to expose the heart for open closure of atrial septal defects [Figure 2], which is done routinely through an incision in the right atrium. In general, these represent an exchange of surgical access for cosmetic appearance. While each has its own set of advantages and disadvantages [Table 1], all have been employed without compromise of surgical results, and overall experience at this point in time would suggest that a full sternotomy is not routinely necessary for closure of an atrial septal defect [12],[13] . Video-assisted endoscopic techniques have not gained wide-spread popularity, probably because of their considerable prolongation of operating time and requirement for expensive equipment to achieve small increments in cosmetic appearance. Robotic closure, which is presently experimental, has applied the methods developed for other types of minimal access cardiac procedures to closure of atrial septal defects in adults, reducing the incisions to four ports of about 1 cm each [18] . Despite approximately five-fold increase in the aortic cross clamp time and quadrupling of the cardiopulmonary bypass period, all patients had resumed a normal lifestyle one week after operation. When a fossa ovalis defect is not excessively large and has adequate surrounding tissue, it can be closed by direct suture [Figure 3]. This is more suitable for slit-like or oblong defects than oval ones. When a patch is needed [Figure 4], autologous pericardium is preferred because it is cheap, readily available, and avoids foreign material within the heart, (and hence the need for long-term antibiotic prophylaxis). It also minimizes any risk of hemolysis, should residual atrioventricular valve regurgitation produce a jet of blood against the patch. A variety of surgical techniques have been employed to repair sinus venosus atrial septal defects and the associated anomalous pulmonary venous connections, with a view to avoiding injury to the sinus node and/or obstruction to systemic or pulmonary venous drainage. The simplest of these is tunneling the pulmonary veins to the interatrial communication with a patch inside the superior caval vein and augmentation of the superior vena cava with a second patch if needed [Figure 5]. This procedure is difficult in small patients or if the pulmonary veins enter high up in the superior caval vein. For such situations, a modification of the Warden [31] or Vargus [32] operations, as described for repair of anomalous pulmonary venous drainage, offers a possible solution. In these procedures, the superior caval vein is divided above the entrance of the pulmonary veins, which are then directed across the atrial septal defect with a pericardial baffle or a flap of free right atrial wall [Figure 6]. The cardiac end of the superior vena cava is closed, while the distal end is joined directly to the right atrial appendage, which is always enlarged in this malformation. In addition to avoiding incisions and sutures in the region of the sinus node, this technique conserves the potential for growth in both the pulmonary and systemic venous pathways and is therefore applicable at any age. Posterior defects also lend themselves to a variety of surgical techniques, depending upon the size of the interatrial communication [Figure 7]. When this is large, a pericardial patch or a flap of right atrial wall may be used to partition the atrium, leaving the pulmonary veins to drain on the left atrial side. Alternatively (and less commonly), when there is a substantial remnant of atrial septum and a small interatrial communication, a flap of septal tissue can be mobilized and brought to the free right atrial wall, superficial to the entrance of the pulmonary veins. The management of coronary sinus defects is dictated by the presence or absence of an associated left superior caval vein. If there is no left superior caval vein, only a small channel, which can be ligated, or an adequate vein connecting it to a right superior caval vein, (which also permits closure of the left SVC Coronary Sinus Junction) the defect is repaired by closing the orifice of the coronary sinus in the right atrium [Figure 8]. Either a patch is used or the edge of the orifice is approximated to the wall of the coronary sinus, in both cases, carrying the suture line inside the vein to avoid injury to the atrioventricular node. The resulting right-to-left shunt of coronary venous blood is hemodynamically and physiologically insignificant. In the presence of a left superior caval vein, the opening of the coronary sinus within the left atrium is closed to route the systemic venous return to the right atrium and obliterate the interatrial communication. This may be accomplished by direct plication of the left atrial wall over a stent or by placement of a patch within the left atrium [Figure 8]. It is usually necessary to create or enlarge a defect in the oval fossa for access to the left atrium, and this second atrial septal defect is also closed using direct sutures or a pericardial patch.
| Results | | |
Survival
Hospital mortality following closure of an atrial septal defect is extremely low and has approached zero in many institutions throughout the world for a remarkable period of time [33] . While a mortality of approximately 6% has been reported among elderly patients undergoing operative closure [28] , neither older age, younger age, coexistent cardiac malformations (because of their infrequent occurrence), the morphology of the defect, or preoperative functional class have been confirmed as risk factors for early mortality [34] . Only elevated pulmonary vascular resistance, at a level exceeding 6 units· m2, has been found to increase hospital death [27],[35] and this is usually in patients greater than 60 years of age at the time of operation. The causes of hospital mortality are generally related to sequel of pulmonary vascular disease, although neurological complications from air embolism have been observed also. Time-dependent or late mortality is generally very low, with most patients achieving an expectation of survival equal to that of the general population. The two groups of patients who may not enjoy such an optimistic outcome, however, are again those with preexisting pulmonary vascular disease and possibly the elderly. While one report of long-term follow up clearly showed that time-related survival depended upon age at the time of closure [Table 2] [35] , other studies have suggested that elderly survivors of atrial septal defect closure have the same life expectancy as the age and gender-matched population [28] . The causes of late deaths, all of which are uncommon, include pulmonary vascular disease, cerebral embolism or hemorrhage, chronic congestive heart failure, and supraventricular arrhythmia.
Functional Status
Patients who are asymptomatic at the time of operation, which includes the vast majority of children and young adults, remain so afterwards; and infants who are in congestive heart failure return to a normal functional class [36] . Improvement in functional status of older patients is related to age at the time of closure: after 60 years of age, 87% of patients improve by one New York Heart Association functional class and only 6% remain in Class III or IV, compared with an improvement of one functional class in all patients between 40 and 60 years of age [28].
Somatic Growth
There has long been a perception that poor growth and small size in children with an asymptomatic atrial septal defect were not due to the cardiac lesion and would not necessarily improve after repair. However, review of 49 such patients with a preoperative height or weight at, or below the 16th percentile at the Boston Childrens Hospital [26] showed that half of the low-weight patients achieved an improvement of 0.5 z-score in 2.6 years (compared with 5.6 years for age, size, and gender-matched controls). Half of the low-height patients similarly increased by 0.5 z-score in 1.7 year after closure of the defect, contrasted with a period of 11.6 years for control patients to achieve the same amount of growth. The chance of improved growth was greater among younger patients and those with lower preoperative weight.
| Ventricular Function | | |
Despite impressive reduction of right ventricular end diastolic volume on echocardiography early after closure of atrial septal defects [37] , this does not return completely to normal in many patients and appears to be influenced by age at the time of surgery [38] . Thus, a normal right ventricular end diastolic volume was found in 64% of children who underwent repair before 10 years of age but only 21% of patients who came to operation after 25 years; and adults who had impaired right ventricular function preoperatively showed less improvement in ejection fraction after closure of the defect [39] . These findings are reflected also in persistence of cardiomegaly on chest x-ray and less complete relief of symptoms. Whether they can be influenced significantly by earlier repair (and thus relief of right ventricular volume overload) or non-operative closure of atrial septal defects remains to be established. Left ventricular function, in contrast, nearly always becomes normal postoperatively. This includes ejection fraction, diastolic dimensions, and geometry [40] . When the left ventricle is small preoperatively as the result of chronic under filling, this returns to normal within about six months. Persistent abnormalities in left ventricular function should suggest the possibility of superimposed, acquired cardiovascular pathology, such as systemic hypertension or coronary artery disease.
| Arrhythmias | | |
Most children remain in sinus rhythm following closure of atrial septal defects and show improved atrioventricular conduction. The occasional but important exceptions are those in whom the sinus node (or its blood supply) or the atrioventricular node are injured during operation with resulting "sick sinus syndrome" or complete heart block, respectively. The former tends to happen variably with repair of sinus venosus defect, while the latter has complicated closure of both coronary sinus defects and very large secundum defects with an attenuated limbus. Careful attention to surgical detail should prevent this complication. Adult patients who are in atrial fibrillation before operation tend to continue in atrial fibrillation after closure of their atrial septal defect, and this is an indication for long-term anticoagulation [41] . Moreover, about half of the patients who undergo atrial septal defect closure after 40 years of age will, at some point in time, develop atrial fibrillation [42] . If this is in part the result of surgical scarring in the right atrium, as has been suggested, transcatheter device closure could offer particular benefit to the older subset of patients.
| Thromboembolic Events | | |
Both systemic and pulmonary emboli constitute recognized hazards following closure of atrial septal defects and may occur more than ten years after operation [43] . Risk factors for embolism include preoperative embolization, pulmonary hypertension, and postoperative atrial fibrillation, as well as operation beyond 40 years of age. It does not appear to be related to the type of operation or patch material used to close the defect.
| Quality of Life | | |
Few investigations have considered the quality of life or psychosocial situation of patients who undergo repair of congenital heart malformations during childhood, but, with improvements in surgical results and long-term survival, these are emerging as increasingly important concerns. In one such study, patients who had repair of Fallot's tetralogy or atrial septal defect at the University of Uppsala, Sweden, between 5 and 15 years of age, were evaluated twenty and thirty years after operation [44] . This protocol included review of medical records, physical examination, extensive interviews by psychologists and cardiologists, and standard self-examination questions. Three principal domains were considered to be of equal importance: 1) external life conditions (housing, quality of work life, quality of economic situation), 2) interpersonal relationships (pair relationships, friendships, parent relationships, relationship to own children), and 3) internal psychological states (engagement in life, energy, self-realization, freedom, general mood, self assurance, self acceptance, emotional access, security). Surprisingly, patients with the less severe cardiac defect and better hemodynamic outcome (atrial septal defect) had a poorer quality of life, which further deteriorated between 20 and 30 years postoperatively [Table 3]. Thus, a comparatively mild congenital cardiac malformation may exert a profound impact on later quality of life, despite apparently successful surgical repair during childhood.
| Reoperation | | |
Although uncommon, reoperation after repair of atrial septal defects has been necessary in about 2% of patients in some series [34] . Recurrence of the interatrial communication is occurs almost exclusively in older patients with preoperative cardiac failure or procedures performed by inexperienced surgeons who fail to recognize the need for patch closure of the defect. Misdirection of the inferior caval vein to the left atrium (a particular liability when the procedure is performed with profound hypothermia and total circulatory arrest), and narrowing of the superior caval vein after repair of a sinus venosus defect are other causes of reintervention. Occasionally, implantation of a cardiac pacemaker is needed for postoperative arrhythmias.
| Comparison of Conventional Repair, Minimally Invasive Operation and Interventional Closure | | |
The introduction of any new therapy requires comparison with existing methods of treatment to judge its relative value and advantages or disadvantages. This is difficult in the case of atrial septal defects because both surgical and percutaneous device closure are continuing to evolve, and device closure is applicable to only one (fossa ovalis) type of atrial septal defect. Few studies have examined concurrent series of patients, and even fewer have randomized them prospectively. Moreover, in the case of operative treatment, survival and closure of the interatrial communication represent fairly crude estimates of success, as reflected in twenty-to-thirty year follow-up; so it will be a considerable period of time before it is known to what extent the cosmetic and/or financial advantages of device closure are supported by hemodynamic outcomes, for example. Recently reported series [45],[46],[47],[48] all have noted a greater incidence of complications and morbidity following surgical closure, as compared with device implantation, as well as a shorter hospital stay and shorter procedure time for catheter interventions. Complications in the surgical patients, however, tended to have little impact on outcome or duration of hospitalization, in contrast to those occurring with device closure. Cardiopulmonary bypass and sternotomy or thoracotomy are, of course, avoided completely by nonsurgical intervention, and the need for blood products is reduced. Some authors have reported better psychological and intellectual achievement following device closure [49] . Successful obliteration of the defect was achieved 96-100% of the time with transcatheter devices, but crossover to the surgical group was significant in most series, and device closure invariably places prosthetic material permanently within the circulation. The undisputed advantage of surgical management has been the capacity to reliably close all defects, regardless of morphology and patient size. Results from one such comparison are summarized in [Table 4] [45].
| Surgical Management of Complications Following Transcatheter Closure of Atrial Septal Defects | | |
The overall incidence of complications which require surgical intervention after device closure of atrial septal defects is unknown, but increasing numbers of case reports [22],[23] and small series [19],[20],[45],[50] suggest that this is not insignificant. In one institution, 8% of patients required operation after attempted transcathter device implantation, mainly for dislocated or malpositioned devices with a significant residual shunt [50] . There was one death among this group, related to left ventricular puncture by a dislocated device. Atrial perforation by the fractured leg of an ASDOS device [19] or arms of the Cardioseal device [23] has resulted in hemorrhage and cardiac tamponade late after implantation [Figure 9], while tamponade six hours after implantation of an Angel Wings device was attributed to perforation of the anterior aortic wall [45] . The technical difficulties in explanting such a foreign body, after seven months of endothelization, may be considerable. Less serious complications have included secondary displacement causing reopening of the interatrial communication, floating thrombus on the device, embolism of a separated device into both the pulmonary artery and the aorta, and femoral arterial injury. In general, the device was removed and the atrial septal defect successfully closed with a patch, the time interval between implantation and explantation of devices ranging from one hour to three years. Optimistically, these complications may be part of the "learning curve" for device implantation and disappear with the passage of time.
| Conclusions | | |
Management of atrial septal defects has diversified enormously with the introduction of percutaneous transcatheter closure techniques. While traditional surgical methods virtually always achieve safe and secure repair for any type of defect, transcatheter closure in selected patients may be cheaper, less invasive, and give superior psychosocial outcome or better late quality of life. The results of long-term follow-up of surgical patients would support repair of all defects before 5 years of age, and ideally at 1-to-2 years, if the diagnosis were known at this time. In that regard, there is no justification to delay closure waiting for somatic growth of the patient to "fit" either cardiopulmonary bypass or an interventional device. Both invasive and noninvasive techniques of atrial septal defect repair are continuing to evolve, and the full impact of these developments will not be known for another 10-to-20 years.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]
[Table 1], [Table 2], [Table 3], [Table 4]
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