Atrial Septal Defect: Acute Left Heart Failure After Surgical Closure Juergen Beyer, M.D.

ABSTRACT Sixteen of 766 patients operated on for sure was no longer being monitored because isolated atrial septal defect developed severe acute of a seemingly uneventful postoperative course. left heart failure that necessitated partial reopening of Only 2 patients demonstrated additional signs the defect; 6 died. The prognosis depended mainly on of forward failure, as shown by low cardiac outprompt surgical intervention. The most frequent put syndrome. pathological and anatomical finding was marked When intensive medical treatment failed to hypoplasia of the left ventricle. Pulmonary hyperten- affect the cardiac status, surgical therapy was sion appeared to be of minor importance. Hemody- applied; this consisted of creation of a small denamic data published by others support the fect (about 1 cm in diameter) in order to reduce hypothesis that this complication is often the result of the preload of the left ventricle. In 10 patients markedly impaired left ventricular compliance as- this led to rapid improvement, but the other 6 sociated with left ventricular hypoplasia. died from progressive heart failure. The prog-

nosis depended mainly on prompt surgical intervention: reopening was successful in most patients (8 of 10) when it was performed before massive pulmonary edema developed; mortality was high (4 of 6) when surgical therapy was delayed. All patients who survived the operation underwent reexamination three months postoperatively and at yearly intervals thereafter. In 6 patients, heart catheterization was performed one to three years postoperatively. One of these patients underwent reoperation for complete closure of the defect because of a high residual shunt volume; this procedure was well tolerMaterials and Methods ated. Another patient, a 53-year-old woman From December, 1958, to December, 1976, 766 who had been suffering from congestive heart patients were operated on for isolated ASD, failure preoperatively, gradually developed mainly of the secundum type. Sixteen patients signs of increasing left and right ventricular fail(2.1%) suffered acute left ventricular failure ure in the years following operation. In the reeither immediately after closure of the defect (10 maining 8 patients long-term follow-up has patients) or u p to 30 hours postoperatively (6 shown good results. Statistical data on the 16 patients were compatients). In the first group this was evidenced by a rapidly increasing left atrial pressure; in the pared to those on a control group consisting of second group acute pulmonary edema was the 100 patients who had isolated ASD. first sign of heart failure, when left atrial presThe repair of an isolated atrial septal defect (ASD) is believed to carry a very low risk compared with other types of open-heart operations. Only marked pulmonary hypertension and preoperative congestive heart failure [2-6, 12, 14, 16-201 are thought to influence the surgical mortality rate. In a small group of our patients, however, closure of the defect was followed by acute left heart failure, even in the absence of these risk factors. This paper reports our experience with this unusual complication and discusses its possible causes.

From the Department of Cardiac Surgery, University of Munich Medical School, Nussbaumstr 20,8000 Mdnchen 2, West Germany.

I would like to thank Prof. Dr. K. Buehlmeyer and Dr. R . Mocellin of the Deutsches Herzzentrum Miinchen for their help in reviewing the cineangiograms of their patients. Accepted for publication May 13, 1977.

36

Results Evaluation of the possible causes contributing to acute left ventricular failure in this group of patients revealed the following facts. There was a significant prevalence (69%) of patients 10 years of age or younger compared with the control

OOO3-4975/78/0025-0108$01.25 @ 1978 by The Society of Thoracic Surgeons

37 Beyer: Atrial Septa1 Defect

group (24%) ( p < 0.003); a second, less prominent peak was seen in the 41- to 50-year age group (Fig 1).The pertinent history was unremarkable in 14 patients. Only 2 patients, both adults, had been suffering from heart failure preoperatively. Except for a patient who had an ostium primum defect, the ASD was of the secundum type in all patients. A large ASD was seen in only 4 patients. Slight mitral stenosis, without hemodynamic significance, was found in 1 patient during operation. Ten patients (8 children and 2 adults) had unusually small left ventricles; 5 were severely hypoplastic. Several times, hypoplasia of the aorta was an additional finding. In this study, the term hypoplastic is used for all ventricles which, on the basis of preoperative cineangiograms (Fig 2) or intraoperative findings, were found to be markedly smaller than those seen in other patients with an ASD; in 2 fatal cases this estimation of left ventricular volume was confirmed at postmortem examination. However, exact calculation of the volume was not possible for two reasons. Cineangiograms had not been performed routinely, as measurement of intracardiac pressures and oxygen saturation appeared to provide sufficient information for establishing the diagnosis of an isolated ASD. Second, the cineangiograms performed in 5 patients were not suitable for calculating left ventricular volume because of lack of a reference grid [ l l ] or exact data regarding tube-to-object and tube-to-film distances [l, 7,

Fig 1 . A g e distribution of patients with ati isolated A S D (controls) atid patierits with acutc left heart failure (LHF) after surgical closure of an A S D . T O controls Ptr with acute of an A S D

4

i'i,

10

4 0 5 0 60

L age

LHF alter closure

131 to permit correcting for roentgenographic distortion and magnification. The incidence of left ventricular hypoplasia was noticeably less in the control group than in the study group: only 12% of the ventricles were classified as small and none as severely hypoplastic, compared with 5 ventricles in each category (= 62%) in the study group (Table 1).It is noteworthy that 1 control group patient whose ventricle had been classified as small died from acute left heart failure with frank pulmonary edema 24 hours postoperatively. For reasons that could not be evaluated from the records, no attempt was made to treat his heart failure by reopening the ASD. None of the other control subjects developed signs of acute left ventricular failure during or after operation. Only 2 patients temporarily suffered from low cardiac output, but this was induced by severe hypovolemia and extreme tachycardia, respectively; there was no evidence of backward failure.

Hemodynamic Data Preoperatively the left-to-right shunt volume, expressed as percentage of total pulmonary blood flow, ranged from 35 to SO% (mean, 59 2 24%); this value did not differ from that of the controls (60 ? 13%). Light to moderate pulmonary hypertension was present in approximately two-thirds of the patients, with almost the same incidence in the control group (Table 2). Average systolic pulmonary artery pressure was 36 k 15 mm Hg in the study group and 32 2 11mm Hg in the control group. In the study group the preoperative cardiac index, as determined by the Fick principle, was 2.73 f 0.56 liters per minute per square meter of body surface area for children and 3.74 +. 1.63for adults. These values were 4.64 +. 1.16 and 3.26 f 1.10, respectively, in the control group. Thus, the children in the study group had a significantly lower cardiac index than those in the control group ( p < 0.001); the difference between the values determined for the adult patients in the two groups was not significant. In the control group systolic arterial pressure measured at the beginning of the operation, 15 to 30 minutes after closure of the ASD, and 1 hour postoperatively was almost constant. Patients with left heart failure showed, on the av-

38 The Annals of Thoracic Surgery Vol 25 No 1 January 1978

LA RA

LA

B Fig 2 . Cineangiograms with lint. interpretations from a patientwijh A S D and left ventricular hypoplasia s h o w marked difference between right (RV) and left (LV) ventricular volumes, zuith the left ventricle representing only a small part of total heart volume. ( A )Anteroposterior v i e w , end-diastole. (B)Anteroposterior v i e w , end-systole. (C) Lateral viero, end-diastole. ( D ) Lateral v i e w , end-systole. (RA = right atrium; LA = left atrium.)

vc.. !mia may have played a role in 2 patients in whom CVP temporarily rose to 13 and 15 mm Hg, respectively. In both patients, however, the left ventricle was hypoplastic. On the other hand, mean values for CVP measured before and during the development of left ventricular failure did not differ significantly from values obtained in the control subjects (Fig 3B). Following closure of the ASD, a slight to erage, a minor fall (-14%) in systolic pressure moderate increase in mean left atrial pressure after closure of the defect; this change ranged was seen in almost all control patients; the averfrom +lo% to -35%. However, the meanvalues age pressure rose from 6.8 ? 2.5 to 11.1& 4.2 mm did not differ significantly from the controls at Hg. In contrast, the patients with acute left heart any time (Fig 3A). failure showed a sharp increase, from an average Central venous pressure (CVP) was monitored of 6.8 k 2.1 to 25.7 k 8.2 mm Hg. When the during operation and for u p to three days post- defect was partly reopened there was a marked operatively. According to these data, hyper- fall to 12.6 & 4.3 mm Hg. The difference between

39 Beyer: Atrial Septa1 Defect

LA LV

LA LV

D

the values measured after closure of the defect in the two groups of patients was statistically significant ( p < 0.001) (Fig 3C).

Recatheterization was performed in 6 of the 10 patients who survived operation. A summary of intracardiac pressures, cardiac index, and left-

40 The Annals of Thoracic Surgery Vol 25

No 1 January 1978

Table 1 . Semiquarititatiur Estimation of Left Ventricular Volume in Control Patients and Study Group

grams in 3 of these patients showed a normal or near-normal left ventricular volume.

Comment A review of our records showed acute left heart failure to be one of the severe, although rare, Severely complications that occur after surgical closure of Patient Group Normal Small Hypoplastic an ASD. In a group of 16 patients this complicaControls 88% 12% 0% tion was treated by partial reopening of the de(N = 100) fect. In 4 of these patients hypervolemia or Study group 6 5 5 preoperative congestive heart failure may have ( N = 16) (= 38%) (== 31%) (= 31%) contributed to the complication; however, in these as well as the remaining 12 patients, an to-right shunt volume in these patients is given additional anatomical anomaly such as left ventricular hypoplasia was evident or, retrospecin Figure 4. The condition of 1of these patients, tively, should have been taken into considerawho had been suffering from beginning heart tion (Table 3). failure preoperatively, had deteriorated in the It is interesting that the hemodynamic mechinterim; clinically and hemodynamically there anism of acute left ventricular failure after clowas evidence of increasing left and right vensure of an ASD has received so little attention tricular failure. The other 5 patients were in good even though left ventricular hypoplasia in these clinical condition. Hemodynamic data invarpatients is well known to cardiologists. Cooley iably showed a tendency toward normal values and Hallman [ 5 ] mentioned pulmonary edema or remained within normal limits. In 1 of these as the most important postoperative complicapatients, however, the residual ASD apparently tion, but they considered massive overtransfuhad increased in size: left and right atrial pression or severe pulmonary hypertension as its sures were almost identical, and the left-to-right main cause. Gerbode and associates [9] lost 1of shunt volume was 50% of total pulmonary blood 77 patients, a 3-year-old girl who had developed flow. This patient underwent reoperation for pulmonary congestion. Sellers and colleagues complete closure of the defect seven years after [17] and Spencer [18] emphasized the importhe initial procedure; no complications occurred tance of hypertension for the development of during or after this operation. In another paacute cardiac failure. On the other hand, pulmotient, recatheterization failed to reveal evidence nary hypertension alone would hardly be exof a persisting interatrial communication; sponpected to lead to this complication. Only 2 of our taneous closure of the residual defect was patients had suffered from moderate hypertenthought to have occurred secondary to postsion preoperatively (systolic pressure, 51 to 75 operative bacterial endocarditis. Cineangiomm Hg). The rest of the group had had normal (N = 6 ) or slightly elevated (N = 8) pulmonary artery pressure. Table 2 . Preoperative Systolic Pulmonary Artery Left ventricular hypoplasia of varying degrees Pressure in Control Patients and Study Group with major reduction in the end-diastolic volume, stroke volume, and cardiac index has been Systolic Pressure (mm Hg) a common finding in patients with an ASD [lo, 13, 151, in infants and children [lo, 131, and in Patient Group 525 26-50 51-75 >75 adults [15]. It is not clear if this finding represents a primary congenital defect which, as an Controls 32% 62 '/o 5O/O 10% obstructive anomaly of the left side, may lead to (N = 100) an acquired ASD, as suggested by Tandon [191: Study 6 (238%) 8 (=50"/,) 2 (212%) 0 pressure overload of the left atrium could result group ( N = 16) in stretching of the atrial septum, including the Left Ventricular Volume

41 Beyer: Atrial Septa1 Defect

4

mm Hg

150-

50-

Part

0

I

begin

A

I

t

-/

15‘after Closure of the ASD

after reopening of the ASD (study group) 1hr postop (controls)

11

mm Hg

16 12

---

8 4

CVP 0 ’

I

begin

B

1

15’ after closure of the ASD

- t

1

before re-opening of the ASD (study group) 1hr postop (controls)

mm Hg

40

t T

30 20 10 PLA

0 I

begin

C

I

1

15’after closure

of the ASD

Fig 3 . ( A ) Systolic arterial pressure (Part),( B ) central venous pressure (CVP), arid (0 mean left atrial pressure (PLA)beforc, and after closure ofASD in patients with acute left heart failure (solid lines) and controls (dashed lines).

valve of the foramen ovale, gradually yielding an ASD. On the other hand, left ventricular hypoplasia could be considered the result of a constantly diminished filling volume secondary to the left-to-right shunt [151.

- t

15‘after re-openlng

of the ASD

Regardless of the mechanism leading to an ASD, the left ventricle shows poor adaptation to a sudden increase in preload. Popio [15]showed that administration of 10% dextran increased the end-diastolic pressure twofold with “minimal, if any, increase in end-diastolic volume index.” This is thought to reflect markedly reduced distensibility of the left ventricle. These results are paralleled by our observations: signs of backward flow through the left ventricle were the most prominent findings, whereas systemic

42 The Annals of Thoracic Surgery Vol 25 No 1 January 1978

mm Hg

A

A

A

A

2015-

10-

-

5P

postop

preop

PRA

1

A rnm Hg

mrn H g

6040

-

20

-

20-

PRV

L-R Shunt Fig 4. Preoperative and postoperative (one to three years) hemodynamic data in patients 7i~ho had partial surgical c l o s u r e g A S D . (PRA= mean right atrial pressure; PLA= mean left atrial pressure; PRV= systolic right ventricular pressure; PPA= systolic pulmonary artery pressure; CI = cardiac index.)

pP A

CI

cause severe backward flow and consequently induce the vicious cycle of pulmonary edemahypoxia-increasing heart failure. Infants and young children appear to be especially sensitive to this mechanism, possibly because of the relatively little exercise to which the heart has prearterial pressure usually changed only little in viously been exposed. O n the other hand, the early phase of the complication. pulmonary hypertension may represent an To date, these findings have not been corre- additional risk primarily in older patients, in lated with the acute left heart failure occasionally whom the discrepancy between performance of seen after closure of an ASD. It is our belief that the right and left ventricles is increased because the sudden removal of the left-to-right shunt of the existing right ventricular hypertrophy. exposes the left ventricle to a sudden increase in Older patients may be threatened by impaired preload which, in combination with the di- myocardial performance, as evidenced by minished distensibility of the chamber, may preoperative congestive heart failure and by ad-

43 Beyer: Atrial Septa1 Defect

Table 3 . Possible Causes of Acute Left Ventricular Failure after Closure of an A S D in 26 Patients Cause

No. of Patients

Left ventricular hypoplasia Alone With pulmonary hypertension and hypervolemia With pulmonary hypertension and preoperative congestive heart failure Pulmonary hypertension and preoperative congestive heart failure Unknown

10 7 2 1 1

5

ditional, although mild, stresses such as hypertension, atrial fibrillation, or mitral regurgitation 1151. The fact that subnormal left ventricular volume is a common finding in ASD but that acute left heart failure is a relatively rare complication after closure of the defect suggests that individual factors play an important role in this regard. First, the degree of hypoplasia appears to determine the tolerance to a sudden change in the hemodynamic pattern. Second, the degree of impairment of left ventricular distensibility due to possible degenerative changes of the myocardium [ 8 ] ,as well as the size of the left atrium and the anatomy and function of the mitral valve, will additionally influence the performance of the left heart. Whereas exact assessment of these three factors may be difficult, the size of the left ventricle can be estimated reliably from a routine cineangiogram and from intraoperative findings. If marked hypoplasia indicates a risk of cardiac failure postoperatively, left atrial pressure should be monitored carefully for u p to two days. If, in the absence of hypervolemia, systolic pressure increases to 25 to 30 mm Hg or pulmonary edema develops, prompt surgical intervention appears mandatory. References Arcilla RA, Tsai P, Thilenius 0, et al: Angiographic method for volume estimation of right and left ventricles. Chest 60:446, 1971 Attai M: Secundum atrial septal defects: results of open surgical repair. NY J Med 69:3007, 1969 Blake HA, Hall RC, Manion WC: Anomalous pulmonary venous return. Circulation 32:406, 1968

4. Coles J, Sears G, McDonald C: Atrial septal defect complicated by pulmonary hypertension: a long term follow up. Ann Surg 166:496, 1967 5. Cooley DA, Hallman GL: Surgical Treatment of Congenital Heart Disease. Philadelphia, Lea & Febiger, 1966 6. Cooley DA, Hallman GL, Leachman RD: Total anomalous pulmonary venous drainage. J Thorac Cardiovasc Surg 51238, 1966 7. Dodge HT, Sandler H, Ballew DW, et al: The use of biplane angiocardiography for the measurement of left ventricular volume in man. Am Heart J 60:762, 1960 8. Gault JH, Morrow AG, Gray WA, et al: Atrial septal defect in patients over the age of forty years. Circulation 37:261, 1968 9. Gerbode F, Harkins GA, Ross JK, et al: Experience with atrial septal defects repaired with the aid of cardiopulmonary bypass. Arch Surg 80:846, 1960 10. Graham TP, Jarmarkani JM, Canent RV: Left heart volume characteristics with a right ventricular volume overload: total anomalous pulmonary venous connection and large atrial septal defect. Circulation 45:389, 1972 11. Greene DG, Carlisle R, Grant C, et al: Estimation of left ventricular volume by one-plane cineangiography. Circulation 35:61, 1967 12. Hanlon CR, Barner HB, Willmann VL, et al: Atrial septal defect: results of repair in adults. Arch Surg 99:275, 1969 13. Mathew RC, Thilenius OG, Arcilla RA: Comparative response of right and left ventricles to volume overload. Am J Cardiol 38:209, 1976 14. McGoon DC, Swan HJC, Brandenburg RO, et al: Atrial septal defect: factors affecting the surgical mortality rate. Circulation 19:195, 1959 15. Popio KA, Gorlin R, Teichholz LE, et al: Abnormalities of left ventricular function and geometry in adults with an atrial septal defect. Am J Cardiol 36:302, 1975 16. Rahimtoola SH, Kirklin JW, Burchell HB: Atrial septal defect. Circulation 37, 38:Suppl 5:2, 1968 17. Sellers RD, Ferlic LP, Sterns LP, et al: Secundum type atrial septal defects: early and late results of surgical repair using extracorporeal circulation i n 275 patients. Surgery 59:155, 1966 18. Spencer FC: Atrial septal defect, anomalous pulmonary veins, and atrioventricular canal, Surgery of the Chest. Edited by JH Gibbon, DC Sabiston, FC Spencer. Philadelphia, Saunders, 1974 19. Tandon R, Edwards JE: Atrial septal defect in infancy: common association with other anomalies. Circulation 49:1005, 1974 20. Tikoff G, Keith TB, Nelson RM, et al: Clinical and hemodynamic observations after surgical closure of large atrial septal defect complicated by heart failure. Am J Cardiol 233310, 1969 21. Wertheimer M, Moller JH, Castaneda AR: Pulmonary hypertension and congenital heart disease. Ann Thorac Surg 16:416, 1973

Atrial septal defect: acute left heart failure after surgical closure.

Atrial Septal Defect: Acute Left Heart Failure After Surgical Closure Juergen Beyer, M.D. ABSTRACT Sixteen of 766 patients operated on for sure was n...
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