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The Surgical Anatomy of Atrial Septal Defects: Experiences with Repair Under Direct Vision'

Minneapolis, Minnesota
From the Department of Surgery, University of Minnesota,


The operations have all been done during hypothermia. The method we have used has been described elsewhere,2-23 so only a brief review of the technic will be given here. After anesthetic induction, the body temperature is lowered over a period of one and one-quarter to three and one-half hours by surface cooling. When the body temperature has reached approximately 300 C. the operation is started but the temperature continues to drop, falling to a low point of between 24.50 and 29.5 C. The chest is open with a transverse, sternal splitting incision made through the fourth interspaces bilaterally. Before the cardiac inflow is interrupted the heart is explored digitally through the right auricular appendage. Then the cardiac inflow and outflow are occluded, and the right atrium is opened widely to expose the defect. After the defect has been repaired, both the right and left heart are filled with saline and the atrium is closed * Presented before the American Surgical Asso- with a clamp. Circulation is resumed before ciation, Philadelphia, Pa., April 27, 1955. This work was supported by Grant Number the atrial wound is sutured. The length of H-1374 of the U. S. Public Health Service and by inflow occlusion has ranged from three to grants from the Minnesota Heart Association and seven and three-quarters minutes (median the Graduate School of the University of Minnesota. of four and three-quarters minutes). Re401

THROUGH USE OF an open repair technic we have become keenly aware of the complex anatomy of atrial septal defects. They vary in form, in size, in position, and even in number-two or more may exist in one heart. Other important anomalies may occur in association with them. Yet, atrial septal defects conform to a logical pattern. Their anatomical nature and development is understandable if it is explained as an embryological growth failure of the complex atrial septal complex25' 28, 31 and the pulmonary veins.7' 9 The classification presented here is based on embryological knowledge but the classification as well as the ideas of surgical anatomy to be described are a result, primarily, of our experience at the operating table. During operation we have not only palpated these defects; we have seen them in the living heart as well. To record this experience, some defects were photographed during operation, and sketches were made of all immediately after the operation. An examination of some rather unsatisfactory fixed specimens from the pathological museum yielded supplementary information. There is nothing new concerning pathological anatomy in this material. We hope merely to

present a rational classification of the defects, and to call attention to several important anatomical features not yet clearly described in the surgical literature. Furthermore, we plan to show how most of these defects may be repaired under direct vision, by simple technics.



Annals of Surgery

September, 19 5 5

Right Atrium

sant..m It



Left Atrium Superior Vena Cava

Septum 1r





Inferior. Veno Cava

FIG. 1. Semi-diagrammatic illustrations modified after Patten (Am. J. Path., 14: 135, 1938), showing the embryological development of the atrial septum. (A) The septum primum has almost reached the endocardial cushion and the ostium secundum has appeared. (B) A later stage illustrating how the septum primum forms the valve of the foramen ovale.
warming is started while the opeiation is in progress, but after the chest has been closed,

it is usually completed by immersing the patient in hot wvater.


The discussion will follow the classification of atrial septal defects which is given in Table I. We have operated upon 35 patients

with atrial septal defects, including the persistent common atrioventricular canal, and one patient who doubtless had an atrial septal defect but whose heart was not opened. Though this is a relatively small number of cases, we have seen defects of each type listed in the table.
TABLE I. Defects of the Atrial Septum.
I Foramen Ovale Defects II High Defects III Continuous defects of both Foramen Ovale and High Septum IV Low Defects

In every case the atrial septal defect was the major anomaly. A number of the defects have been complicated by mitral valve disease or partial anomalous pulmonary venous drainage, but none were found in combina-

pulmonary stenosis, tricuspid atresia, total anomalous pulmonary drainage, etc. Of course, from a purely anatomical point of view the atrial septal component of these latter anomalies would probably fit into the classification as well. Though they are important associated deformities, the classification holds no special place for mitral valve disease or partial anomalous pulmonary venous drainage. Presumably mitral stenosis or insufficiency could occur with any of the defects. As a matter of fact, however, we have encountered mitral valve disease, presumed to be rheumatic in origin, only with the Type I defects, while a congenitally deformed mitral cusp, on the other hand, is apparently a constant feature of the Type IV anomaly. Associated partial anomalous pulmonary venous drainage has been found with the first three types, and it seems to be an integral part of the high defect (Types II and III). This classification is similar to that of Edwards and associates,.10 19 but in our classification non-surgical probe patency of the foramen ovale has been omitted, and the high defects are listed as a major type rather than as part of a poorly defined group called "atrial septal defects in unusual location."

tion with anatomical


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FIG. 2. Figures 2 through 8 depict atrial septal defects from the surgeon's point of view he stands on the right side of the supine patient with the patient's head to the left. This is as a foramen ovale defect in which the valvula foraminis ovalis is absent. (A) A variation of the foramen ovale defect in which part of the valve remains as a fenestrated membrane.
A. FORAMEN OVALE DEFECTS are basically similar to one another. The structure

Morphologically these defects

of this commonest type of atrial septal defect-can best be understood by a study of the embryological development of the septum. This has been particularly well explained by Patten28 (Fig. 1). The margins of the clinical defect superiorly, anteriorly, and usually posteriorly are formed by the relatively thick edge of the septum secundum, which- normally forms the limbus foraminis ovalis (Fig. 2). This defect may be caused by a developmental arrest of the septum secundum, which results in an opening too big to be closed by the septum primum. Or the septum primum, which normally forms the valvula foraminis ovalis within the oval limits of the limbus, may have reabsorbed too far in the process that

the normal ostium secundum. Thus, excessive reabsorption, the septum priby mum will no longer-form a valve adequate to close the foramen ovalis. This latter process-excessive reabsorption-seems to be the more important one, for the valvula foraminis ovalis (septum primum) usually appears to be inadequate. Part of the septum primum may remain, and when it does it may form the lower edge of the defect, or in some cases the remaining septum primum may be found as a membrane with numerous perforations (sub-type A, Table II, and Fig. 2A). In still other cases it may be present only as a few thin strands. Finally, the septum primum may be totally absent in this area (sub-type B, Table II, and Fig. 2). When this occurs there is no clear lower margin of the defect above the orifice of the inferior vena cava, and the caudal -wall



Aiuials of Surgery5 September, 1 9 5

Septal leaflet of tricuspid valve



alve of l.V.C.

FIG. 3. In this foramen ovale defect the valvula foraminis ovalis is absent and the prominent valve of the inferior vena cava creates a false lower margin. (A) First repair stitch in place. (B) First repair stitch tied.

of the left atrium then blends imperceptibly into the wall -of the right atrium, or into the medial wall of the inferior vena cava at the lower part of the defect. An important variation of this type of defect-the foramen ovale defect with absence of the septum primum-at least to surgeons, occurs when a prominent valve of the inferior vena cava forms a confusing false margin (sub-type C, Table II, and Fig. 3). Here the anterior and posterior extremities of the caval valve blend into the true edges of the defect. The excellent illustrations of Licata, which show the appearance of the septum in the embryo,25 clarify the origin of this variation. During a certain period of embryonic life the right venous valve, which ultimately becomes the valve of the inferior vena cava, is so large that it almost covers the foramen ovale on the right. This valve doubtless regresses incom-

pletely in some cases to produce the variation just described.

What this all means to the surgeon is evident in the illustrations. In the simple foramen ovale defect, with or without a lower margin, repair is easy. We have usually employed a continuous stitch of 2-0 silk. If
TABLE II. Foramen Ovale Defects.
No. of Patients A. Part of the valvula foraminis ovalis present as a fenestrated membrane or caudal margin ..... B. Valvula foraminis ovalis absent; no lower margin C. Valvula foraminis ovalis absent; true margins continuous with valve of inferior vena cava. .
14* 3


Total ..................................

(3 deaths)

*One patient had a separate anomalous pulmonary vein entering the superior vena cava and another patient had a double superior vena cava. tOne patient had an anomalous pulmonary vein entering the right atrium. $Four patients had mitral stenosis.


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Anomalous right superior pulmonary vein

Right inferior pulmonary

FIG. 4. Usually anomalous pulmonary veins are closely related to the septal defect (Fig. 5), but in this case the right superior pulmonary vein enters the superior vena cava at a distance from the foramen valve defect. (A) The anomalous vein has been transferred to the left side of the heart by means of an end-to-side anastomosis to the inferior pulmonary vein.

there are a number of small holes in a mem- caval valve, is closed by first placing the brane at the lower part of the defect (Fig. lowermost stitch to the left of the caval 2A), the whole thing should be closed as orifice, with some of its bites in the left atrial one defect. When there is no lower margin, wall, as is illustrated in Figures 3 A and B. the lowest stitch, consisting of several bites, It is obviously quite possible to err and use is placed first. Some of the bites are taken the valve of the vena cava in the repair, thus in the lowest part of the left atrial wall. This diverting the inferior vena cava into the left stitch is tied before closing the rest of the atrium. This has been done with a blind defect. Similarly, the more difficult defect, technic of repair,5 but it is an error that characterized by a prominent and confusing could be made with an open technic, too. 405


Annals of

19 5 5 September,Surgery

"' Foramen ovale


FIG. 5. High defect in association with a separate, small ovale defect. repair stitch is placed above the anomalous pulmonary vein. foramen repair stitch (A) The first (B) First tied.

into the left atrium. The degree of mitral stenosis in these cases has been less than

did in four of the foramen ovale defects, a commissurotomy may be done with the finger inserted through the atrial septal defect

The right inferior pulmonary vein may drain directly into the right atrium if the posterior margin of the defect is poorly formed. In correcting this it is a relatively simple matter to place the stitches to the right of the vein orifice, and thus direct the pulmonary vein to its proper termination in the left atrium. In one case the right superior pulmonary vein entered the superior vena cava at a distance from the septal defect. Repair of the defect, and an end-to-side anastomosis, remedied the condition (Fig. 4). When mitral valve disease coexists, as it

that ordinarily found in mitral stenosis.



ovale defect, yet the distinction is not clearly made in the surgical literature. It is obvious from descriptions and illustrations that other surgeons have encountered these defects just as we have.5 14, 15, 26 They have failed, however, to delineate them as a distinct, relatively uniform type with an embryological origin which must be entirely different from that of either the foramen ovale or the low defect. We came to an understanding of these defects with a sense of discovery only to find that they have been described by a number of pathologists, anatomists, and

High defects

are not a

type of foramen


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NVaIve of I.V.C.

FIG. 6. Large defect which has the characteristics of both a high defect and a foramen ovale defect. (A) The upper stitch is the same as the first repair stitch of a high defect. The lower stitch is identical to the first repair stitch of a Type C, foramen ovale defect (Fig. 3). (B) Upper and lower stitches tied.

clinicians whose work dates back





2, 8, 12, 13, 17, 18, 35, 36

Usually these

defects have been set forth as an extremely anomaly, but in our relatively small series three were definitely of this type and two probably were. It has been at least as common as the persistent ostium primum. Located just below the superior vena cava the high defect has three important characteristics. First of all, the defect is above the fossa ovalis and separate from it. Before we knew this we failed to search for the fossa ovalis, and therefore failed to identify it in two patients who doubtless had this defect.

Then, in a third patient, an easily identifiable patent foramen ovale, independent of the high defect, forced us to recognize the nature of the anomaly (Fig. 5). After this we looked about more carefully, and found a normal fossa ovalis in both of the last two patients with high defects. As a second anatomical feature, the high defect lacks a complete margin. Characteristically there is no margin superiorly, and an incomplete one posteriorly. Finally, the defect is regularly associated with anomalous drainage of the right superior, and sometimes of the right middle or inferior, pulmonary vein. This fea-



Annals of

195 September,Surgerya

Septal leaflet of tricuspid valve -Cleft mitral

leaf let

FIG. 7. Persistent ostium primum with closed foramen ovale. (A) Repair of this defect employing the lowermost part of the left atrial wall to avoid injuring the conduction system. (B) First stitch tied.

ture was not always noticed by earlier authors perhaps because the hearts they examined were removed from the body without the pulmonary veins and the cavae.36 The embryological development of high defects has not been clearly explained. The defect has sometimes been described as an abnormal entry of the superior vena cava into both the right and left atria rather than as a defect of the atrial septum.12' 18 Such a description suggests, of course, that the defect represents an anomaly of venous development rather than an anomaly of the atrial septal complex. In its completed form, however, the defect is in the position of the ostium secundum of the septum primum. Normally this ostium is covered by the upper

proper attachments developmental failure here would almost certainly involve both the atrial septum and the large veins. The articles of Brown and Davis on the development
in this area. A

must be a failure of the

part of the septum secundum, the septun sperious, and the left sinus valve, so there

High Defects.

A. Single defects (foramen ovale closed) .......... B. Combined with Separate patent foramen ovale.

Total ............................

(no deaths)
*The evidence that these are high defects is direct in twothe closed foramen ovale was identified during surgery. The other two were earlier cases and we did not look for the fossa ovalis.


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posterior valve

Common valves are not fused to ventricular septum

ventricular septum by numerous

FIG. 8. Common atrioventricular canal with small foramen ovale defect. (A) Detail of dorsal, atrioventricular valve which has been split to show how it is suspended above the


of the pulmonary veins help to explain this complicated embryology.7 9 To repair this defect, the first, and most difficult, stitch is placed superiorly and then tied down before continuing (Fig. 5 A and B). Properly placed, this stitch directs the right superior pulmonary vein into the left atrium. The rest of the closure is simple. In some cases the atrial wall incision has been carried up into the lower part of the superior vena cava in order to expose the orifice of the superior pulmonary vein. Even with this extension, repair of the incision has not ob-

structed the vena cava. Some high defects have been repaired improperly, however. The anomalous pulmonary vein was not recognized in the first high defect encountered. This error was not discovered until a catheter was passed into the vein during postoperative cardiac catheterization.21 In another case the right phrenic nerve was accidently included in the repair stitches. Neither of these mistakes will be made

The foramen ovale defect was repaired independently in the one patient who had



Annals of Surgery September, 19 5 5



FIG. 9. A common atrioventricular canal with an additional foranen ovale defect. The hemostat runs beneath the dorsal, common, atrioventricular valve to illustrate the ventricular component of the defect.

this double defect. Apparently, as will be described in the next section, these two defects may occur together as one continuous, large defect instead of two separate defects.

some foramen ovale defects. It is possible,

The appearance and size of one defect led us to call it a continuous combined defect of both the foramen ovale and the high types (Fig. 6). Superiorly it continued into the superior vena cava, and posteriorly the pulmonary veins emptied anomalously. These features characterize the high defect. Inferiorly, its margins continued into the valve of the inferior vena cava in a way typical of

of course, that this defect represents simply

an enormous foramen ovale defect, with an

almost complete growth failure of the sepsecundum. But the features illustrated, especially the anomalous entry of the pulmonary vein into the superior vena cava, caused us to classify it as a high defect plus a foramen ovale defect. In any case, surgical repair must combine the technics used in the high defect, and in one variety of the foramen ovale defect. By placing the first two stitches as shown in Figure 6A, a technical problem that seemed formidable at first was satisfactorily solved. Postoperative catheterization studies of this case demonstrated that the defect is closed. This defect may have been called "complete absence of the atrial septum" by others.3' 5, 6, 10, 16, 30 It is also possible that very large foramen ovale defects or large ostium primum defects have been labeled, absence of the septum. Of course, in any of


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TABLE IV. Low Defects.

term fits as well as the other, for though the orifice itself is a persistent ostium primum, it is clear that the septum primum in these Number hearts fails to fuse with the endocardial A. Persistent ostium primum; Atrioventricular cushions and the ventricular septum as it valves fused to ventricular septum and mitral valve notched ............... 3* should. The important developmental error B. Common Atrioventricular Canal; primitive in the entire group of low defects, however, valves usually suspended above ventricular septum .................................. 3* probably concerns the endocardial cushions *One patient in each group had a separate foramen ovale primarily rather than the septum pridefect in addition. mum.16, 29, 31 If this type of defect is not actually a defective septum primum, then the designation "persistent ostium primum," these cases some septal tissue would remain, which emphasizes the most obvious part of but in the reported cases of "complete de- the defect without implication concerning fects," too, a rim of septal tissue has been its origin, should be preferred. described and so this explanation is not In the persistent ostium prinium the atrioinvalidated. ventricular valves are fused to the upper crest of the ventricular septum. The triD. LOW DEFECTS-PART OF PERSISTENT cuspid valve is usually complete, while the COMMON ATRIOVENTRICULAR CANAL aortic cusp of the mitral is notched or deformed. Superiorly the two valves have a Low defects offer a formidable challenge continuous surface, but inferiorly they are to the surgeon. Some seem at present to be divided by the ventricular septum (Fig. 7). irreparable. Others may be closed surgically, The edges of such defects can be stitched but the incidence of serious postoperative together without great difficulty while the complications has been distressingly high. heart is open, but the repair itself often In short, treatment is still unsatisfactory, due causes serious complications. The atriovenin large part to the complicated surgical tricular node which lies near the caudal anatomy (Figs. 7 and 8). edge of the defect, adjacent to the coronary In order to describe and classify these sinus, may be injured. The three patients defects we have referred to the terminology upon whom we have operated all developed and concepts of Edwards and his associ- complete heart block with an idioventricular ates.'0 11, 19, 31 In some of these defects the rhythm. One developed this arrhythmia impatent ostium primum apparently stands out mediately and died suddenly on the third as the only important deformity, but Ed- postoperative day. Presumably she died of wards has shown that all of these low defects cardiac arrest, for autopsy disclosed no have in common evidence of a persistent cause. The second patient had a temporary common atrioventricular canal. In some this complete heart block immediately after opcommon canal may remain as nothing more eration, which became permanent one week than a notching of the mitral valve, but it is thereafter. The third patient did not show still this feature that draws all of the low complete heart block until one month after defects into one group. Within the group two operation, but in her case, too, this arrhythmain sub-types, each presenting different mia now seems to be permanent. surgical problems, can be discerned (Table In the case of this last patient we made a IV). careful effort to avoid the conduction sysThe defect designated "persistent ostium tem by placing the stitches as illustrated in primum" in Table IV has been referred to as Figure 7 A and B. The inferior point of the a septum primum defect. Superficially one left atrium reaches approximately the same 411
(Part of persistent, common, atrioventricular canal)


Annals of 1 95 5 ~~~~~~September. Surgery

level as the inferior margin of the defect, so that the left atrial wall may easily be brought into the repair at this dangerous angle. Perhaps this type of repair-further modified-will be the answer. It should be possible to avoid injury to the conduction system, but there is still another danger. Both of our surviving patients may have some mitral insufficiency which was not present preoperatively. After encountering so much trouble in these three patients, we are consoled by knowing that our experience is not unique.4 37 The second anomaly in Table IV (illustrated in Fig. 8) is even more difficult to repair. Called a common atrioventricular canal or an incomplete double heart,' it consists of an ostium primum defect above two primitive atrioventricular valves. These ventral and dorsal common valves should normally have joined together, and each should have developed into part of the mitral and the tricuspid valve. Below one or both of the primitive common valves a free passage between the ventricular cavities is usually found, and it is this additional deformity, especially (a ventricular septal defect), that distinguishes the defect from the persistent ostium primum. The primitive valves of the common atrioventricular canal are suspended above the crest of the ventricular septum by numerous chordae (Fig. 8A), creating an unusual ventricular septal defect. To cure the anomaly the entire defect, including the ventricular component, must be repaired. This is an appalling problem. Three patients with this defect have been operated upon during hypothermia. The first two, one four years old and the other seven months old, were operated upon two years ago. The preoperative diagnosis was simply interatrial septal defect, and we did not, unfortunately, make a correct diagnosis even during the operation. This error led in each case to a fatal attempt at repair. We did at least learn how to recognize the defect at operation, and when to suspect preopera-

tively that it might be present. The third patient was operated upon with the correct presumptive diagnosis and a suture repair was done, stitching the posterior arch of the atrial component down to the valves, and the ventricular septum beneath them. Stitches were taken deep through the valves in order to include the ventricular septum, and thus close the ventricular defect. Nevertheless, the entire ventricular component of the defect was not closed; on top of this, a significant mitral insufficiency was created, and the child did not survive the operation. Figure 9 is a photograph of this defect.

The open technic, employing hypothermia, is a good technic for repairing atrial septal defects of the first three types (Table I). Among 29 patients, only three died. Even these deaths, in the light of experience, could have been prevented, with the possible exception of one which was due to irreversible ventricular fibrillation. This low mortality rate has been achieved without employing an age limitation for the operation. Eight patients were over 30, and the oldest, an apparent cure, was 52. The median age was 19. If the three patients with ostium primum defects (Table IV, sub-type A), and the one patient who did not have a cardiotomy are added, survival statistics are still good (four deaths among 33 patients) . It seems reasonable, when trying to estimate the risk of an operation for atrial septal defects, to exclude the three patients who had common atrioventricular canal defects, for these defects have a ventricular component. By objective criteria the operation has made good in the first three types of defect. Twelve patients have had postoperative, cardiac catheterization studies to date, and the defect was completely closed in all but two. In both of these the shunt is only a fraction of its former value. In one the remaining shunt is due to an anomalous pulmonary vein which was associated with a high de-


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fect; it was unnoticed at the time of surgery (Type II defect). The other patient with a small remaining shunt had a large foranten ovale defect and mitral stenosis. Except for the patients with low defects, the survivors have improved clinically in every case.

The most disturbing complication of this technic is ventricular fibrillation. It occurred in 11 patients, but with massage, intracardiac adrenalin and electrical shock the hearts were successfully defibrillated in every case but one. This one was a 39-year-old man whose heart fibrillated while the chest was being opened. He was the only patient cooled rapidly in an ice water bath. In one other patient ventricular fibrillation started before the heart was exposed, but in the nine remaining patients it occurred just before, during, or just after the open cardiotomy.

Some experimental evidence has indicated that the addition of C02 to the respiratory mixture during cooling might lower the MULTIPLE DEFECTS incidence of ventricular fibrillation,27 but we have been able to test this concept in There is with multionly one patient. Despite the fact that she ple defects no mystery associatedThey do not of the atrial septum. was a poor operative risk, 31 years old, with mitral stenosis, mitral insufficiency, and con- occur in random fashion but seem, rather, to be of two general types. The first type is gestive failure, ventricular fibrillation did simply an association of either a high or a not occur. low defect with a patent foramen ovale. The Experimentally, coronary perfusion during hypothermia has extended the time limit second type of multiple defect is merely a for inflow occlusion, and it was used in two variation of the foramen ovale defect. It is of the patients in this series.33 It has not, found when the membranous valve of the remains either as a perforated however, done away with the problem of fossa ovalis or as a number of strands membrane, crossventricular fibrillation. ing the defect (Fig. 2A). It has been well illustrated and described by Patten,28 and REPAIER OF LOW DEFECTS much earlier by Rokitansky.32 The perEven with the advantages of an open forated foramen ovale defect could, of technic we have not yet mastered low de- course, coexist with either a low or high fects. In the persistent ostium primum, re- defect, and conceivably all three principal pair may injure the conduction system or the defects could occur, isolated from one anmitral valve. For the common atrioventricu- other, in the same septum, but we have not lar canal defect, suture repair is even more yet seen or read about such a fantastic troublesome. In all of the low defects stitches pathological cluster.

needed for the repair may cause trouble. It would be advisable to do without them. Of course this cannot be accomplished by simply using a graft or a plastic patch, for stitches are still necessary. We have developed various plastic devices to close ventricular septal defects, experimentally at least, without stitches or with only one stitch,24' 34 but such devices do not fit into these low defects. There is still another disconcerting complication. In low defects the scarring which follows repair may cause late complications. In the foramen ovale defects and the high defects there is plenty of room for a scar, but not in the low defects. In these the repair scar may impede valve function, or even cause late damage to the conduction system. Both patients who survived repair of low defects developed complete heart block some time after surgery. In one it became permanent one week after operation, and in the other it did not occur until one month thereafter.



September, 1955

1. The surgical anatomy of atrial septal defects described here is based upon observations made during 35 operations to repair these defects under direct vision, during hypothermia. 2. Defects of the atrial septum have been classified into four main types: foramen ovale defects, high defects, continuous defects of both the foramen ovale and the high septum, and low defects. Partial anomalous pulmonary venous drainage is found occasionally with the first type of defect, and it is invariably associated with high defects,
in our experience.

3. The first three types of defect, even when complicated, can be satisfactorily repaired under direct vision by carefully drawing the true margins together with stitches. Attempts to repair low defects, on the other hand, have so far been unrewarding, if not catastrophic. Nonetheless, at least one category of low defect, the persistent ostium primum, should be reparable at the present time.
BIBLIOGRAPHY Abbott, M. E.: Atlas of Congenital Cardiac Dis-

ease. American Heart Association, New York, 1936, p.62. 2 Atkinson, W. J., J. L. Dean, E. H. Kennendell and C. J. Lambertsen: A Multiple Anomaly of the Human Heart and Pulmonary Veins. Anat. Rec., 78: 383, 1940. 3 Bailey, C. P., D. F. Downing, G. Geckeler, W. Likoff, H. Goldberg, J. C. Scott, 0. Janton and H. P. Redondo-Ramirez: Congenital Interatrial Communications: Clinical and Surgical Considerations With a Description of a New Surgical Technic: Atrio-SeptoPexy. Ann. Int. Med., 37: 888, 1952. 4 Bailey, C. P., H. T. Nichols, H. E. Bolton, W. L. Jamison and M. Gomez-Almeida: Surgical Treatment of Forty-six Interatrial Septal Defects by Atrio-Septo-Pexy. Ann. Surg., 140: 805, 1954. 5 Bailey, C. P.: Surgery of the Heart. Lea & Febiger, Philadelphia, 1955, p. 1062. 6 Bedford, D. E., C. Papp and J. Parkinson:

Atrial Septal Defect. Brit. Heart J., 3: 37, 1941. 7 Brown, A. J.: The Development of the Pulmonary Vein in the Domestic Cat. Anat. Rec., 7: 299, 1913. 8 Cabot, R. C.: Facts on the Heart. W. B. Saunders Co., Philadelphia, 1926, p. 754. 9 Davis, F., and M. A. MacConaill: Cor Biloculare, With a Note on the Development of the Pulmonary Veins. J. Anat. 71: 437, 1937. 10 Edwards, J. E.: Congenital Malformations of the Heart and Great Vessels. In Gould, S. E.: Pathology of the Heart. C. C. Thomas, Springfield, 1953, p. 266. Edwards, J. E., T. J. Dry, R. L. Parker, H. B. Burchell, E. H. Wood and A. H. Bulbulian: Congenital Anomalies of the Heart and Great Vessels. Charles C. Thomas, Springfield, 1954. p. 202. 12 Geddes, A. C.: Abnormal Superior Vena Cava. Anat. Anz., 41: 449, 1912. 13 Greenfield, WV. S.: A Case of Malformation of the Heart, with Large Deficiency in the Interauricular Septum, Patency of the Foramen Ovale, and Stenosis of the Aortic Orifice. J. Anat. & Physiol., 24: 423, 1890. 14 Gross, R. E.: The Surgery of Infancy and Childhood. W. B. Saunders Co., Philadelphia, 1953, p. 1000. 15 Gross, E., E. Watkins, Jr., A. Pomeranz and T. Goldsmith: A Method for Surgical Closure of Interauricular Septal Defects. Surg., Gynec. & Obst., 96: 1, 1953. 16 Gunn, F. C., and J. M. Dieckmann: Malformations of the Heart Including Two Cases With Common Atrioventricular Canal and Septum Defects and One With Defect of the Atrial Septum. Am. J. Path., 3: 595, 1927. 17 Hepburn, D.: Double Superior Vena Cava, Right Pulmonary Veins Opening Into the Right Auricle, and a Special Interauricular Foramen. J. Anat. & Physiol., 21: 438, 1887. 18 Ingalls, N. W.: Report. Communication Between the Right Pulmonary Veins and the Superior Vena Cava. Anat. Rec., 1: 14, 1907. 19 Kirklin, J. W., H. J. C. Swan, E. H. Wood, H. B. Burchell and J. E. Edwards: Anatomic, Physiologic, and Surgical Considerations in Repair of Interatrial Communications in Man. J. Thoracic Surg., 29: 37, 1955. 20 Lewis, F. J., and M. Taufic: Closure of Atrial Septal Defects With the Aid of Hypothermia; Experimental Accomplishments and the Report of One Successful Case. Surgery, 33: 52, 1953. 21 Lewis, F. J., R. L. Varco and M. Taufic: Repair of Atrial Septal Defects in Man Under


Number 3

Volume 142


Rogers, H. M., and J. E. Edwards: Incomplete Division of the Atrioventricular Canal With Patent Interatrial Foramen Primum (Persistent Common Atrioventricular Ostium). Am. Heart J., 36: 28, 1948. 32 Rokitansky, C. F.: Die Defect der Scheidewande des Herzens. Wilhelm Braumiiller, Vienna, 1875, p. 153. 33 Shumway, N. E., and M. L. Gliedman: Coronary Perfusion for Longer Periods of Cardiac Occlusion Under Hypothermia. Presented at Am. Assoc. for Thoracic Surg. Meeting. April, 1955. 34 Taufic, M., and F. J. Lewis: Production and Repair of Experimental Interventricular Septal Defects Under Direct Vision With Aid of Hypothermia. Surg. Forum. American College of Surgeons, W. B. Saunders Co., Phliadelphia, 4: 67, 1953. 35 Van Cleave, C. D.: A Multiple Anomaly of the Great Veins and Interatrial Septum in a Human Heart. Anat. Rec., 50: 45, 1931. 36 Wagstaffee, W. W.: Two Cases of Free Communication Between the Auricles, by Deficiency of the Upper Part of the Septum Auricularum. Tr. Path. Soc. London, 19: 96, 1868. 37 Watkins, E., Jr., and R. E. Gross: Experiences With Surgical Repair of Atrial Septal Defects. Presented at Am. Assoc. for Thoracic Surg. Meeting, April, 1955.








Direct Vision With the Aid of Hypothermia. Surgery, 36: 538, 1954. Lewis, F. J.: Hypothermia in Cardiac and General Surgery. Minnesota Med., 38: 77, 1955. .-----: Repair of Atrial Septal Defects During Hypothermia. Postgraduate Med., 17: 293, 1955. Lewis, F. J., and M. Taufic: The Repair of Experimental Interventricular Septal Defects, During Hypothermia, with a Molded Polyvinyl Sponge. Surg., Gynec. & Obst., 100: 583, 1955. Licata, R. H.: The Human Embryonic Heart in the Ninth Week. Am. J. Anat., 94: 73, 1954. Muller, W. H., Jr., S. W. Smith, J. F. Dammann, Jr., F. H. Adams and M. L. Darsie: Considerations and Physiologic Studies in the Closure of Interauricular Septal Defects. Surgery, 37: 1, 1955. Niazi, S. A., and F. J. Lewis: The Effect of Carbon Dioxide on Heart-Block and Ventricular Fibrillation During Hypothermia in Rats and Dogs. Surg. Forum Am. Coll. of Surg., 1954. In press. Patten, B. M.: Developmental Defects at the Foramen Ovale. Am. J. Path., 14: 135, 1938. Robson, G. M.: Congenital Heart Disease. A Persistent Ostium Atrioventriculare Commune With Septal Defects in a Mongolian Idiot. Am. J. Path. 7: 229, 1931. Roesler, H.: Interatrial Septal Defect. Arch. Int. Med., 54: 339, 1934.

DIscUSSION.-DR. HARus B. SCHUMACKER, JR., Indianapolis, Indiana: I would like to congratulate Dr. Swan and his co-workers, and Dr. Lewis and his group, upon their very informative and stimulating papers. Dr. Lewis mentioned the problem of the prevention of ventricular fibrillation, and I arise primarily to tell you briefly of some experiences we have had in the experimental laboratory with normal dogs. The situation may not be entirely the same with the diseased human heart, but it has been possible for us to carry out without ventricular fibrillation right ventriculotomies in cooled dogs during complete occlusion of venous inflow provided we did one of several things. One is to block the sino-auricular node with procaine. Under such circumstances the heart slows remarkably, becomes quite free of irritability, and the animal seems to be well protected. A second is to perform a sympathetic de-

nervation by removing the upper dorsal and lower cervical sympathetic chain. Finally, although our work in this respect is as yet quite preliminary, it seems that the use of the blocking agent, arfonad, accomplishes almost as much as the other methods. All the control animals undergo ventricular fibrillation when right ventriculotomy is carried out in the hypothermic state. These methods have indeed changed the picture in the experimental animal to this extent, that we have been able to open the right ventricle and produce and close ventricular septal defects in a fairly large series of animals without mortality.
DR. HENRY T. BAHNSON, Baltimore, Maryland: I can give nothing but compliments to the two preceding speakers, and hope that my comments will not be taken as a criticism of their papers. Knowing that Dr. Lewis and others are so well bracketed by hypothermia, and knowing that all of