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Hemodynamic determinants of risk in pulmonary artery banding
Hemodynamic Determinants of Risk in Pulmonary Artery Banding Joe R. Utley, MD, Lexington, Kentucky
Banding of the pulmonary artery is a palliative procedure for several types of congenital heart disease; the most common is ventricularseptal defect with intractable heart failure. In ventricular septal defect and more complex lesions such as endoe.ardial cushion defect, transposition of the great vessels with ventricular septal defect, double outlet right ventricle,and truncus arteriosus,banding has also been performed to decrease pulmonary blood in patients with heart failureand to prevent and reverse pulmonary vascular disease. The results of banding have been variable. The mortality for banding in isolated ventricular septal defects has been low but the risk is greater when performed for endocardial cushion defects or atrial septal defect plus ventricular septal defect [I-4]. Although the risk of banding is greater with more complex lesions, the hemodynamics may be as important as the anatomy in determining the risk.~ of pulmonary artery banding. There has been no hemodynamic basis for selecting patients with atrial septal defect plus ventricular septal defect or endocardial cushion defect for pulmonary artery banding. Despite the high risk of banding the pulmona~ artery in patients with atrial and ventricular shunts, no criteria have been available for predicting which patients are at greatest risk for banding. As results for cor-
From the Departmentof Surgery, Division of Cardiothoracic Surgery. University of Kentucky School of Medicine. Lexington. Kentucky 40506. Reprint requests should be addressed to Dr Utley. Division of Cardiothoracic Surgery. University of Kentucky School of Medicine. Lexington. Kentucky40506.
30
rective procedures in infants improve, the proper selection of patients for correctiveversus palliative surgery becomes increasinglyimportant. In this study patients with left to right shunts have been classifiedaccording to the magnitude of the shunt (QP/Qs) and the pulmonary artery pressure (APp/APs). The study shows that the risk of banding is great in patients with either low right ventriculilrpressure (APp/APs < 0.{3)or low flow ratios (QP/Qs < 2.0) and that patients with high pulmonary artery pressures and high flow ratios have the lowest mortality for pulmonary artery banding. Material The results of cardiac catheterization in patients with left to right shunts without right to left shunting were reviewed to classify the hemodynamics of the
shunt. Rs/Rp was used rather than Rp/Rs because the relationof Rs/Rp to QP/Qs in nonrestrictiveshunts is linear.The patientswith ventricularseptal defectwere grouped according to the ratioof right to leftventricular pressure (PRY/PLY) and were considered restrictive when PRY/PLY was less than 0.6 and nonrestrictive when Pav/PLv was greaterthan 0.6. Patent ductus arteriosuswas considered nonrestrictiveifmean or phasic aortic and pulmonary artery pressureswere equal. The flow ratios(QP/Qs) were plotted against the resistance ratios (Rs/Rp). Patients who did w-.~ have banding but who were incorporated in the c',.assification included six with nonrestrictive ventricular septal defect, eight with restrictive ventricular septal defect, five with nonrestrictive patent du'ctus arteriosus: fifteen with secundum atrial septal defect, two with left ventricular to .right atrial shunts, and eighteen with endocardial cushion defect.
The Arnedcan Journal of Surgery
Hemodynamic Determinants in Pulmonary Artery Banding •
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Qp s Figure 1. Flow ratios ( Q p / Q ~ and resistance ratios (Rs/Rp) for non. restrictive patent ductus arteriosus and nonrestrictive ventricular septal defect. All pressure ratios are above 0.6 and flow ratios (QP/Qs) largely determined by resistance ratios (Rs/Rp).
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The results of prebanding cardiac catheterization were reviewed in twenty-two patients with yentricular septal defect, ten patients with endocardial cushion defect, and ten patients with atrial septal defect and ventricular septal defect. In eighteen of the twenty-two banded patients with ventricular septal defect the Piw/PLv was greater than 0.6. Nine of ten banded patients with atrial septal defect and ventricular septal defect had a P~v/PLv greater than 0.6. All ten patients with endocardial cushion defect had a PRY/PLY greater than 0.6. Cardiac catheterization of forty-nine patients with atrial septal defect plus pulmonic stenosis was reviewed to determine the effect of increased right ventricular afterload on atrial shunting.
tricular septal defect or nonrestrictive p a t e n t ductus arteriosus. In these lesions the pressure ratios (APp/APs) are relatively fLxed near 1.0 and flow ratios (QP/Qs) are dependent on resistance ratios (Rs/Rp). In these pat!ents pressure ratios (APP/APs) declined as flow ratios (QP/Qs) increased because of increased left atrial pressures in both ventricular septal defect and p a t e n t ductus arteriosus and decreasing mean p u l m o n a r y artery pressure because of greater diastolic runoff in ventricular septal defect. All patients with nonrestrictive ventricular defects are above the A p p / APs ffi 0.6 line. Figure 2 shows the same hemodynamic relationship for patients with atrial septal defect or restrictive left ventricular to right atrial shunts or restrictive ventricular septal defect. T h e relationship of QP/Qs to Rs/Rp is very similar in these lesions. Figure 3 shows the patients with endocardial cushion defect or atrial septal defect
Results Figure 1 shows the relation of pulmonic to systemic flow ratios and systemic to pulmonary resistance ratios for patients with nonrestrictive ven•
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Q.__~e Figure 2. Relationship of flow ratios (Op/Qs) to resistance ratios (R.~/Rp) for atrial septal defect, restrictive Ventricular septal defact, and restrictive left ventricular to right atrial shunL Flow ratios (QP/Qs) are largely independent of resistance ratios (R.~/Rp).
V o l u m e 126, July 1 | 7 3
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Rs/Rp and restrictive or nonrestrictive ventricular septal defect plotted in a similar way. The hemodynamie situation in these more complex lesions is determined mainly by the size of the ventricular communication. Nonrestrictive ventricular communications with atrial septal defect behave much like an isolated nonrestrictive ventricular septal defect although the shunts tend to be larger. Restrictive ventricular shunts with atrial septal defect behave much like the isolated restrictive ventricular defect although the shunts tend to be larger but right ventricular and pulmonary artery pressures remain low. Endocardial cushion defect may be similar to an atrial or restrictive ventricular shunt 6 5
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Rs/Rp Figure 4. Hemodynamic classification of left to right shunts based on flow ratios ( O p / O ~ ) , resistance ratios (R~/RI,), and pressure ratios ( A p p / A p s ) . Group A: Rs/Rp greater than 2.0, App/APs greater than 0.6. Qp/Os Usually greater than 2.0. Group B: R.~/Rp less than 2.0. O p / O s less than 2.0. APp/ APs usually greater than 0.6. Group C: R.~/Rp greater than 2.0. A p p / Ap~ less than 0.6.
32
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Figure 3. Ratio of flows (Qp/Qs) and resistances with endocardlal cushion defect and atrial sePtal defect and restrictive and nonrestrictive ventricular septal defect. Flow ratios are dependent mainly on resistance ratios with nonrestrictive ventricular communications but are much less dependent on resistance ratios with restrictive ventricular defects.
or it m a y behave like a nonrestrictive ventricular shunt. Figure 4 shows three hemodynamic groups based on this classification. Patients with ventrieular septal defect with or without atrial septal defect and endocardial cushion defect may be in group A, B, or C depending on the flow ratios (QP/Qs) and pressure ratio or resistance ratios. Nonrestrictive ventrieular shunts with pressure rfitios (APp/APs) greater t h a n 0.6 and QP/Qs greater than 2.0 are in group A. These patients have relatively nonrestrictive ventricular shunts and low pulmonary vascular resistance, ng~ht ventricular systolic pressure (Pays) is near left ventricular systolic pressure (PLvs), and banding_will not. greatly increase the afterload on the right ventricle. Group C patients are those with low right ventricular pressures (APp/APs < 0.6). The patients have either atrial shunts or restrictive ventricular shunts. B a n d i n g the pulmonary artery in group C patients with ventricular defects will not abolish the venticular shunting, unless right ventricular systolic pressure rises to,equal left ventri• I cular systohc pressure. Such a n acute increase in right ventricular afterload may cause ).he. right ventricle to fail. Thus, banding "may be detrimental in this group of patients. Table I shows the results of banding in hemodynamic groups A, B, and C with ventricular septal defect, ventricular septal defect and atrial septal defect, and endoeardial cushion d e f e c t : Ninetyseven per cent of group A patients survived banding. The mortality was 38 per cent in group B and 50 per cent in group C. In addition to postopera• l:ive death, banding was considered contraindicat-
T h e A m e r i c a n J o u r n a l of
Surgery
Hemodynamlc Determlnants In Pulmonary Artery Banding ed if a gradient across the band could not be tolerated. Banding was contraindicated in five of eight group B patients (62 per cent) and two of four group C patients (50 per cent). W h e n pulmonic to systemic flow ratio (QP/Qs) is less than 2.0 .(group B), pulmonary vascular resistance is increased whether the defect is atrial or ventricular. Patients with endocardial cushion defect which previously behaved like an atrial or restrictive ventricular communication (APp/APs > 0.6) may be poor candidates for banding (group C to B) whereas those who have always had nonrestrictive shunts (group A to B) m a y tolerate a band. Thus, in group B patients with endocardial cushion defect the prior hemodynamic status m a y be important. T w o group B patients who were previously in group, A with high pulmonary artery flows and pressures survived banding. The b~atient who was previously in group C died"after banding. (Table I..) The effect of banding on atrial shunting depends largely on the effect of increased afterload on diastolic compliance. Figure 5 shows the relationship of-the ratio of pulmonic to systemic flow (QP/Qs) to the ratio of ventricular systolic pressures (PIws/PLvs) in forty-nine patients with pulmonic stenosis and atrial septal defect. In this lesion the right ventricular afterload is comparable to the ventricular systolic pressure ratios and the TABLE I
diastolic compliance is comparable to the flow ratios. In general, those patients with greater afterloads and higher right ventricular pressures have lower flow ratios, but right ventricular pressure may be greater than left ventricular pressure with significant left to right shunting still occurring. The great variability in shunting in patients with right ventricular pressures at systemic levels indicates that other factors are important determinants of diastolic ventricular compliance. Patients with pulmonic insufficiency and stenosis had right to left shunting at low right ventricular pressures. From these observations changes in right ventricular afterload would be expected to have an unpredictable effect on atrial shunting particularly with valvular insufficiency. After banding, one patient with endocardial cushion defect had a greatly elevated-'P-ev./~PLv (1:5) and pulmonic to systemic flow ratio of 2.0. Comments
The results-of~banding in isolated ventricular septal defect have been good b u t m o r t a l i t y has been high in patients with both an atrial septal defect and ventricular septal defect or endocardial cushion defect. Gamelgaard et al [5] found that no patients with endocardial cushion defect were
R e s u l t s of P u l m o n a r y A r t e r y B a n d i n g in H e m o d y n a m i c G r o u p s A, B, a n d C
Anatomic Lesion Ventrlcular septal defect Group A Group B Group C Ventricular septal defect and atrial septal deject Group A Group C Endocardial cushion defect GroupA Group B C "-'* B A -'* B Tota~ Group A Group B Group C
Number with Banding
Number of Deaths
Number with Intolerance to Banding
Survival
p*
Banding Contraindicated'l"
15 4 3
0 2 1"
1 1 0
15(100%) 2(50%) 2(66%)
__ "03 NS
1 (7~o) 3(75%) 1 (33%)
... .01 NS
9 1
0 1
0 0
9(100%) 0(0%)
... NS
0(0%) 1 (100%)
... NS
6 4 I 2
I 1 1 0
t 1 0 0
5 (83%) 3(75%) 0(0%) 2(100%)
... NS ... ...
2(33%) 2(50%) 1 (100%) 0(0%)
NS ,.. ...
30 8 4
1 3 2
2 2 0
29(97%) 5(62%) 2(50%)
... .01 .01
3(10%) 5(62%) 2(50%)
... .01 .01
* p determined by comparing groups B and C to group A with Fisher's exact chi square test. 1" Died or would not tolerate band,
Volume 126, July 1973
33
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Figure 5. Ratio of purmonl'c 'tO systemic flow (Op/Os) to right venfricular to left ventricular systotic pressure (Pavs/PLv~ in pulmp'nic stenosis and atria] septal detect. Many flow ratios--ote'-elevafed to 2.Cl with equal systolic pressures in the two ventricles. Flow ratios are much less at the same level of righ,t ventricular pressure when pulrnonic value is insufficient as well as stenotic.
benefited by banding and no patients with this lesion survived banding in the series of Sirak and Craig [3]. Somerville and colleagues [2,4] reported five deaths in twelve cases of endocardial cushion defect treated by banding, and Goldblatt [6] reported a 20 per cent mortality in such patients. Rudolph [7] has recently pointed out that banding may be contraindicated in endocardial cushion defect with a n obligatory left ventricular to right atrial shunt. Somerville et al [4] noted that patients with endocardial cushidn defect most likely to benefit from pulmonary artery banding were those with predominantly ventricular shunts and T A B L E II
Results of liulmonary Artery Banding in Endocardial Cushion Defect
Author Goldblatt et a! [6] Caylor et al Willman et al [ 14] Coles, Gergely, and Buttigliero I2J Higashimo and Moss [ 1 5 ] Reid et al [10] Somerville et a! [4} Idriss, Riker. and Paul [9] Hunt et al [8] Stark et a1177] Present series Total* *Combined morta(ity was 37 per cent.
34
Number with Banding
Number of Deaths
10 3
2 1
4
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6
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little mitral regurgitation. H u n t et al [81 believed predominant mitral insufficiency in e n d o ~ r d i a l cushion defect to be a contraindication to pulmonary artery banding. Little attention has been given to the problems of banding restrictive ventricular septal defedts with or without an atrial shunt. It is generally agreed that banding an isolated atrial defect is contraindicated. Although banding m a y occasionally be helpful in endocardial cushion defect, patients with this lesion or ventricular septal defect and atrial septal defect must be carefully selected on the basis of hem0dynamic criteria. Classifying left to right shunts into the three groups (A, B, and C) based on the magnitude of the shunt and ratio of pulmonary artery to aortic pressure m a y allow better prediction of the outcome of puhnonary artery banding. This experience indicates that the h e m o d y n a m ic status of the patient is probably as important as the anatomic lesion in predicting the results of pulmonary artery banding. Pulmonary artery banding in endocardial cushion defect has carried a high risk in all reported series as shown in Table It. The combined mortality in this group of eighty-one patients was 37 per cent. There are several reasons for the high mortality in pulmonary artery banding for endocardial cushion defect "including the presence of shunting at the atrial and ventricular levels. The risk of pulmonary artery banding in atrial septal defect and ventricular septal defect is m u c h greater than in ventricular septal defect alone for perhaps similar reasons. The mortality for banding in patients with ventricular ~eptal defect and atrial septal defect has been high in all reported series [9-1/]. Wakai, Swan, and W o o d [12] showed the great variability of ventricuiar and atrial shunting in endocardial cushion defect. It m a y be difficult to determine whether shunting is occurring at the atrial or ventricular level from saturation in various cardiac chambers. Plotting QP/Qs, Rs/Rp, and APp/APs m a y help to solve this dilemma. If a patient with an atrioventricular canal has a flow ratio ( Q P / Q s ) greater than 2.0 and a pressure ratio (APp/APs) above 0.6, the shunt may:be predominantly ventricular. As mentioned before, an atrial or restrictive ventricular communication may have a APp/APs greater than 0.6 in the presence of severe pulmonary vascular disease, b u t QP/Qs is usually less than 2.0. Therefore, the patients with endocardial cushion defect Who are the
The American Journal of Ss~rgery
Hemodynamic Determinants in Pulmonary Arlery Banding
best candidates for banding are those with large shunts without high pulmonary vascular resistance (group A). Three of four patients in this group survived pulmonary artery banding. Those patients with predominant atrial or restrictive ventricular communications with puhnonary hypertension and pulmonic to systemic flow r a t i o s less than 2.0 may not be candidates for banding. The results of previous cardiac catheterizations before the development of pulmonary vascular disease may be helpful in such cases. Those who previously h a d low pulmonary artery pressure (APp/APs less than 0.6; group C to B) probably should not have banding; the one patient in this group did not survive banding. Much of their debility m a y be right ventricular failure or tricuspid insufficiency which could be made worse by increasing right ventricular afterload with banding. Those with high pulmonary artery pressure (APp/APs greater than 0.6) on previous catheterization may have banding (group A to B!, and both patients in this group survived banding. With high pulmonary vascular resistances only a small gradient can be produced across a band without producing right to left shunting through a ventricular defect. The long-term benefit of banding in group B may depend on whether deterioration in the patient's condition is cardiac or pulmonaT" in origin. If pulmonary vascular disease develops in a patient with an atrial shunt, restrictive ventricular shunt, or both (such as an endocardial cushion defect), clinical deterioration may be a result of either of two effects. First, with high pulmonary artery pressure the lungs are less compliant and the work of breathing is increased; banding may lower pulmonary artery pressure and possibly improve lung compliance. On the other hand, if increased afterload has led to right ventricular failure and caused or exacerbated tricuspid insufficiency, banding will only raise the right ventricular afterload and increase the tricuspid insufficiency. These effects may be particularly important in endocardial cushion defects because these patients may be prone to pulmonary vascular disease. T h i s study not only implies t h a t hemodynamic considerations are very important in the results of pulmonary artery banding but also t h a t the relative risks of banding versus total correction must be compared on the basis of the hemodynamic state. The presence of pulmonary vascular disease is the main factor t h a t increases the risk of either banding or total correction of isolated ventricular
Volume 15'6,July 11)73
septal defect. Cartmill et al [13] report a hospital mortality of less than 1.0 per cent in patients with ventricular septal defect comparable to hemodynamic group C (low right ventricular pressure). Their mortality in patients with hemodynamics comparable to group B (high pulmonary vascular resistance) was 54 per cent and in those with hemodynamics comparable to group A was 14 per cent. It appears that the risk of banding or closure of the ventricular septal defect is similar in groups A and B and the results of both procedures are dependent on the level of pulmonary vascular resistance. The results of corrective surgery were distinctly better than those of banding in group C. Restrictive shunts and lesions with low right ventricular pressures (atrial septal defect, restrictive ventricular septal defect and atrial septal defect, and restrictive endocardial cushion defect) should not be banded. The risk of correction of these defects largely depends on the anatomic lesion.
Summary A classification of left to right shunts is presented based on pulmonary to systemic flow and resistance ratios as well as right ventricular and left ventricular systolic pressure ratios. The results of banding are poor when the ratio of pulmonary flow to systemic flow (QP/Qs) is less than 2.0. Banding may be detrimental when right ventricular systolic pressure is low. Patients at the lowest risk for banding are those with high right ventricular pressures and large shunts.
Acknowledgment: I would like to t h a n k Dr A. M. Rudolph and Dr Carl E. H u n t for kindly furnishing catheterization data on their patients, and Drs Benson B. Roe, L. Henry Edmunds, Julien I. E. Hoffman, and A. M. Rudolph for many helpful suggestions during the preparation of the manuscript. References 1. Tassopoulos NM, Carter DR: Pulmonary artery banding in infants with cardiac anomalies other than ventricular septa! defect. Dis Chest 47: 88, 1963. 2. Coles JC, Gergely NF, Buttigliero J: Banding the pulmonary artery. C/in Pediat 2: 316, 1963. 3. Sirak HD, Craig TV: Pulmonary artery banding. J Thorac Cardiovasc Surg 45: 599, 1963. 4. Somerville J, Agnew T, Start J, Waterston D J: Banding of the pulmonary artery for common atrioventrioular canal Brit HeartJ 29: 816, 1967. 5. Gametg,~ad A, Thorkelsen F, Boesen I, Terslev E: Ventricular septal defects in infancy treated with surgical
35
Utley
6. 7.
8. 9. 10.
36
narrowing of the pulmonary artery. Acta Chit Scand Suppl 283: 84, 1961. Goldblatt A, Bernhard WF. Nadas AS, Gross RE: Pulmonary artery banding. Circu/ation 32:172, 1965. Rudolph AM: The role of pulmonary circulation In infants and children. The Natural History and Progress in Treatment of Congenital Heart Defects (Langford Kidd BS and Keith JD, ed). Springfield, III, Thomas, 1971. Hunt CE, Foramanek G, Levine MA, Castaneda A, Miller JH: Banding of the pulmonary artery. Circulation 43: 395, 1971. Idriss FS, Riker WL, Paul MH: Banding of the pulmonary artery: a palliative surgical procedure. J Pecllat Surg 3: 465, 1968. Reid JM, Barclay RS, Coleman EN, Stevenson JG, Welsh TM, McSwan N: Pulmonary artery banding In congenital heart disease associated with pulmonary hyperten-
slon. Thorax 23: 385, 1968. 11. Stark J, Aberdeen E, Waterson DJ, Bonham-Carter RE, Tynan M: Pulmonary artery constrictlor, (banding): a report of 146 cases. Surgery 65: 808, 1£69. 12. Wakal CS, Swan HJC, Wood EH: He~nodynamic data and findings of diagnostic value in .~ine proved cases of persistent c o m m o n , atrioventricular canal. Proc Staff Meet Mayo C/in 31: 500, 1956. 13. Cartmlll TB, Dushane JW, McGoon DC, KIrklln JW: Resuits of repair of ventricular septal defect. J Thorac Cardiovasc Surg 52: 486, 1966. 14. Willman VL, Cooper T, Mudd JG, et ah Treatment of ventricutar septal defect by constriction of pulmonary artery. Arch Surg 85: 745, 1962. 15. Higashino SM, Moss AJ: Pulmonary artery banding: the electrocardiogram as an aid in selection of patient for operation. Brit HeartJ 29: 252, 1967.
The American Journal et Surgery
Banding of the pulmonary artery is a palliative procedure for several types of congenital heart disease; the most common is ventricularseptal defect with intractable heart failure. In ventricular septal defect and more complex lesions such as endoe.ardial cushion defect, transposition of the great vessels with ventricular septal defect, double outlet right ventricle,and truncus arteriosus,banding has also been performed to decrease pulmonary blood in patients with heart failureand to prevent and reverse pulmonary vascular disease. The results of banding have been variable. The mortality for banding in isolated ventricular septal defects has been low but the risk is greater when performed for endocardial cushion defects or atrial septal defect plus ventricular septal defect [I-4]. Although the risk of banding is greater with more complex lesions, the hemodynamics may be as important as the anatomy in determining the risk.~ of pulmonary artery banding. There has been no hemodynamic basis for selecting patients with atrial septal defect plus ventricular septal defect or endocardial cushion defect for pulmonary artery banding. Despite the high risk of banding the pulmona~ artery in patients with atrial and ventricular shunts, no criteria have been available for predicting which patients are at greatest risk for banding. As results for cor-
From the Departmentof Surgery, Division of Cardiothoracic Surgery. University of Kentucky School of Medicine. Lexington. Kentucky 40506. Reprint requests should be addressed to Dr Utley. Division of Cardiothoracic Surgery. University of Kentucky School of Medicine. Lexington. Kentucky40506.
30
rective procedures in infants improve, the proper selection of patients for correctiveversus palliative surgery becomes increasinglyimportant. In this study patients with left to right shunts have been classifiedaccording to the magnitude of the shunt (QP/Qs) and the pulmonary artery pressure (APp/APs). The study shows that the risk of banding is great in patients with either low right ventriculilrpressure (APp/APs < 0.{3)or low flow ratios (QP/Qs < 2.0) and that patients with high pulmonary artery pressures and high flow ratios have the lowest mortality for pulmonary artery banding. Material The results of cardiac catheterization in patients with left to right shunts without right to left shunting were reviewed to classify the hemodynamics of the
shunt. Rs/Rp was used rather than Rp/Rs because the relationof Rs/Rp to QP/Qs in nonrestrictiveshunts is linear.The patientswith ventricularseptal defectwere grouped according to the ratioof right to leftventricular pressure (PRY/PLY) and were considered restrictive when PRY/PLY was less than 0.6 and nonrestrictive when Pav/PLv was greaterthan 0.6. Patent ductus arteriosuswas considered nonrestrictiveifmean or phasic aortic and pulmonary artery pressureswere equal. The flow ratios(QP/Qs) were plotted against the resistance ratios (Rs/Rp). Patients who did w-.~ have banding but who were incorporated in the c',.assification included six with nonrestrictive ventricular septal defect, eight with restrictive ventricular septal defect, five with nonrestrictive patent du'ctus arteriosus: fifteen with secundum atrial septal defect, two with left ventricular to .right atrial shunts, and eighteen with endocardial cushion defect.
The Arnedcan Journal of Surgery
Hemodynamic Determinants in Pulmonary Artery Banding •
*/Gvv./et'srPt~rl~ pAI'fNT DMCTU$~Rl£4425MJr
0
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The results of prebanding cardiac catheterization were reviewed in twenty-two patients with yentricular septal defect, ten patients with endocardial cushion defect, and ten patients with atrial septal defect and ventricular septal defect. In eighteen of the twenty-two banded patients with ventricular septal defect the Piw/PLv was greater than 0.6. Nine of ten banded patients with atrial septal defect and ventricular septal defect had a P~v/PLv greater than 0.6. All ten patients with endocardial cushion defect had a PRY/PLY greater than 0.6. Cardiac catheterization of forty-nine patients with atrial septal defect plus pulmonic stenosis was reviewed to determine the effect of increased right ventricular afterload on atrial shunting.
tricular septal defect or nonrestrictive p a t e n t ductus arteriosus. In these lesions the pressure ratios (APp/APs) are relatively fLxed near 1.0 and flow ratios (QP/Qs) are dependent on resistance ratios (Rs/Rp). In these pat!ents pressure ratios (APP/APs) declined as flow ratios (QP/Qs) increased because of increased left atrial pressures in both ventricular septal defect and p a t e n t ductus arteriosus and decreasing mean p u l m o n a r y artery pressure because of greater diastolic runoff in ventricular septal defect. All patients with nonrestrictive ventricular defects are above the A p p / APs ffi 0.6 line. Figure 2 shows the same hemodynamic relationship for patients with atrial septal defect or restrictive left ventricular to right atrial shunts or restrictive ventricular septal defect. T h e relationship of QP/Qs to Rs/Rp is very similar in these lesions. Figure 3 shows the patients with endocardial cushion defect or atrial septal defect
Results Figure 1 shows the relation of pulmonic to systemic flow ratios and systemic to pulmonary resistance ratios for patients with nonrestrictive ven•
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Q.__~e Figure 2. Relationship of flow ratios (Op/Qs) to resistance ratios (R.~/Rp) for atrial septal defect, restrictive Ventricular septal defact, and restrictive left ventricular to right atrial shunL Flow ratios (QP/Qs) are largely independent of resistance ratios (R.~/Rp).
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Rs/Rp and restrictive or nonrestrictive ventricular septal defect plotted in a similar way. The hemodynamie situation in these more complex lesions is determined mainly by the size of the ventricular communication. Nonrestrictive ventricular communications with atrial septal defect behave much like an isolated nonrestrictive ventricular septal defect although the shunts tend to be larger. Restrictive ventricular shunts with atrial septal defect behave much like the isolated restrictive ventricular defect although the shunts tend to be larger but right ventricular and pulmonary artery pressures remain low. Endocardial cushion defect may be similar to an atrial or restrictive ventricular shunt 6 5
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5
6
7
8
9
Rs/Rp Figure 4. Hemodynamic classification of left to right shunts based on flow ratios ( O p / O ~ ) , resistance ratios (R~/RI,), and pressure ratios ( A p p / A p s ) . Group A: Rs/Rp greater than 2.0, App/APs greater than 0.6. Qp/Os Usually greater than 2.0. Group B: R.~/Rp less than 2.0. O p / O s less than 2.0. APp/ APs usually greater than 0.6. Group C: R.~/Rp greater than 2.0. A p p / Ap~ less than 0.6.
32
:,4
~
ze
~0
Figure 3. Ratio of flows (Qp/Qs) and resistances with endocardlal cushion defect and atrial sePtal defect and restrictive and nonrestrictive ventricular septal defect. Flow ratios are dependent mainly on resistance ratios with nonrestrictive ventricular communications but are much less dependent on resistance ratios with restrictive ventricular defects.
or it m a y behave like a nonrestrictive ventricular shunt. Figure 4 shows three hemodynamic groups based on this classification. Patients with ventrieular septal defect with or without atrial septal defect and endocardial cushion defect may be in group A, B, or C depending on the flow ratios (QP/Qs) and pressure ratio or resistance ratios. Nonrestrictive ventrieular shunts with pressure rfitios (APp/APs) greater t h a n 0.6 and QP/Qs greater than 2.0 are in group A. These patients have relatively nonrestrictive ventricular shunts and low pulmonary vascular resistance, ng~ht ventricular systolic pressure (Pays) is near left ventricular systolic pressure (PLvs), and banding_will not. greatly increase the afterload on the right ventricle. Group C patients are those with low right ventricular pressures (APp/APs < 0.6). The patients have either atrial shunts or restrictive ventricular shunts. B a n d i n g the pulmonary artery in group C patients with ventricular defects will not abolish the venticular shunting, unless right ventricular systolic pressure rises to,equal left ventri• I cular systohc pressure. Such a n acute increase in right ventricular afterload may cause ).he. right ventricle to fail. Thus, banding "may be detrimental in this group of patients. Table I shows the results of banding in hemodynamic groups A, B, and C with ventricular septal defect, ventricular septal defect and atrial septal defect, and endoeardial cushion d e f e c t : Ninetyseven per cent of group A patients survived banding. The mortality was 38 per cent in group B and 50 per cent in group C. In addition to postopera• l:ive death, banding was considered contraindicat-
T h e A m e r i c a n J o u r n a l of
Surgery
Hemodynamlc Determlnants In Pulmonary Artery Banding ed if a gradient across the band could not be tolerated. Banding was contraindicated in five of eight group B patients (62 per cent) and two of four group C patients (50 per cent). W h e n pulmonic to systemic flow ratio (QP/Qs) is less than 2.0 .(group B), pulmonary vascular resistance is increased whether the defect is atrial or ventricular. Patients with endocardial cushion defect which previously behaved like an atrial or restrictive ventricular communication (APp/APs > 0.6) may be poor candidates for banding (group C to B) whereas those who have always had nonrestrictive shunts (group A to B) m a y tolerate a band. Thus, in group B patients with endocardial cushion defect the prior hemodynamic status m a y be important. T w o group B patients who were previously in group, A with high pulmonary artery flows and pressures survived banding. The b~atient who was previously in group C died"after banding. (Table I..) The effect of banding on atrial shunting depends largely on the effect of increased afterload on diastolic compliance. Figure 5 shows the relationship of-the ratio of pulmonic to systemic flow (QP/Qs) to the ratio of ventricular systolic pressures (PIws/PLvs) in forty-nine patients with pulmonic stenosis and atrial septal defect. In this lesion the right ventricular afterload is comparable to the ventricular systolic pressure ratios and the TABLE I
diastolic compliance is comparable to the flow ratios. In general, those patients with greater afterloads and higher right ventricular pressures have lower flow ratios, but right ventricular pressure may be greater than left ventricular pressure with significant left to right shunting still occurring. The great variability in shunting in patients with right ventricular pressures at systemic levels indicates that other factors are important determinants of diastolic ventricular compliance. Patients with pulmonic insufficiency and stenosis had right to left shunting at low right ventricular pressures. From these observations changes in right ventricular afterload would be expected to have an unpredictable effect on atrial shunting particularly with valvular insufficiency. After banding, one patient with endocardial cushion defect had a greatly elevated-'P-ev./~PLv (1:5) and pulmonic to systemic flow ratio of 2.0. Comments
The results-of~banding in isolated ventricular septal defect have been good b u t m o r t a l i t y has been high in patients with both an atrial septal defect and ventricular septal defect or endocardial cushion defect. Gamelgaard et al [5] found that no patients with endocardial cushion defect were
R e s u l t s of P u l m o n a r y A r t e r y B a n d i n g in H e m o d y n a m i c G r o u p s A, B, a n d C
Anatomic Lesion Ventrlcular septal defect Group A Group B Group C Ventricular septal defect and atrial septal deject Group A Group C Endocardial cushion defect GroupA Group B C "-'* B A -'* B Tota~ Group A Group B Group C
Number with Banding
Number of Deaths
Number with Intolerance to Banding
Survival
p*
Banding Contraindicated'l"
15 4 3
0 2 1"
1 1 0
15(100%) 2(50%) 2(66%)
__ "03 NS
1 (7~o) 3(75%) 1 (33%)
... .01 NS
9 1
0 1
0 0
9(100%) 0(0%)
... NS
0(0%) 1 (100%)
... NS
6 4 I 2
I 1 1 0
t 1 0 0
5 (83%) 3(75%) 0(0%) 2(100%)
... NS ... ...
2(33%) 2(50%) 1 (100%) 0(0%)
NS ,.. ...
30 8 4
1 3 2
2 2 0
29(97%) 5(62%) 2(50%)
... .01 .01
3(10%) 5(62%) 2(50%)
... .01 .01
* p determined by comparing groups B and C to group A with Fisher's exact chi square test. 1" Died or would not tolerate band,
Volume 126, July 1973
33
Utley • INS~JC-/£#r PULO~dW/C V~LY£ ANDAt'RIAL $£PYAL 12~F'lrC¥
25o 20.
o
d~
0
PRY= 1.5o
% I0-
o
OOo@O~e°
o o
• 0
0
o:~
°°
o G°oO o ~ o
,;o ...........,:5 '2'o OP/Os
o o
o
o
3'o
z'~
i5
Figure 5. Ratio of purmonl'c 'tO systemic flow (Op/Os) to right venfricular to left ventricular systotic pressure (Pavs/PLv~ in pulmp'nic stenosis and atria] septal detect. Many flow ratios--ote'-elevafed to 2.Cl with equal systolic pressures in the two ventricles. Flow ratios are much less at the same level of righ,t ventricular pressure when pulrnonic value is insufficient as well as stenotic.
benefited by banding and no patients with this lesion survived banding in the series of Sirak and Craig [3]. Somerville and colleagues [2,4] reported five deaths in twelve cases of endocardial cushion defect treated by banding, and Goldblatt [6] reported a 20 per cent mortality in such patients. Rudolph [7] has recently pointed out that banding may be contraindicated in endocardial cushion defect with a n obligatory left ventricular to right atrial shunt. Somerville et al [4] noted that patients with endocardial cushidn defect most likely to benefit from pulmonary artery banding were those with predominantly ventricular shunts and T A B L E II
Results of liulmonary Artery Banding in Endocardial Cushion Defect
Author Goldblatt et a! [6] Caylor et al Willman et al [ 14] Coles, Gergely, and Buttigliero I2J Higashimo and Moss [ 1 5 ] Reid et al [10] Somerville et a! [4} Idriss, Riker. and Paul [9] Hunt et al [8] Stark et a1177] Present series Total* *Combined morta(ity was 37 per cent.
34
Number with Banding
Number of Deaths
10 3
2 1
4
4
2
0
6
2
2 13 15 3 13 10 81
2 4 7 2 4 2 30
little mitral regurgitation. H u n t et al [81 believed predominant mitral insufficiency in e n d o ~ r d i a l cushion defect to be a contraindication to pulmonary artery banding. Little attention has been given to the problems of banding restrictive ventricular septal defedts with or without an atrial shunt. It is generally agreed that banding an isolated atrial defect is contraindicated. Although banding m a y occasionally be helpful in endocardial cushion defect, patients with this lesion or ventricular septal defect and atrial septal defect must be carefully selected on the basis of hem0dynamic criteria. Classifying left to right shunts into the three groups (A, B, and C) based on the magnitude of the shunt and ratio of pulmonary artery to aortic pressure m a y allow better prediction of the outcome of puhnonary artery banding. This experience indicates that the h e m o d y n a m ic status of the patient is probably as important as the anatomic lesion in predicting the results of pulmonary artery banding. Pulmonary artery banding in endocardial cushion defect has carried a high risk in all reported series as shown in Table It. The combined mortality in this group of eighty-one patients was 37 per cent. There are several reasons for the high mortality in pulmonary artery banding for endocardial cushion defect "including the presence of shunting at the atrial and ventricular levels. The risk of pulmonary artery banding in atrial septal defect and ventricular septal defect is m u c h greater than in ventricular septal defect alone for perhaps similar reasons. The mortality for banding in patients with ventricular ~eptal defect and atrial septal defect has been high in all reported series [9-1/]. Wakai, Swan, and W o o d [12] showed the great variability of ventricuiar and atrial shunting in endocardial cushion defect. It m a y be difficult to determine whether shunting is occurring at the atrial or ventricular level from saturation in various cardiac chambers. Plotting QP/Qs, Rs/Rp, and APp/APs m a y help to solve this dilemma. If a patient with an atrioventricular canal has a flow ratio ( Q P / Q s ) greater than 2.0 and a pressure ratio (APp/APs) above 0.6, the shunt may:be predominantly ventricular. As mentioned before, an atrial or restrictive ventricular communication may have a APp/APs greater than 0.6 in the presence of severe pulmonary vascular disease, b u t QP/Qs is usually less than 2.0. Therefore, the patients with endocardial cushion defect Who are the
The American Journal of Ss~rgery
Hemodynamic Determinants in Pulmonary Arlery Banding
best candidates for banding are those with large shunts without high pulmonary vascular resistance (group A). Three of four patients in this group survived pulmonary artery banding. Those patients with predominant atrial or restrictive ventricular communications with puhnonary hypertension and pulmonic to systemic flow r a t i o s less than 2.0 may not be candidates for banding. The results of previous cardiac catheterizations before the development of pulmonary vascular disease may be helpful in such cases. Those who previously h a d low pulmonary artery pressure (APp/APs less than 0.6; group C to B) probably should not have banding; the one patient in this group did not survive banding. Much of their debility m a y be right ventricular failure or tricuspid insufficiency which could be made worse by increasing right ventricular afterload with banding. Those with high pulmonary artery pressure (APp/APs greater than 0.6) on previous catheterization may have banding (group A to B!, and both patients in this group survived banding. With high pulmonary vascular resistances only a small gradient can be produced across a band without producing right to left shunting through a ventricular defect. The long-term benefit of banding in group B may depend on whether deterioration in the patient's condition is cardiac or pulmonaT" in origin. If pulmonary vascular disease develops in a patient with an atrial shunt, restrictive ventricular shunt, or both (such as an endocardial cushion defect), clinical deterioration may be a result of either of two effects. First, with high pulmonary artery pressure the lungs are less compliant and the work of breathing is increased; banding may lower pulmonary artery pressure and possibly improve lung compliance. On the other hand, if increased afterload has led to right ventricular failure and caused or exacerbated tricuspid insufficiency, banding will only raise the right ventricular afterload and increase the tricuspid insufficiency. These effects may be particularly important in endocardial cushion defects because these patients may be prone to pulmonary vascular disease. T h i s study not only implies t h a t hemodynamic considerations are very important in the results of pulmonary artery banding but also t h a t the relative risks of banding versus total correction must be compared on the basis of the hemodynamic state. The presence of pulmonary vascular disease is the main factor t h a t increases the risk of either banding or total correction of isolated ventricular
Volume 15'6,July 11)73
septal defect. Cartmill et al [13] report a hospital mortality of less than 1.0 per cent in patients with ventricular septal defect comparable to hemodynamic group C (low right ventricular pressure). Their mortality in patients with hemodynamics comparable to group B (high pulmonary vascular resistance) was 54 per cent and in those with hemodynamics comparable to group A was 14 per cent. It appears that the risk of banding or closure of the ventricular septal defect is similar in groups A and B and the results of both procedures are dependent on the level of pulmonary vascular resistance. The results of corrective surgery were distinctly better than those of banding in group C. Restrictive shunts and lesions with low right ventricular pressures (atrial septal defect, restrictive ventricular septal defect and atrial septal defect, and restrictive endocardial cushion defect) should not be banded. The risk of correction of these defects largely depends on the anatomic lesion.
Summary A classification of left to right shunts is presented based on pulmonary to systemic flow and resistance ratios as well as right ventricular and left ventricular systolic pressure ratios. The results of banding are poor when the ratio of pulmonary flow to systemic flow (QP/Qs) is less than 2.0. Banding may be detrimental when right ventricular systolic pressure is low. Patients at the lowest risk for banding are those with high right ventricular pressures and large shunts.
Acknowledgment: I would like to t h a n k Dr A. M. Rudolph and Dr Carl E. H u n t for kindly furnishing catheterization data on their patients, and Drs Benson B. Roe, L. Henry Edmunds, Julien I. E. Hoffman, and A. M. Rudolph for many helpful suggestions during the preparation of the manuscript. References 1. Tassopoulos NM, Carter DR: Pulmonary artery banding in infants with cardiac anomalies other than ventricular septa! defect. Dis Chest 47: 88, 1963. 2. Coles JC, Gergely NF, Buttigliero J: Banding the pulmonary artery. C/in Pediat 2: 316, 1963. 3. Sirak HD, Craig TV: Pulmonary artery banding. J Thorac Cardiovasc Surg 45: 599, 1963. 4. Somerville J, Agnew T, Start J, Waterston D J: Banding of the pulmonary artery for common atrioventrioular canal Brit HeartJ 29: 816, 1967. 5. Gametg,~ad A, Thorkelsen F, Boesen I, Terslev E: Ventricular septal defects in infancy treated with surgical
35
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6. 7.
8. 9. 10.
36
narrowing of the pulmonary artery. Acta Chit Scand Suppl 283: 84, 1961. Goldblatt A, Bernhard WF. Nadas AS, Gross RE: Pulmonary artery banding. Circu/ation 32:172, 1965. Rudolph AM: The role of pulmonary circulation In infants and children. The Natural History and Progress in Treatment of Congenital Heart Defects (Langford Kidd BS and Keith JD, ed). Springfield, III, Thomas, 1971. Hunt CE, Foramanek G, Levine MA, Castaneda A, Miller JH: Banding of the pulmonary artery. Circulation 43: 395, 1971. Idriss FS, Riker WL, Paul MH: Banding of the pulmonary artery: a palliative surgical procedure. J Pecllat Surg 3: 465, 1968. Reid JM, Barclay RS, Coleman EN, Stevenson JG, Welsh TM, McSwan N: Pulmonary artery banding In congenital heart disease associated with pulmonary hyperten-
slon. Thorax 23: 385, 1968. 11. Stark J, Aberdeen E, Waterson DJ, Bonham-Carter RE, Tynan M: Pulmonary artery constrictlor, (banding): a report of 146 cases. Surgery 65: 808, 1£69. 12. Wakal CS, Swan HJC, Wood EH: He~nodynamic data and findings of diagnostic value in .~ine proved cases of persistent c o m m o n , atrioventricular canal. Proc Staff Meet Mayo C/in 31: 500, 1956. 13. Cartmlll TB, Dushane JW, McGoon DC, KIrklln JW: Resuits of repair of ventricular septal defect. J Thorac Cardiovasc Surg 52: 486, 1966. 14. Willman VL, Cooper T, Mudd JG, et ah Treatment of ventricutar septal defect by constriction of pulmonary artery. Arch Surg 85: 745, 1962. 15. Higashino SM, Moss AJ: Pulmonary artery banding: the electrocardiogram as an aid in selection of patient for operation. Brit HeartJ 29: 252, 1967.
The American Journal et Surgery