Determinants of left ventricular function following aorto-coronary bypass surgery Bruce H. Brundage, M.D., Lieutenant Colonel, (MC) USA Warren T. Anderson, M.D., Major, (MC) USA James E. Davia, M.D., Lieutenant Colonel, (MC) USA Melvin D. Cheitlin, M.D., Colonel, (MC) USA Carlos M. deCastro, M.D., Colonel, (MC) USA Denver, Colo., Washington, D.C., and San Francisco, Calif.
There continues to be controversy over the effects of coronary artery bypass surgery on left ventricular function. 1-5 T h i r t y patients were studied in order to evaluate ventricular function before and an average of 5 months after surgery. The patients were grouped according to operative indications, preoperative condition, perioperative events, and postoperative status in an effort to elucidate the determinates of postoperative function. Materials and methods
T h i r t y patients undergoing saphenous vein bypass grafting of the coronary arteries at Walter Reed Army Medical Center form the basis of this study. Th e surgery was performed during an 18 m o n t h period spanning 1972 and 1973. Each patient underwent cardiac catheterization prior to surgery. All patients were fasted for 12 hours and had no~ taken propranolol for at least 2 days and digoxin for 5 days prior to the study. The subjects were premedicated 45 minutes before catheterization with 50 mg. of meperidine, 25 mg. of promethazine, and 0.4 mg. of atropine. All pressure measurements were recorded on an Electronics for Medicine DR-12, from a P 23 DB S t a t h a m strain gauge, connected to a fluid-filled polyethylene catheter. Left ventricular end-diastolic pressure (LVEDP) was recorded at high amplification and at a paper speed of 100 mm. per F r o m Fitzsimons A r m y Medical Center. Walter Reed A r m y Medical Center. a n d the University of California Medical School. Received for publication J a n . 23. 1976. Reprint requests: Bruce H. Brundage, M.D.. {LTC). {MC) USA, Cardiology Service, Fitzsimons A r m y Medical Center. Denver. Colo. 80240.
June, 1977, Vol. 93, No. 6, pp. 687-698
second. L V E D P was measured at the point of rapid rise in pressure after the "a" wave or at the peak of the R wave on the electrocardiogram (ECG). Aortic pressure was electronically meaned. Cardiac out put was determined by the green dye or thermodilution indicator technique2- 7 Stroke work index was calculated from the formula: SWI = (aortic mean press u r e - L V E D P ) x stroke volume index x 1.36/ 100. All measurements were obtained prior to the use of any contrast agent. The ventriculogram was performed by injecting 0.8 ml. per kilogram or 60 ml. (whichever was less) of methyglucamine diatriazoate (Renografin 76) through a polyethylene pigtail catheter over a 4 second period. The patients were positioned in the right anterior oblique and ejection fractions were calculated from this single plane by the area-length method. The hemodynamic measurements were repeated 3 to 5 minutes following left ventricular angiography. T he volume stress from the hyperosmotic contrast material used produces changes in L V E D P and stroke work index so that ventricular function curves can be constructed. 8 Coronary arteriograms were done after ventriculography by Judkin's technique. Narrowing of a major coronary artery of greater than 50 per cent of the diameter was considered significant. The patients were restudied an average of 5 months (range, 3 to 9 months) following their coronary artery surgery. T he restudy protocol was identical to the preoperative study and also included angiographic demonstration of graft patency. Treadmill stress tests were performed, when possible, before each study. T he exercise protocol has previously been reported. 9 There were 76 patients
American Heart Journal
687
Brundage et al.
Table I. Pre- a n d p o s t o p e r a t i v e v e n t r i c u l a r f u n c t i o n d a t a
Group
A. B. C. D. E. F. G. H. I. J. K. L. M N. O. P. Q. R. S. T. U.
All patients Stable angina Unstable angina Previous infarct No previous infarct Poor preop, function Fair preop, function Good preop, function Operated for markedly positive stress test Stress test >2 mm. Main left lesion No periop, infarct Periop. infarct One or more grafts closed 100%graft patency No periop, infarct and 100% patency Asymptomatic postop. Neg. stress test postop. Ischemic postop. Change in native circulation No change in native circulation
* p < 0.05. t p < 0.02. $ p < 0.Ol.
L VEDP preangio. (ram. Hg preop. postop.)
L VEDP postangio. (ram. Hg preop.postop.)
10•177 10• 8 • 1-9 ___2 10•177 9•177 14+1-12• 10•177 1 8•177 10• 1-9 • 2
20•177 19+1-19• 20 • 6-22 • 2 22•177 18•177 25•177 21•177 16+2-17-+1 22 • 2-17 • 2
6.1+0.3-6.1• 5.7•177 8.5•177 6.5•177 5.8•177 5.6• 6.1•177 6.5•177 5.6+0.3-6.2•
7.6•177 7.0•177 9.8• 7.5•177 7.7•177 6.5•177 7.6•177 8.2•177 7.5•177
96•177 99•177 97•177 99•177 93•177 89•177 99~5-92• 96•177 86•177
10.+1-9• 11+_1-9• 9•177 11•177 11_+1-8+1" 9•177 9•177
23•177 24.+3-19• 19+2-18• 22•177 22•177 18•177 19+2-18•
5.4•177 5.3+0.4-6.7• 5.9•177 6.5•177 6.1•177 6.1•177 5.9•177
7.5•177 7.3• 7.6•177 7.6•177 7.4•177 7.8•177 7.7•177
95• 99•177 93•177 99• 95•177 97• 95-+5-99•
9•177 9• 1-9• 1 11•177 10 • 1-9 _+1 10• 1-9• 1
19•177 21•177 1 21•177 19-+ 1-19 • 1 23•177
6.3+0.4-6.2• 6.3•177 6.1•177 6.3+0.4-6.2+0.6 5.9•
7.7• 7.8•177 7.6+0.6-7.4+0.9 7.7+0.4-6.9+0.5 7.4•177
93•177 96•177 100• 97•177 90•
CO preangio. (L. rain. preop.-postop.)
CO postangio. (L. /min. preop.-postop.)
Aortic mean preangm. (ram. Hg preop.-postop.)
wp < 0.001. 82 p < 0.0001. [[ p < 0.00001.
who underwent coronary bypass grafting during t h e p r o t o c o l period. T h e r e were 6 o p e r a t i v e d e a t h s . T h i r t y - n i n e p a t i e n t s were e x c l u d e d f r o m t h e s t u d y b e c a u s e p r e o p e r a t i v e or p o s t o p e r a t i v e c a t h e t e r i z a t i o n d a t a were i n c o m p l e t e a n d o n e p a t i e n t w a s lost t o follow-up.
Results T h e 30 p a t i e n t s i n t h i s s t u d y were all m a l e . E i g h t e e n (60 p e r c e n t ) were o p e r a t e d o n b e c a u s e of severe b u t s t a b l e a n g i n a , u n c o n t r o l l e d b y m e d i c a l m a n a g e m e n t . F i v e (17 p e r c e n t ) h a d u n s t a b l e a n g i n a t h a t did n o t s t a b i l i z e a f t e r a d m i s s i o n to t h e c o r o n a r y - c a r e u n i t . S e v e n p a t i e n t s (23 p e r c e n t ) h a d a m a r k e d l y i s c h e m i c r e s p o n s e to exercise ( g r e a t e r t h a n 2 m m . S T - s e g m e n t depress i o n ) a n d were o p e r a t e d o n b e c a u s e t h e y h a d a n g i n a a n d a m a i n left c o r o n a r y o b s t r u c t i o n , a m a i n left e q u i v a l e n t ( p r o x i m a l o b s t r u c t i o n of left anterior descending and circumflex coronary arteries), or severe t h r e e - v e s s e l disease. P r e o p e r a -
688
_ S.E.M.)
tive c o r o n a r y a r t e r i o g r a p h y d e m o n s t r a t e d t h r e e vessel disease i n 20 p a t i e n t s (67 p e r cent), twovessel disease in s e v e n (23 per c e n t ) , a n d onevessel disease i n t h r e e (10 per cent}. I n o n e case, o n l y t h e r i g h t c o r o n a r y was b y p a s s e d , b u t it s u p p l i e d a n u n u s u a l l y l a r g e p o r t i o n of t h e p o s t e r o l a t e r a l w a l l of t h e left v e n t r i c l e . O n e p a t i e n t r e c e i v e d f o u r grafts (3 p e r cent), 15 t h r e e grafts (50 p e r cent}, 10 t w o g r a f t s (33 p e r c e n t ) , a n d f o u r o n l y o n e g r a f t (14 p e r cent}. R e v a s c u l a r i z a t i o n w a s c o n s i d e r e d to be c o m p l e t e in 25 (83 per cent} of t h e p a t i e n t s . A t t h e t i m e of r e s t u d y 24 p a t i e n t s (80 per c e n t ) d e n i e d s y m p t o m s a n d six (20 per cent} h a d residual a n g i n a b u t s t a t e d it w a s i m p r o v e d . P o s t o p e r a t i v e t r e a d m i l l stress t e s t s were negative for i s c h e m i a i n I5 a n d p o s i t i v e in five. S t r e s s t e s t s e i t h e r were n o t o b t a i n e d i n t h e o t h e r 10 p a t i e n t s or were t e c h n i c a l l y i n a d e q u a t e for i n t e r p r e t a t i o n . P e r i o p e r a t i v e infarcts, d e f i n e d as n e w Q w a v e s o n p o s t o p e r a t i v e E C G ' s , were n o t e d i n 12
J u n e , 1977, Vol. 93, No. 6
Function after aorto-coronary bypass
Table I., continued Aorhc mean postangio. (ram. Hg preop.postopJ
HR preangio(b./ min. preop.postop.)
HR postangio. (b./min. preop. postor.)
SV preangio,
SV postangio.
(ml.
(ml.
preop.postop.)
preop.postop.)
SWI preangio. (Gm.-M./M. 2 preop.postop.)
SWI postangio (Gm.-M./M# preop.postopJ
Ejection frac~on preop.postopj
No.
103_+4-97_+3" 106_+5-98_+4" 105_+10--103_+8 108_+7-100_+6 99_+4--94_+4 90-+8--82_+5 103_+6--101_+6 109_+7-100_+4" 92_+8--88_+8
78_+2-89_+3: 82_+3--87_+3 80_+3-91_+3" 85_+5--88_+3 78_+1--82_+3 79_+5-84_+4 81_+4-84_+3 84_+4--85_+3 75_+2-94_+5580_+4--89_+4* 78_+5--80_+5 76_+5--83_+4 77_+3--93_+4587_+5--89_+3 78_+5--90_+6 79_+5-89_+5 72_+3--89_+1075_+4--89_+8
80_+4-70_+5* 95_+4--81_+55 50_+3--41_+3t 57_+3--44_+3w62_+3--62_+2 30 75_+5--66_+6 88_+5--76+_6* 48_+4-39_+3 54_+3--43_+3564-+3--63_+3 18 100_+9--82_+18 114_+7-77_+6" 66_+11-49_+11 74_+11--51_+8 64_+6--56_+7 5 78_+6--68_+7 87_+5-73_+7* 52_+6--41_+4 58_+5--40_+4558_+4--58_+3 14 82_+4--71_+7 102_+6--86_+7t 48_+2--40_+4* 57_+4--47_+35 66_+3--66_+3 16 72_+4-61_+8 84_+3--69_+10 40_+3-31_+35 44_+3--33_+4 43_+6--61_+85 6 82_+3--69_+9 93_+4-75_+6t 55_+5-42_+6* 56_+5-43_+4* 66_+11--59_+4 12 83_+9--75_+6 104_+10--93_+9 50_+6-44_+3 66_+5-50+_45 68_+2--66_+2 12 78_+5--70_+3 101_+11--76_+4t 43_+4--38_+5* 54_+7-41_+6" 57_+6--65_+5* 7
101_+7-97_+6 103_+9--104_+7 102_+6--98_+4 103_+6--94_+6" 100_+6--92_+4 106_+5--101_+4 106_+5--101_+4
73_+2--91_+6t 80_+3--89_+5 72_+2--85_+4576-+5--83-+4 78_+3--90_+5* 84_+5--94_+7 77_+3--88_+3* 78_+3-87_+3 78_+3--86_+3 80_+4-85_+3 77_+4--93_+5t 84_+5--90_+4 75_+3--94_+6584_+6--90_+5
74_+4--64_+35 73_+5--77-+12 77_+6--70_+4 84_+4--69_+10 79_+4--69_+7 81_+6--71_+6 79_+7-72_+6
96_+7-76_+35 99+13-79_+4 94_+7--85_+7 97_+4--75_+85 93_+5--79_+75 106_+9-83_+85 99_+9-85_+8
44_+3--38_+4* 46_+5--46-+6 47_+4-42_+3 53_+4-39_+6t 47_+3-37_+5t 53_+6-44_+3 50_+6--44_+3
55_+6--43_+4t 60_+4--65_+4 56_+10-49_+4 63_+4--69-+5 58_+5--46_+3t 64_+3--66_+3 57_+5--40_+45 59_+5--57_+4 52_+3--41_+35 59_+4--60_+4 64_+6-47_+4t 65_+2--64_+3 60-+6-48_+4* 64-+2--64_+3
11 6 18 12 16 14
99_+5-96_+4 100_+6-97_+5 106_+7-96_+5 99_+5--92_+4* 103_+6--100_+4
79_+3-89_+4* 83_+4-89___3 80_+4--71_+5 73 _+3-92 _+5:~ 79-+3-89_+4* 84_+5--71_+6" 71_+2--84_+5"75_+3--81_+3 85_+6-73-+11 75+3--94_+45 81_+4--92_+3t 85_+4--68_+65 78_+3--80_+3 80_+4-78_+3 76-+6--75_+9
96_+5-82_+65 99_+6--79_+35 102-+8-91-+13 98•182 94_+10-89_+11
48_+4--40_+3* 53_+5-41_+4t 53-+5-43+7 51-+4-36 _+3~: 49_+6-50_+5
56-+4--43_+35 64_+3--61_+3 59_+5--42_+35 64_+3--62_+3 61-+4-50+5" 58_+6--68-+4* 60_+4--39_+31] 61_+3--60_+3 52_+6-52_+5 64_+6--66__4
24 15
patients (40 per cent). Postoperative c o r o n a r y arteriography d e m o n s t r a t e d p a t e n c y in 53 of the 73 grafts placed (73 per cent). T h e purpose of this s t u d y was to investigate a n y changes in ventricular function following c o r o n a r y a r t e r y bypass surgery and elucidate their causes. Global ventricular function was evaluated by developing pre- and postoperative ventricular function curves from the v o l u m e stress of left ventricular a n g i o g r a p h y and by measuring pre- and postoperative ejection fractions. Previous work has s h o w n t h a t hyperosmotic c o n t r a s t material produces increases in cardiac o u t p u t , p r e s u m a b l y due to increases in blood volume. T h e increased blood volume results in greater venous r e t u r n and increased ventricular end-diastolic volume. Cardiac o u t p u t is thereby e n h a n c e d by the F r a n k - S t a r l i n g m e c h a nism. T h e r e s u l t a n t changes in cardiac o u t p u t and L V E D P m a k e the c o n s t r u c t i o n of v e n t r i c u l a r function curves possible. 8 T a b l e I includes the
American Heart J o u r n a l
9
19 10
d e t e r m i n a n t s of the ventricular f u n c t i o n curves ( L V E D P and SWI), ejection fractions (EF), and the h e m o d y n a m i c values t h a t influence these measurements: cardiac o u t p u t (CO), m e a n aortic pressure, heart rate (HR), and stroke volume (SV). Pre- and postoperative values are listed side by side with the s t a n d a r d error of the m e a n (S.E.M.). A n y statistically significant differences are a n n o t a t e d . Line A of Table I indicates the mean values for the entire group. T h e r e were significant decreases in pre- and p o s t a n g i o g r a m S W I postoperatively. Since there was no change from pre- to postoperative L V E D P , depression of the ventricular f u n c t i o n curve occurred after surgery (Fig. 1). T h e r e was no change in postoperative EF. A significant increase in postoperative resting H R was observed. In an a t t e m p t to obtain a more meaningful understanding of changes in postoperative ventricular function, patients were grouped according to indications for operation, condition prior to oper-
689
Brundage
e t al.
M~
ilO
---t
i
60-
20-~
=.I
w gr
3= e,4
40-
30-
30-
I
I
I
10
20
30
LV EOP
mm HE
Fig. 1. Pre- and postoperative ventricular function curves for all patients. Solid line = preoperative; broken line = postoperative; S W I = stroke work index; L V E D P = left ventricular end-diastolic pressure.
ation, i n t r a o p e r a t i v e events, and p o s t o p e r a t i v e status. T h e s e categories are included in T a b l e I. S e p a r a t i n g p a t i e n t s b y t y p e of p r e o p e r a t i v e angina (stable, G r o u p B; unstable, G r o u p C) did not a l t e r the effect of b y p a s s surgery on postoperative v e n t r i c u l a r function. T h e r e was evidence for depression of function in b o t h groups, a l t h o u g h the n u m b e r of p a t i e n t s w i t h u n s t a b l e angina was too small for statistical significance. A history of an old m y o c a r d i a l i n f a r c t i o n prior to surgery (Group D) was associated with a greater depression of the p o s t o p e r a t i v e ventricu l a r function curve, b u t a significant decrease in function occurred in the p a t i e n t s w i t h o u t previous infarction (Group E; Figs. 2A a n d 2B). Ejection fractions were u n c h a n g e d a f t e r surgery b u t were lower in the infarct group. T h e group w i t h o u t previous infarction h a d a significant increase in p o s t o p e r a t i v e h e a r t r a t e s whereas the infarct group did not. P a t i e n t s were categorized as h a v i n g poor, fair, or good p r e o p e r a t i v e v e n t r i c u l a r function (Groups F, G, a n d H). P a t i e n t s w i t h resting L V E D P ' s of 12 m m . H g or less, ejection fractions
690
I tO LVEOP
0
I 20
I 20
mmH|
Fig. 2A. Pre- and postoperative ventricular function curves in patients with prior myocardial infarction. Solid line = preoperative; broken line = postoperative; S W I = stroke work index; L V E D P = left ventricular end-diastolic pressure. 60--
50-
I
f f
40-
30-
l 10
I 20 I. VEDP
I 30
mmHg
Fig. 2B. Pre- and postoperative ventricular function curves in patients without prior myocardial infarction. Symbols as in Fig. 2.4.
J u n e , 1977, Vol. 93, No. 6
Function after aorto-coronary bypass
N-
W-
u m
40--
I-
I = m
30-
W-
I !0
I 20 LVEDP
I 30
nmHl[
Fig. 3A. Pre- and postoperative ventricular function curves in patients with poor preoperative ventricular function. Solid line = preoperative; broken line = postoperative; S W I = stroke work index; L V E D P = left ventricular enddiastolic pressure. "
30-
i 10 LVEDP
I 20
i
mmHI
Fig. 3C. Pre- and postoperative ventricular function curves in patients with good preoperative ventricular function. Symbols as in Fig. 3A.
50-I
40--
m-
I
10 LVEDP
I
I
20
30
WaHl[
Fig. 3B. Pre- and postoperative ventricular function curves in patients with fair preoperative ventricular function. Symbols as in Fig. 3A.
American Heart Journal
55 per cent or greater, a n d n o r m a l preoperative ventricular function curves were r a t e d as good, patients meeting none of these criteria as poor, and the remainder as fair. Postoperative ventricular function curves were depressed by equivalent a m o u n t s in all groups (Figs. 3A, 3B, and 3C). Postoperative ejection fractions were significantly increased (43 to 61, p < 0.01) in patients with poor preoperative v e n t r i c u l a r function; however, there was a significant decrease in postoperative aortic m e a n pressure in this group. Ejection fraction did not change significantly in patients with fair or good preoperative ventricular function. There was a group of patients with evidence of a r a t h e r m a r k e d l y ischemic ventricle preoperatively as defined by very positive stress tests (greater t h a n 2 mm. S T - s e g m e n t depression). M a n y of these patients (five of 11) h a d significant main left c o r o n a r y obstruction. Seven of these
6 91
Brundage
e t al.
60-
m50I
U-
i
40--
N
O30-
I O
10 LVEDP
I
I
20 mmHg
30
N
Fig. 4A. Pre- and postoperative ventricular function curves
in patients with evidence of markedly ischemic ventricular function preoperatively (markedly positive stress test). Solid line = preoperative; broken line = postoperative; S W I = stroke work index; L V E D P = left ventricular enddiastolic pressure. 60--
50-
I
L
40-
30-
I 10 L Y E D P
I 20 mm HI[
I 30
Fig, 4B, Pre- and postoperative ventricular function curves in patients with evidence of markedly ischemic ventricular function preoperatively {stress test > 2 mm.). Symbols as in Fig. 4A.
692
0
l 10
I 20
LVEDP
I 30
mmHI
Fig. 4C. Pre- and postoperative ventricular function curves in patients with evidence of markedly ischemic ventricular function preoperatively (main left lesions). Symbols as in Fig. 4A. patients were operated on primarily because of the m a r k e d l y positive stress test. Their angina was mild or m o d e r a t e a n d n o t sufficient to be considered as indication for operation alone (Group I). T h e y h a d severe three-vessel disease, main left lesions, or main left equivalent lesions. While there was a decrease in stroke work index postoperatively, there was also a significant decrease in postoperative L V E D P after angiography. For this reason, the postoperative ventricular f u n c t i o n curve was only slightly depressed (Fig. 4A). There was a significant i m p r o v e m e n t in the ejection fraction from 57 to 65 (p < 0.05) and the postoperative aortic m e a n pressure was unchanged. All patients with preoperative stress tests showing greater t h a n 2 mm. S T - s e g m e n t depression (Group J) h a d a decrease in postoperative stroke work index b u t this also was associated with a significant decrease in postangio. L V E D P so the v e n t r i c u l a r function curve was changed little after surgery (Fig. 4B). T h e ejection fraction increased from 60 to 65 b u t this was not statistically significant. P a t i e n t s with signifi-
J u n e , 1977, Vol. 93, No. 6
Function after aorto-coronary bypass
W--
N-
i
/1/
s/
u
u
3t r
i
3t
(
30
I 10 LVtDP
I 28
I m
Illl
0
I 10 LV[DP
I 20
I 10
mmHI
Fifl. 5A. Pre- and postoperative ventricular curves in patients w i t h o u t a perioperative infarct. Solid line = preoperative; broken line = postoperative; S W I = stroke work index; LVEDP = left ventricular end-diastolic pressure.
I::ifl.5B. Pre- and postoperative ventricular curves in patients with perioperative infarct. Symbolsas in Fig. 5A.
cant main left coronary lesions (Group K) had no postoperative depression of the ventricular function curve (Fig. 4C) and ejection fraction improved but not to levels of statistical significance. A perioperative infarct could b e expected to depress postoperative ventricular function. However, patients without a perioperative infarct (Group L) likewise had significant depression of postoperative ventricular function. The perioperative infarction groups, however, did h a v e a greater reduction in postoperative stroke work indices (Group M; Figs. 5A and 5B). Ejection fractions were unchanged in both groups. The finding of one or more closed grafts at restudy (16 patients) was associated with a depressed postoperative ventricular function curve (Group N; Fig. 6A). Only four patients had all grafts occluded. The 14 patients with 100 per cent graft patency (Group O) also h a d significantly lower postoperative ventricular function curves (Fig. 6B). Even patients who did not have a perioperative infarct and had 100 per cent patency on restudy (Group P) were found to have depressed ventricular function curves postopera-
tively (Fig. 6C). Ejection fractions were unchanged after surgery in these three groups. Lack of myocardial ischemia postoperatively, whether the subjective lack of anginal symptoms (24 patients, Group Q) or, more objectively, a negative treadmill stress test (15 patients, Group R), did not prevent depression of ventricular function curves. However, the presence of angina and/or a positive stress test (nine patients, Group S} after surgery appeared to produce contradictory data. There was a decrease in the postoperative stroke work indices but ejection fraction and LVEDP improved. However, there was a significant decrease in postoperative aortic mean pressure in these patients. Similar results were previously noted in the patients with poor preoperative ventricular function (Group F). When all patients were categorized according to changes in postoperative ejection fraction, the group of patients with improved ejection fractions showed a significant decrease (p < 0.01} in postoperative aortic mean pressure (Table II). Finally, in this study, the most important determinant of postoperative ventricular function was the state of the native circulation at
American Heart Journal
593
Brundage et al.
I
N60~
m 50-3E B t
40 40--
30]
I
I
I0
20
30
L VEDP
ininH|
I lO
o
Fig. 6A. Pre- and postoperative ventricular function curves
I 20
L V E OP
in patients with graft closure (one or more grafts occluded). Solid line = preoperative; broken line = postoperative; S W I = Stroke work index; L V E D P = left ventricular enddiastolic pressure.
i 30
minHI
Fig. 6B. Pre- and postoperative ventricular function curves in patients with 100 per cent graft patency. Symbols as in Fig. 6A.
T a b l e II. Effect of aortic pressure on ejection fraction
Postop: EF increased 5% or more (n = 10) Preop.
Aortic mean S.E.M. p value
94 6.4 < 0.01
I
Postop.
Preop.
83 6.6
99 6.5 < 0.5
recatheterization. T h e 19 patients (Group T) who d e m o n s t r a t e d progression of preoperative obstructions (10 per cent increase or more), or a new occlusion in the native circulation, showed the most s i g n i f i c a n t dePression in postoperative ventricular function (Fig. 7A). T h e changes were 100 per cent occlusion of a previously p a t e n t vessel in 24 instances and an increase in a preoperative obstruction in six instances. In 18 patients at least one of the changes was a new complete occlusion. T w e n t y - t w o (73 per cent) of these
694
Postop. E F unchanged (n = 10) I
Postop. EF decreased 5% or more (n = 9)
Postop.
Preop.
98 5.3
93 4.6
I
Postop.
93 3.9 < 0.5
changes were associated with a p a t e n t graft distal to the change, seven (23 per cent) with an occluded graft, and one (4 per cent) change in native circulation occurred in an ungrafted area. T h e 10 patients w i t h o u t a change in postoperative n a t i v e circulation (Group U) had no evidence, by a n y parameter, of deterioration in ventricular function (Fig. 7B). T h e group with the progression of disease in native circulation d e m o n s t r a t e d v e r y significant increases in h e a r t rate and decreases in aortic m e a n pressures post-
June, 1977, Vol. 93, No. 6
Function after aorto-coronary bypass
I
60--
50
-I
E
m
40
30
I
I
I
10
20
30
L V E D P mm HE
Fig. 6C. Pre- and postoperative ventricular function curves in patients with 100 per cent graft patency plus no perioperative infarct. Symbols as in Fig. 6A.
operatively. One p a t i e n t did not h a v e the native circulation opacified a d e q u a t e l y enough at res t u d y for i n t e r p r e t a t i o n , Discussion
T h e r e continues to be c o n t r o v e r s y as to the effects of c o r o n a r y a r t e r y b y p a s s surgery on left v e n t r i c u l a r function. S o m e studies h a v e demons t r a t e d i m p r o v e m e n t , others no change, a n d still others h a v e s h o w n deterioration. 1-~ T h e d a t a f r o m our entire group would suggest there has been s o m e deterioration of v e n t r i c u l a r function following c o r o n a r y b y p a s s surgery. I t is evident t h a t the p a t i e n t s having this o p e r a t i o n are not a h o m o g e n eous group and this m a y in p a r t explain the conflicting reports in the literature on the effects of this operation on v e n t r i c u l a r function. Therefore, we subdivided our p a t i e n t s into groups according to the indications for operation, condition prior to operation, i n t r a o p e r a t i v e events, and p o s t o p e r a t i v e status. S y m p t o m a t o l o g y a n d the q u a l i t y of v e n t r i c u l a r f u n c t i o n p r e o p e r a t i v e l y were of some prognostic value in predicting the effect of the operation on p o s t o p e r a t i v e function.
American Heart Journal
P a t i e n t s with a history of a previous infarct h a d poorer p o s t o p e r a t i v e v e n t r i c u l a r function t h a n p a t i e n t s who did not. However, p a t i e n t s w i t h o u t prior infarctions also d e m o n s t r a t e d decreased p o s t o p e r a t i v e function as a group (Figs. 2A a n d 2B). T h e group of p a t i e n t s with t h e best chance of m a i n t a i n i n g v e n t r i c u l a r function were those with v e r y ischemic ventricles preoperatively, as evidenced by m a r k e d l y positive stress tests. T h i s group included p a t i e n t s with significant m a i n left c o r o n a r y a r t e r y lesions. T h e y showed improvem e n t in p o s t o p e r a t i v e ejection fractions w i t h o u t decreases in aortic m e a n pressure. T h e y did h a v e lower values for pre- and p o s t a n g i o g r a m stroke work index at r e s t u d y b u t left v e n t r i c u l a r enddiastolic pressures were also lower so there was little or no change in the v e n t r i c u l a r function curve (Figs. 4A, 4B, and 4C}. Therefore, in this group of patients, there was no significant deterioration in v e n t r i c u l a r function and by some criteria an i m p r o v e m e n t was noted. T h e patients who sustained a perioperative infarction or were shown to h a v e one or m o r e grafts occluded p o s t o p e r a t i v e l y could be expected to show a decrease in p o s t o p e r a t i v e v e n t r i c u l a r function. However. p a t i e n t s who did not h a v e a perioperative infarct, who had 100 per cent graft patency, or both, also d e m o n s t r a t e d a significant depression in p o s t o p e r a t i v e v e n t r i c u l a r function curves (Figs. 5A, 5B, 6A. 6B, a n d 6C). T h e m o s t i m p o r t a n t predictor of the s t a t e of p o s t o p e r a t i v e v e n t r i c u l a r f u n c t i o n was the condition of the n a t i v e c o r o n a r y circulation at restudy. T h e m a j o r i t y of t h e changes in t h e native circulation were progression to 100 per cent occlusion of a c o r o n a r y a r t e r y p r o x i m a l to a p a t e n t graft, a c o m m o n finding reported by others. ~~ T h i s group showed a very significant depression in p o s t o p e r a t i v e v e n t r i c u l a r function curves (Fig. 7A ). If there was no change in native circulation, p o s t o p e r a t i v e h e m o d y n a m i c values were v i r t u a l l y identical to those of the p r e o p e r a t i v e s t u d y (Fig. 7BI. T h e o b s e r v a t i o n t h a t p a r t i a l l y o b s t r u c t e d c o r o n a r y arteries occlude p r o x i m a l to a p a t e n t vein graft has not caused m u c h a l a r m . 1~However, t h e d a t a presented here would suggest t h a t these occlusions h a v e a very d e t r i m e n t a l effect on v e n t r i c u l a r function. Possibly s m a l l b r a n c h e s n e a r the o b s t r u c t i o n are lost w i t h the occlusion and viable m y o c a r d i u m is sacrificed, resulting in loss of ventricular function. In a n y
695
B r u n d a g e et al.
80-
/ /
/
e~
w
u-
N-
I 10 LVEOP
0
I 20
] 30
mmHg
Fig. 7A. Pre- and postoperative ventricular function curves in patients with postoperative changes in native coronary circulation. Solid line = preoperative; broken line = postoperative; S W I = stroke work index: L V E D P = left ventricular end-diastolic pressure.
i,[ 50I
I r~
40-
30-
I
0
10 20 L V E D P mm HI(
!
30
Fig. 7B. Pre- and postoperative ventricular function curves in patients without postoperative changes in native coronary circulation. Symbols as in Fig. 7A.
696
regard, the m a i n t e n a n c e of a p a t e n t native circulation is s o m e h o w i m p o r t a n t to the p r e s e r v a t i o n of m y o c a r d i u m in the grafted area, even in the presence of a p a t e n t graft. T h e incidence of perioperative infarction was 21~ times g r e a t e r in the p a t i e n t s with changes in native circulation (53 per cent} t h a n in p a t i e n t s w i t h o u t changes in native circulation (20 per cent). This would suggest t h a t the loss of m y o c a r dium due to infarction m a y occur w h e n the native circulation occludes even t h o u g h a p a t e n t graft m a y be present distal to the occlusion. C o m p a r ison of groups with a n d w i t h o u t E C G evidence of m y o c a r d i a l infarction (L a n d M) was n o t as discriminating as changes in native circulation. This m a y be related to the insensitivity of E C G to recognize new m y o c a r d i a l d a m a g e in the postoperative period. Vectorcardiographic 14 a n d enz y m e 1~ techniques suggest t h a t the incidence of perioperative infarction m a y be quite high in this operation. T h e incidence of perioperative infarction by E C G was u n u s u a l l y high (40 per cent) in the group of p a t i e n t s restudied. This m a y well bias t h e entire group t o w a r d worse postoperative v e n t r i c u l a r function. However, the purpose of this s t u d y was to determine factors t h a t influence v e n t r i c u l a r function following b y p a s s surgery. Perioperative infarction b y E C G criteria is only one factor t h a t affects p o s t o p e r a t i v e function and comparison of Groups L and M indicates t h a t it is not the m o s t differentiating. T h e p a t i e n t s who h a d either angina, a positive stress test, or b o t h p o s t o p e r a t i v e l y (Group S) had an increased ejection fraction and a reduction in L V E D P postoperatively. T h i s could be interpreted as a n i m p r o v e m e n t in v e n t r i c u l a r function in a group of p a t i e n t s in w h o m deterioration m i g h t well be expected. However, this group also h a d a significant drop in resting aortic m e a n pressure and decreased a f t e r l o a d is k n o w n to improve ejection fraction a n d L V E D P . 1~ Stroke work indices, however, were depressed postoperatively in these patients. T h e s e observations p r o m p t e d us to f u r t h e r investigate the relationship of postoperative changes in resting aortic m e a n pressure on changes in ejection fraction. I t was found t h a t the p a t i e n t s w i t h improved p o s t o p e r a t i v e ejection fractions as a group had a significant decrease in baseline aortic m e a n pressure (Table II). T h e cause of the lower p o s t o p e r a t i v e aortic m e a n pressures in our patients is u n k n o w n . I t is possible
June, 1977. Vol. 93, No. 6
Function after aorto-coronary bypass
t h a t this represents a c o m p e n s a t o r y m e c h a n i s m to preserve cardiac o u t p u t in a group of p a t i e n t s who h a v e f u r t h e r depression of v e n t r i c u l a r function a f t e r b y p a s s surgery. A n o t h e r u n e x p l a i n e d o b s e r v a t i o n in our p a t i e n t s is t h e increased resting h e a r t r a t e postoperatively. T h i s has been r e p o r t e d b y others. 12-14 T h e e x p l a n a t i o n t h a t it is due to a high c a t e c h o l a m i n e s t a t e f r o m the stress of operation does n o t seem plausible in a group of p a t i e n t s studied an average of 5 m o n t h s a f t e r surgery and this increase in h e a r t r a t e has been observed by others as late as 1 y e a r p o s t o p e r a t i v e ly. TM T h i s could r e p r e s e n t a b a r o r e c e p t o r reflex because of lower aortic pressure. T h e observation t h a t a drop in p o s t o p e r a t i v e aortic m e a n pressure correlates with i m p r o v e d ejection fraction m a k e s it i m p e r a t i v e t h a t this h e m o d y n a m i c p a r a m e t e r be k n o w n before i n t e r p r e t i n g increased ejection fractions a f t e r surgery as i m p r o v e d v e n t r i c u l a r function. Since our p a t i e n t s often h a d increases in posto p e r a t i v e h e a r t r a t e with c o n c o m i t a n t decreases in stroke v o l u m e a n d often with decreases in blood pressure it is a p p a r e n t t h a t the decreases in stroke work index would occur. However, these changes should h a v e produced an a p p r o p r i a t e decrease in L V E D P according to the F r a n k S t a r l i n g m e c h a n i s m unless there h a d been alterations in v e n t r i c u l a r function or compliance. T h e fact t h a t L V E D P did not decrease postoperatively explains t h e p o s t o p e r a t i v e depression of v e n t r i c u l a r function curves seen in m a n y of our patients.
Conclusion M a n y of the p a t i e n t s in this s t u d y d e m o n s t r a t e d depressed v e n t r i c u l a r function a f t e r c o r o n a r y a r t e r y b y p a s s surgery. T h e m o s t import a n t d e t e r m i n a n t of deterioration was a new occlusion in the native circulation, even t h o u g h the m a j o r i t y of p a t i e n t s h a d a p a t e n t graft distal to t h e new occlusion. P a t i e n t s with very ischemic ventricles p r e o p e r a t i v e l y a p p e a r to h a v e the best c h a n c e of showing m a i n t e n a n c e or i m p r o v e m e n t in p o s t o p e r a t i v e v e n t r i c u l a r function. C a u t i o n m u s t be used in i n t e r p r e t i n g increases in postoperative ejection fraction as i m p r o v e m e n t in v e n t r i c u l a r function, because of t h e often seen decrease in p o s t o p e r a t i v e aortic m e a n pressure. T h i s decrease in aortic pressure m a y explain t h e increased p o s t o p e r a t i v e h e a r t r a t e observed by us a n d others. ~
American Heart Journal
Summary V e n t r i c u l a r function was e v a l u a t e d b y the d e v e l o p m e n t of v e n t r i c u l a r function curves f r o m the v o l u m e stress of angiographic c o n t r a s t m e d i a in 30 p a t i e n t s before a n d a n average of 5 m o n t h s a f t e r c o r o n a r y b y p a s s surgery. P a t i e n t s were grouped according to p r e o p e r a t i v e operative indications, perioperative events, and p o s t o p e r a t i v e s t a t u s to d e t e r m i n e the m o s t i m p o r t a n t factors affecting p o s t o p e r a t i v e v e n t r i c u l a r function. Pro: gression of lesions in t h e n a t i v e c o r o n a r y circulation correlated m o s t significantly with a decrease in p o s t o p e r a t i v e v e n t r i c u l a r function. In 18 of 19 p a t i e n t s t h e changes in n a t i v e c o r o n a r y circulation were progression to c o m p l e t e occlusion. S e v e n t y - t h r e e per cent of these changes were associated with a p a t e n t graft distal to the change. P a t i e n t s with v e r y ischemic ventricles as evidenced b y a m a r k e d l y positive stress test ( > 2 m m . S T depression) a n d / o r m a i n left c o r o n a r y obstruction m a i n t a i n e d or i m p r o v e d p o s t o p e r a tively v e n t r i c u l a r function. Increase in p o s t o p e r a tive ejection fraction was often associated with decrease in aortic m e a n pressure, m a k i n g it difficult to use this p a r a m e t e r to e v a l u a t e p o s t o p e r a tive v e n t r i c u l a r function.
REFERENCES 1. Itscoitz, S. B., Shepherd, R. L., Glancy, D. L., Olinger, G. N., Stinson, E. B., and Epstein, S. E.: Deterioration of myocardial function following aortocoronary bypass operation (abst.), Clin. Res. 21:427, 1973. 2. Campeau, L., Ghanem, E., Esplugas, E., Lesperance, J., Bourassa, M., and Grondin, C. M.: Left ventricular performance during exercise before and one year after aortocoronary bypass for angina pectoris, Circulation 49, 50 (Suppl. II):103, 1974. 3. Rees, G., Bristow, J. D., Kremkau, E. L., Green, G. S., Herr, R. H., Griswold, H. E., and Starr, A.: Influence of aortocoronary bypass surgery on left ventricular performance, N. Engl. J. Med. 284:1116, 1971. 4. Hammermeister, K. E., Kennedy, J. W., Hamilton, G. W., Steward, D. K., Gould, K. L., Lipscomb, K., and Murray, J. A.: Aortocoronary saphenous vein bypass: Failure of successful grafting to improve left ventricular function in chronic angina, N. Engt. J. Med. 290:183, 1974. 5. Chatterjee, K., Swan, H. J. C., Parmley, W. W., Sustaita, H, Marcus, H. S., and Matloff, J.: Influence of direct myocardial revascularization on left ventricular asynergy and function in patients with coronary heart disease: With and without previous myocardial infarction, Circulation 47:276, 1973. 6. Symposium on indocyanine green and its clinical applications: Proc. Staff Meet. Mayo Clin. 35:729, 1960. 7. Ganz, W., Donoso, R., Marcus, H. S., Forrester, J. S., and Swan, H. J. C.: A new techn!que for the measurement of cardiac output by thermodilution in man, Am. J. Cardiol. 27:392, 1971. 8. Brundage, B. H., and Cheitlin, M. D.: Ventricular func-
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ti0n curves from the cardiac response to angiographic contrast: A sensitive detector of ventricular dysfunction in coronary artery disease, AM. HEART J. 88:281, 1974. 9. Cheitlin, M. D., Davia, J. E., deCastro, C. M., Barrow, E. A., and Anderson, W. T.: Correlation of "critical" left coronary artery lesions with positive submaximal exercise tests in patients with chest pain, AM. HEART J. 89:305, 1975. 10. Griffith, L. S. C., Achuff, S. C., Conti, C. R., Humphries, J. 0., Brawley, R. K., Goth, V. L., and Ross, R. S.: Changes in intrinsic coronary circulation and segmental ventricular motion after saphenous vein coronary bypass graft surgery, N. Engl. J. Med. 288:589, 1973. 11. Bousvaros, G., Piracha, A. R., Chaudhry, M. A., Grant, C., Older, T. M., and Pifarr~, R.: Increase in severity of proximal coronary disease after successful distal aortocoronary grafts. Its nature and effects, Circulation 48:915, 1973.
698
12. Levine, J. A., Bechtel, D. J., Gorlin, R., Cohn, P. F., Herman, H. V., Cohn, L. V., and Collins, J. J., Jr.: Coronary artery anatomy before and after direct revascularization surgery: clinical and cinearteriographic studies in 67 selected patients, AM. HEART J. 89:561, 1975. 13. Urschel, C. W., Covell, J. W., Sonnenblick, E. H., Ross, J., Jr., and Braunwald, E.: The effects of decreased aortic compliance on performance of the left ventricle, Am. J. Physiol. 214:298, 1968. 14. Anderson, W. T., Brundage, B. H., andCheitlin, M. D.: Vectorcardiographic changes following coronary artery bypass surgery, AM. HEART J 87:421, 1974. 15. Dixon, S. H., Limbird, B. S., Roc, C. R., Wagner, G. S., Oldham, M. D~ Jr., and Sabiston, D. C., Jr.: Recognition of postoperative acute myocardial infarction: Application of isoenzyme techniques, Circulation 47, 48 (Suppl. 111):137, 1973.
June, 1977, Vol. 93, No. 6
There continues to be controversy over the effects of coronary artery bypass surgery on left ventricular function. 1-5 T h i r t y patients were studied in order to evaluate ventricular function before and an average of 5 months after surgery. The patients were grouped according to operative indications, preoperative condition, perioperative events, and postoperative status in an effort to elucidate the determinates of postoperative function. Materials and methods
T h i r t y patients undergoing saphenous vein bypass grafting of the coronary arteries at Walter Reed Army Medical Center form the basis of this study. Th e surgery was performed during an 18 m o n t h period spanning 1972 and 1973. Each patient underwent cardiac catheterization prior to surgery. All patients were fasted for 12 hours and had no~ taken propranolol for at least 2 days and digoxin for 5 days prior to the study. The subjects were premedicated 45 minutes before catheterization with 50 mg. of meperidine, 25 mg. of promethazine, and 0.4 mg. of atropine. All pressure measurements were recorded on an Electronics for Medicine DR-12, from a P 23 DB S t a t h a m strain gauge, connected to a fluid-filled polyethylene catheter. Left ventricular end-diastolic pressure (LVEDP) was recorded at high amplification and at a paper speed of 100 mm. per F r o m Fitzsimons A r m y Medical Center. Walter Reed A r m y Medical Center. a n d the University of California Medical School. Received for publication J a n . 23. 1976. Reprint requests: Bruce H. Brundage, M.D.. {LTC). {MC) USA, Cardiology Service, Fitzsimons A r m y Medical Center. Denver. Colo. 80240.
June, 1977, Vol. 93, No. 6, pp. 687-698
second. L V E D P was measured at the point of rapid rise in pressure after the "a" wave or at the peak of the R wave on the electrocardiogram (ECG). Aortic pressure was electronically meaned. Cardiac out put was determined by the green dye or thermodilution indicator technique2- 7 Stroke work index was calculated from the formula: SWI = (aortic mean press u r e - L V E D P ) x stroke volume index x 1.36/ 100. All measurements were obtained prior to the use of any contrast agent. The ventriculogram was performed by injecting 0.8 ml. per kilogram or 60 ml. (whichever was less) of methyglucamine diatriazoate (Renografin 76) through a polyethylene pigtail catheter over a 4 second period. The patients were positioned in the right anterior oblique and ejection fractions were calculated from this single plane by the area-length method. The hemodynamic measurements were repeated 3 to 5 minutes following left ventricular angiography. T he volume stress from the hyperosmotic contrast material used produces changes in L V E D P and stroke work index so that ventricular function curves can be constructed. 8 Coronary arteriograms were done after ventriculography by Judkin's technique. Narrowing of a major coronary artery of greater than 50 per cent of the diameter was considered significant. The patients were restudied an average of 5 months (range, 3 to 9 months) following their coronary artery surgery. T he restudy protocol was identical to the preoperative study and also included angiographic demonstration of graft patency. Treadmill stress tests were performed, when possible, before each study. T he exercise protocol has previously been reported. 9 There were 76 patients
American Heart Journal
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Table I. Pre- a n d p o s t o p e r a t i v e v e n t r i c u l a r f u n c t i o n d a t a
Group
A. B. C. D. E. F. G. H. I. J. K. L. M N. O. P. Q. R. S. T. U.
All patients Stable angina Unstable angina Previous infarct No previous infarct Poor preop, function Fair preop, function Good preop, function Operated for markedly positive stress test Stress test >2 mm. Main left lesion No periop, infarct Periop. infarct One or more grafts closed 100%graft patency No periop, infarct and 100% patency Asymptomatic postop. Neg. stress test postop. Ischemic postop. Change in native circulation No change in native circulation
* p < 0.05. t p < 0.02. $ p < 0.Ol.
L VEDP preangio. (ram. Hg preop. postop.)
L VEDP postangio. (ram. Hg preop.postop.)
10•177 10• 8 • 1-9 ___2 10•177 9•177 14+1-12• 10•177 1 8•177 10• 1-9 • 2
20•177 19+1-19• 20 • 6-22 • 2 22•177 18•177 25•177 21•177 16+2-17-+1 22 • 2-17 • 2
6.1+0.3-6.1• 5.7•177 8.5•177 6.5•177 5.8•177 5.6• 6.1•177 6.5•177 5.6+0.3-6.2•
7.6•177 7.0•177 9.8• 7.5•177 7.7•177 6.5•177 7.6•177 8.2•177 7.5•177
96•177 99•177 97•177 99•177 93•177 89•177 99~5-92• 96•177 86•177
10.+1-9• 11+_1-9• 9•177 11•177 11_+1-8+1" 9•177 9•177
23•177 24.+3-19• 19+2-18• 22•177 22•177 18•177 19+2-18•
5.4•177 5.3+0.4-6.7• 5.9•177 6.5•177 6.1•177 6.1•177 5.9•177
7.5•177 7.3• 7.6•177 7.6•177 7.4•177 7.8•177 7.7•177
95• 99•177 93•177 99• 95•177 97• 95-+5-99•
9•177 9• 1-9• 1 11•177 10 • 1-9 _+1 10• 1-9• 1
19•177 21•177 1 21•177 19-+ 1-19 • 1 23•177
6.3+0.4-6.2• 6.3•177 6.1•177 6.3+0.4-6.2+0.6 5.9•
7.7• 7.8•177 7.6+0.6-7.4+0.9 7.7+0.4-6.9+0.5 7.4•177
93•177 96•177 100• 97•177 90•
CO preangio. (L. rain. preop.-postop.)
CO postangio. (L. /min. preop.-postop.)
Aortic mean preangm. (ram. Hg preop.-postop.)
wp < 0.001. 82 p < 0.0001. [[ p < 0.00001.
who underwent coronary bypass grafting during t h e p r o t o c o l period. T h e r e were 6 o p e r a t i v e d e a t h s . T h i r t y - n i n e p a t i e n t s were e x c l u d e d f r o m t h e s t u d y b e c a u s e p r e o p e r a t i v e or p o s t o p e r a t i v e c a t h e t e r i z a t i o n d a t a were i n c o m p l e t e a n d o n e p a t i e n t w a s lost t o follow-up.
Results T h e 30 p a t i e n t s i n t h i s s t u d y were all m a l e . E i g h t e e n (60 p e r c e n t ) were o p e r a t e d o n b e c a u s e of severe b u t s t a b l e a n g i n a , u n c o n t r o l l e d b y m e d i c a l m a n a g e m e n t . F i v e (17 p e r c e n t ) h a d u n s t a b l e a n g i n a t h a t did n o t s t a b i l i z e a f t e r a d m i s s i o n to t h e c o r o n a r y - c a r e u n i t . S e v e n p a t i e n t s (23 p e r c e n t ) h a d a m a r k e d l y i s c h e m i c r e s p o n s e to exercise ( g r e a t e r t h a n 2 m m . S T - s e g m e n t depress i o n ) a n d were o p e r a t e d o n b e c a u s e t h e y h a d a n g i n a a n d a m a i n left c o r o n a r y o b s t r u c t i o n , a m a i n left e q u i v a l e n t ( p r o x i m a l o b s t r u c t i o n of left anterior descending and circumflex coronary arteries), or severe t h r e e - v e s s e l disease. P r e o p e r a -
688
_ S.E.M.)
tive c o r o n a r y a r t e r i o g r a p h y d e m o n s t r a t e d t h r e e vessel disease i n 20 p a t i e n t s (67 p e r cent), twovessel disease in s e v e n (23 per c e n t ) , a n d onevessel disease i n t h r e e (10 per cent}. I n o n e case, o n l y t h e r i g h t c o r o n a r y was b y p a s s e d , b u t it s u p p l i e d a n u n u s u a l l y l a r g e p o r t i o n of t h e p o s t e r o l a t e r a l w a l l of t h e left v e n t r i c l e . O n e p a t i e n t r e c e i v e d f o u r grafts (3 p e r cent), 15 t h r e e grafts (50 p e r cent}, 10 t w o g r a f t s (33 p e r c e n t ) , a n d f o u r o n l y o n e g r a f t (14 p e r cent}. R e v a s c u l a r i z a t i o n w a s c o n s i d e r e d to be c o m p l e t e in 25 (83 per cent} of t h e p a t i e n t s . A t t h e t i m e of r e s t u d y 24 p a t i e n t s (80 per c e n t ) d e n i e d s y m p t o m s a n d six (20 per cent} h a d residual a n g i n a b u t s t a t e d it w a s i m p r o v e d . P o s t o p e r a t i v e t r e a d m i l l stress t e s t s were negative for i s c h e m i a i n I5 a n d p o s i t i v e in five. S t r e s s t e s t s e i t h e r were n o t o b t a i n e d i n t h e o t h e r 10 p a t i e n t s or were t e c h n i c a l l y i n a d e q u a t e for i n t e r p r e t a t i o n . P e r i o p e r a t i v e infarcts, d e f i n e d as n e w Q w a v e s o n p o s t o p e r a t i v e E C G ' s , were n o t e d i n 12
J u n e , 1977, Vol. 93, No. 6
Function after aorto-coronary bypass
Table I., continued Aorhc mean postangio. (ram. Hg preop.postopJ
HR preangio(b./ min. preop.postop.)
HR postangio. (b./min. preop. postor.)
SV preangio,
SV postangio.
(ml.
(ml.
preop.postop.)
preop.postop.)
SWI preangio. (Gm.-M./M. 2 preop.postop.)
SWI postangio (Gm.-M./M# preop.postopJ
Ejection frac~on preop.postopj
No.
103_+4-97_+3" 106_+5-98_+4" 105_+10--103_+8 108_+7-100_+6 99_+4--94_+4 90-+8--82_+5 103_+6--101_+6 109_+7-100_+4" 92_+8--88_+8
78_+2-89_+3: 82_+3--87_+3 80_+3-91_+3" 85_+5--88_+3 78_+1--82_+3 79_+5-84_+4 81_+4-84_+3 84_+4--85_+3 75_+2-94_+5580_+4--89_+4* 78_+5--80_+5 76_+5--83_+4 77_+3--93_+4587_+5--89_+3 78_+5--90_+6 79_+5-89_+5 72_+3--89_+1075_+4--89_+8
80_+4-70_+5* 95_+4--81_+55 50_+3--41_+3t 57_+3--44_+3w62_+3--62_+2 30 75_+5--66_+6 88_+5--76+_6* 48_+4-39_+3 54_+3--43_+3564-+3--63_+3 18 100_+9--82_+18 114_+7-77_+6" 66_+11-49_+11 74_+11--51_+8 64_+6--56_+7 5 78_+6--68_+7 87_+5-73_+7* 52_+6--41_+4 58_+5--40_+4558_+4--58_+3 14 82_+4--71_+7 102_+6--86_+7t 48_+2--40_+4* 57_+4--47_+35 66_+3--66_+3 16 72_+4-61_+8 84_+3--69_+10 40_+3-31_+35 44_+3--33_+4 43_+6--61_+85 6 82_+3--69_+9 93_+4-75_+6t 55_+5-42_+6* 56_+5-43_+4* 66_+11--59_+4 12 83_+9--75_+6 104_+10--93_+9 50_+6-44_+3 66_+5-50+_45 68_+2--66_+2 12 78_+5--70_+3 101_+11--76_+4t 43_+4--38_+5* 54_+7-41_+6" 57_+6--65_+5* 7
101_+7-97_+6 103_+9--104_+7 102_+6--98_+4 103_+6--94_+6" 100_+6--92_+4 106_+5--101_+4 106_+5--101_+4
73_+2--91_+6t 80_+3--89_+5 72_+2--85_+4576-+5--83-+4 78_+3--90_+5* 84_+5--94_+7 77_+3--88_+3* 78_+3-87_+3 78_+3--86_+3 80_+4-85_+3 77_+4--93_+5t 84_+5--90_+4 75_+3--94_+6584_+6--90_+5
74_+4--64_+35 73_+5--77-+12 77_+6--70_+4 84_+4--69_+10 79_+4--69_+7 81_+6--71_+6 79_+7-72_+6
96_+7-76_+35 99+13-79_+4 94_+7--85_+7 97_+4--75_+85 93_+5--79_+75 106_+9-83_+85 99_+9-85_+8
44_+3--38_+4* 46_+5--46-+6 47_+4-42_+3 53_+4-39_+6t 47_+3-37_+5t 53_+6-44_+3 50_+6--44_+3
55_+6--43_+4t 60_+4--65_+4 56_+10-49_+4 63_+4--69-+5 58_+5--46_+3t 64_+3--66_+3 57_+5--40_+45 59_+5--57_+4 52_+3--41_+35 59_+4--60_+4 64_+6-47_+4t 65_+2--64_+3 60-+6-48_+4* 64-+2--64_+3
11 6 18 12 16 14
99_+5-96_+4 100_+6-97_+5 106_+7-96_+5 99_+5--92_+4* 103_+6--100_+4
79_+3-89_+4* 83_+4-89___3 80_+4--71_+5 73 _+3-92 _+5:~ 79-+3-89_+4* 84_+5--71_+6" 71_+2--84_+5"75_+3--81_+3 85_+6-73-+11 75+3--94_+45 81_+4--92_+3t 85_+4--68_+65 78_+3--80_+3 80_+4-78_+3 76-+6--75_+9
96_+5-82_+65 99_+6--79_+35 102-+8-91-+13 98•182 94_+10-89_+11
48_+4--40_+3* 53_+5-41_+4t 53-+5-43+7 51-+4-36 _+3~: 49_+6-50_+5
56-+4--43_+35 64_+3--61_+3 59_+5--42_+35 64_+3--62_+3 61-+4-50+5" 58_+6--68-+4* 60_+4--39_+31] 61_+3--60_+3 52_+6-52_+5 64_+6--66__4
24 15
patients (40 per cent). Postoperative c o r o n a r y arteriography d e m o n s t r a t e d p a t e n c y in 53 of the 73 grafts placed (73 per cent). T h e purpose of this s t u d y was to investigate a n y changes in ventricular function following c o r o n a r y a r t e r y bypass surgery and elucidate their causes. Global ventricular function was evaluated by developing pre- and postoperative ventricular function curves from the v o l u m e stress of left ventricular a n g i o g r a p h y and by measuring pre- and postoperative ejection fractions. Previous work has s h o w n t h a t hyperosmotic c o n t r a s t material produces increases in cardiac o u t p u t , p r e s u m a b l y due to increases in blood volume. T h e increased blood volume results in greater venous r e t u r n and increased ventricular end-diastolic volume. Cardiac o u t p u t is thereby e n h a n c e d by the F r a n k - S t a r l i n g m e c h a nism. T h e r e s u l t a n t changes in cardiac o u t p u t and L V E D P m a k e the c o n s t r u c t i o n of v e n t r i c u l a r function curves possible. 8 T a b l e I includes the
American Heart J o u r n a l
9
19 10
d e t e r m i n a n t s of the ventricular f u n c t i o n curves ( L V E D P and SWI), ejection fractions (EF), and the h e m o d y n a m i c values t h a t influence these measurements: cardiac o u t p u t (CO), m e a n aortic pressure, heart rate (HR), and stroke volume (SV). Pre- and postoperative values are listed side by side with the s t a n d a r d error of the m e a n (S.E.M.). A n y statistically significant differences are a n n o t a t e d . Line A of Table I indicates the mean values for the entire group. T h e r e were significant decreases in pre- and p o s t a n g i o g r a m S W I postoperatively. Since there was no change from pre- to postoperative L V E D P , depression of the ventricular f u n c t i o n curve occurred after surgery (Fig. 1). T h e r e was no change in postoperative EF. A significant increase in postoperative resting H R was observed. In an a t t e m p t to obtain a more meaningful understanding of changes in postoperative ventricular function, patients were grouped according to indications for operation, condition prior to oper-
689
Brundage
e t al.
M~
ilO
---t
i
60-
20-~
=.I
w gr
3= e,4
40-
30-
30-
I
I
I
10
20
30
LV EOP
mm HE
Fig. 1. Pre- and postoperative ventricular function curves for all patients. Solid line = preoperative; broken line = postoperative; S W I = stroke work index; L V E D P = left ventricular end-diastolic pressure.
ation, i n t r a o p e r a t i v e events, and p o s t o p e r a t i v e status. T h e s e categories are included in T a b l e I. S e p a r a t i n g p a t i e n t s b y t y p e of p r e o p e r a t i v e angina (stable, G r o u p B; unstable, G r o u p C) did not a l t e r the effect of b y p a s s surgery on postoperative v e n t r i c u l a r function. T h e r e was evidence for depression of function in b o t h groups, a l t h o u g h the n u m b e r of p a t i e n t s w i t h u n s t a b l e angina was too small for statistical significance. A history of an old m y o c a r d i a l i n f a r c t i o n prior to surgery (Group D) was associated with a greater depression of the p o s t o p e r a t i v e ventricu l a r function curve, b u t a significant decrease in function occurred in the p a t i e n t s w i t h o u t previous infarction (Group E; Figs. 2A a n d 2B). Ejection fractions were u n c h a n g e d a f t e r surgery b u t were lower in the infarct group. T h e group w i t h o u t previous infarction h a d a significant increase in p o s t o p e r a t i v e h e a r t r a t e s whereas the infarct group did not. P a t i e n t s were categorized as h a v i n g poor, fair, or good p r e o p e r a t i v e v e n t r i c u l a r function (Groups F, G, a n d H). P a t i e n t s w i t h resting L V E D P ' s of 12 m m . H g or less, ejection fractions
690
I tO LVEOP
0
I 20
I 20
mmH|
Fig. 2A. Pre- and postoperative ventricular function curves in patients with prior myocardial infarction. Solid line = preoperative; broken line = postoperative; S W I = stroke work index; L V E D P = left ventricular end-diastolic pressure. 60--
50-
I
f f
40-
30-
l 10
I 20 I. VEDP
I 30
mmHg
Fig. 2B. Pre- and postoperative ventricular function curves in patients without prior myocardial infarction. Symbols as in Fig. 2.4.
J u n e , 1977, Vol. 93, No. 6
Function after aorto-coronary bypass
N-
W-
u m
40--
I-
I = m
30-
W-
I !0
I 20 LVEDP
I 30
nmHl[
Fig. 3A. Pre- and postoperative ventricular function curves in patients with poor preoperative ventricular function. Solid line = preoperative; broken line = postoperative; S W I = stroke work index; L V E D P = left ventricular enddiastolic pressure. "
30-
i 10 LVEDP
I 20
i
mmHI
Fig. 3C. Pre- and postoperative ventricular function curves in patients with good preoperative ventricular function. Symbols as in Fig. 3A.
50-I
40--
m-
I
10 LVEDP
I
I
20
30
WaHl[
Fig. 3B. Pre- and postoperative ventricular function curves in patients with fair preoperative ventricular function. Symbols as in Fig. 3A.
American Heart Journal
55 per cent or greater, a n d n o r m a l preoperative ventricular function curves were r a t e d as good, patients meeting none of these criteria as poor, and the remainder as fair. Postoperative ventricular function curves were depressed by equivalent a m o u n t s in all groups (Figs. 3A, 3B, and 3C). Postoperative ejection fractions were significantly increased (43 to 61, p < 0.01) in patients with poor preoperative v e n t r i c u l a r function; however, there was a significant decrease in postoperative aortic m e a n pressure in this group. Ejection fraction did not change significantly in patients with fair or good preoperative ventricular function. There was a group of patients with evidence of a r a t h e r m a r k e d l y ischemic ventricle preoperatively as defined by very positive stress tests (greater t h a n 2 mm. S T - s e g m e n t depression). M a n y of these patients (five of 11) h a d significant main left c o r o n a r y obstruction. Seven of these
6 91
Brundage
e t al.
60-
m50I
U-
i
40--
N
O30-
I O
10 LVEDP
I
I
20 mmHg
30
N
Fig. 4A. Pre- and postoperative ventricular function curves
in patients with evidence of markedly ischemic ventricular function preoperatively (markedly positive stress test). Solid line = preoperative; broken line = postoperative; S W I = stroke work index; L V E D P = left ventricular enddiastolic pressure. 60--
50-
I
L
40-
30-
I 10 L Y E D P
I 20 mm HI[
I 30
Fig, 4B, Pre- and postoperative ventricular function curves in patients with evidence of markedly ischemic ventricular function preoperatively {stress test > 2 mm.). Symbols as in Fig. 4A.
692
0
l 10
I 20
LVEDP
I 30
mmHI
Fig. 4C. Pre- and postoperative ventricular function curves in patients with evidence of markedly ischemic ventricular function preoperatively (main left lesions). Symbols as in Fig. 4A. patients were operated on primarily because of the m a r k e d l y positive stress test. Their angina was mild or m o d e r a t e a n d n o t sufficient to be considered as indication for operation alone (Group I). T h e y h a d severe three-vessel disease, main left lesions, or main left equivalent lesions. While there was a decrease in stroke work index postoperatively, there was also a significant decrease in postoperative L V E D P after angiography. For this reason, the postoperative ventricular f u n c t i o n curve was only slightly depressed (Fig. 4A). There was a significant i m p r o v e m e n t in the ejection fraction from 57 to 65 (p < 0.05) and the postoperative aortic m e a n pressure was unchanged. All patients with preoperative stress tests showing greater t h a n 2 mm. S T - s e g m e n t depression (Group J) h a d a decrease in postoperative stroke work index b u t this also was associated with a significant decrease in postangio. L V E D P so the v e n t r i c u l a r function curve was changed little after surgery (Fig. 4B). T h e ejection fraction increased from 60 to 65 b u t this was not statistically significant. P a t i e n t s with signifi-
J u n e , 1977, Vol. 93, No. 6
Function after aorto-coronary bypass
W--
N-
i
/1/
s/
u
u
3t r
i
3t
(
30
I 10 LVtDP
I 28
I m
Illl
0
I 10 LV[DP
I 20
I 10
mmHI
Fifl. 5A. Pre- and postoperative ventricular curves in patients w i t h o u t a perioperative infarct. Solid line = preoperative; broken line = postoperative; S W I = stroke work index; LVEDP = left ventricular end-diastolic pressure.
I::ifl.5B. Pre- and postoperative ventricular curves in patients with perioperative infarct. Symbolsas in Fig. 5A.
cant main left coronary lesions (Group K) had no postoperative depression of the ventricular function curve (Fig. 4C) and ejection fraction improved but not to levels of statistical significance. A perioperative infarct could b e expected to depress postoperative ventricular function. However, patients without a perioperative infarct (Group L) likewise had significant depression of postoperative ventricular function. The perioperative infarction groups, however, did h a v e a greater reduction in postoperative stroke work indices (Group M; Figs. 5A and 5B). Ejection fractions were unchanged in both groups. The finding of one or more closed grafts at restudy (16 patients) was associated with a depressed postoperative ventricular function curve (Group N; Fig. 6A). Only four patients had all grafts occluded. The 14 patients with 100 per cent graft patency (Group O) also h a d significantly lower postoperative ventricular function curves (Fig. 6B). Even patients who did not have a perioperative infarct and had 100 per cent patency on restudy (Group P) were found to have depressed ventricular function curves postopera-
tively (Fig. 6C). Ejection fractions were unchanged after surgery in these three groups. Lack of myocardial ischemia postoperatively, whether the subjective lack of anginal symptoms (24 patients, Group Q) or, more objectively, a negative treadmill stress test (15 patients, Group R), did not prevent depression of ventricular function curves. However, the presence of angina and/or a positive stress test (nine patients, Group S} after surgery appeared to produce contradictory data. There was a decrease in the postoperative stroke work indices but ejection fraction and LVEDP improved. However, there was a significant decrease in postoperative aortic mean pressure in these patients. Similar results were previously noted in the patients with poor preoperative ventricular function (Group F). When all patients were categorized according to changes in postoperative ejection fraction, the group of patients with improved ejection fractions showed a significant decrease (p < 0.01} in postoperative aortic mean pressure (Table II). Finally, in this study, the most important determinant of postoperative ventricular function was the state of the native circulation at
American Heart Journal
593
Brundage et al.
I
N60~
m 50-3E B t
40 40--
30]
I
I
I0
20
30
L VEDP
ininH|
I lO
o
Fig. 6A. Pre- and postoperative ventricular function curves
I 20
L V E OP
in patients with graft closure (one or more grafts occluded). Solid line = preoperative; broken line = postoperative; S W I = Stroke work index; L V E D P = left ventricular enddiastolic pressure.
i 30
minHI
Fig. 6B. Pre- and postoperative ventricular function curves in patients with 100 per cent graft patency. Symbols as in Fig. 6A.
T a b l e II. Effect of aortic pressure on ejection fraction
Postop: EF increased 5% or more (n = 10) Preop.
Aortic mean S.E.M. p value
94 6.4 < 0.01
I
Postop.
Preop.
83 6.6
99 6.5 < 0.5
recatheterization. T h e 19 patients (Group T) who d e m o n s t r a t e d progression of preoperative obstructions (10 per cent increase or more), or a new occlusion in the native circulation, showed the most s i g n i f i c a n t dePression in postoperative ventricular function (Fig. 7A). T h e changes were 100 per cent occlusion of a previously p a t e n t vessel in 24 instances and an increase in a preoperative obstruction in six instances. In 18 patients at least one of the changes was a new complete occlusion. T w e n t y - t w o (73 per cent) of these
694
Postop. E F unchanged (n = 10) I
Postop. EF decreased 5% or more (n = 9)
Postop.
Preop.
98 5.3
93 4.6
I
Postop.
93 3.9 < 0.5
changes were associated with a p a t e n t graft distal to the change, seven (23 per cent) with an occluded graft, and one (4 per cent) change in native circulation occurred in an ungrafted area. T h e 10 patients w i t h o u t a change in postoperative n a t i v e circulation (Group U) had no evidence, by a n y parameter, of deterioration in ventricular function (Fig. 7B). T h e group with the progression of disease in native circulation d e m o n s t r a t e d v e r y significant increases in h e a r t rate and decreases in aortic m e a n pressures post-
June, 1977, Vol. 93, No. 6
Function after aorto-coronary bypass
I
60--
50
-I
E
m
40
30
I
I
I
10
20
30
L V E D P mm HE
Fig. 6C. Pre- and postoperative ventricular function curves in patients with 100 per cent graft patency plus no perioperative infarct. Symbols as in Fig. 6A.
operatively. One p a t i e n t did not h a v e the native circulation opacified a d e q u a t e l y enough at res t u d y for i n t e r p r e t a t i o n , Discussion
T h e r e continues to be c o n t r o v e r s y as to the effects of c o r o n a r y a r t e r y b y p a s s surgery on left v e n t r i c u l a r function. S o m e studies h a v e demons t r a t e d i m p r o v e m e n t , others no change, a n d still others h a v e s h o w n deterioration. 1-~ T h e d a t a f r o m our entire group would suggest there has been s o m e deterioration of v e n t r i c u l a r function following c o r o n a r y b y p a s s surgery. I t is evident t h a t the p a t i e n t s having this o p e r a t i o n are not a h o m o g e n eous group and this m a y in p a r t explain the conflicting reports in the literature on the effects of this operation on v e n t r i c u l a r function. Therefore, we subdivided our p a t i e n t s into groups according to the indications for operation, condition prior to operation, i n t r a o p e r a t i v e events, and p o s t o p e r a t i v e status. S y m p t o m a t o l o g y a n d the q u a l i t y of v e n t r i c u l a r f u n c t i o n p r e o p e r a t i v e l y were of some prognostic value in predicting the effect of the operation on p o s t o p e r a t i v e function.
American Heart Journal
P a t i e n t s with a history of a previous infarct h a d poorer p o s t o p e r a t i v e v e n t r i c u l a r function t h a n p a t i e n t s who did not. However, p a t i e n t s w i t h o u t prior infarctions also d e m o n s t r a t e d decreased p o s t o p e r a t i v e function as a group (Figs. 2A a n d 2B). T h e group of p a t i e n t s with t h e best chance of m a i n t a i n i n g v e n t r i c u l a r function were those with v e r y ischemic ventricles preoperatively, as evidenced by m a r k e d l y positive stress tests. T h i s group included p a t i e n t s with significant m a i n left c o r o n a r y a r t e r y lesions. T h e y showed improvem e n t in p o s t o p e r a t i v e ejection fractions w i t h o u t decreases in aortic m e a n pressure. T h e y did h a v e lower values for pre- and p o s t a n g i o g r a m stroke work index at r e s t u d y b u t left v e n t r i c u l a r enddiastolic pressures were also lower so there was little or no change in the v e n t r i c u l a r function curve (Figs. 4A, 4B, and 4C}. Therefore, in this group of patients, there was no significant deterioration in v e n t r i c u l a r function and by some criteria an i m p r o v e m e n t was noted. T h e patients who sustained a perioperative infarction or were shown to h a v e one or m o r e grafts occluded p o s t o p e r a t i v e l y could be expected to show a decrease in p o s t o p e r a t i v e v e n t r i c u l a r function. However. p a t i e n t s who did not h a v e a perioperative infarct, who had 100 per cent graft patency, or both, also d e m o n s t r a t e d a significant depression in p o s t o p e r a t i v e v e n t r i c u l a r function curves (Figs. 5A, 5B, 6A. 6B, a n d 6C). T h e m o s t i m p o r t a n t predictor of the s t a t e of p o s t o p e r a t i v e v e n t r i c u l a r f u n c t i o n was the condition of the n a t i v e c o r o n a r y circulation at restudy. T h e m a j o r i t y of t h e changes in t h e native circulation were progression to 100 per cent occlusion of a c o r o n a r y a r t e r y p r o x i m a l to a p a t e n t graft, a c o m m o n finding reported by others. ~~ T h i s group showed a very significant depression in p o s t o p e r a t i v e v e n t r i c u l a r function curves (Fig. 7A ). If there was no change in native circulation, p o s t o p e r a t i v e h e m o d y n a m i c values were v i r t u a l l y identical to those of the p r e o p e r a t i v e s t u d y (Fig. 7BI. T h e o b s e r v a t i o n t h a t p a r t i a l l y o b s t r u c t e d c o r o n a r y arteries occlude p r o x i m a l to a p a t e n t vein graft has not caused m u c h a l a r m . 1~However, t h e d a t a presented here would suggest t h a t these occlusions h a v e a very d e t r i m e n t a l effect on v e n t r i c u l a r function. Possibly s m a l l b r a n c h e s n e a r the o b s t r u c t i o n are lost w i t h the occlusion and viable m y o c a r d i u m is sacrificed, resulting in loss of ventricular function. In a n y
695
B r u n d a g e et al.
80-
/ /
/
e~
w
u-
N-
I 10 LVEOP
0
I 20
] 30
mmHg
Fig. 7A. Pre- and postoperative ventricular function curves in patients with postoperative changes in native coronary circulation. Solid line = preoperative; broken line = postoperative; S W I = stroke work index: L V E D P = left ventricular end-diastolic pressure.
i,[ 50I
I r~
40-
30-
I
0
10 20 L V E D P mm HI(
!
30
Fig. 7B. Pre- and postoperative ventricular function curves in patients without postoperative changes in native coronary circulation. Symbols as in Fig. 7A.
696
regard, the m a i n t e n a n c e of a p a t e n t native circulation is s o m e h o w i m p o r t a n t to the p r e s e r v a t i o n of m y o c a r d i u m in the grafted area, even in the presence of a p a t e n t graft. T h e incidence of perioperative infarction was 21~ times g r e a t e r in the p a t i e n t s with changes in native circulation (53 per cent} t h a n in p a t i e n t s w i t h o u t changes in native circulation (20 per cent). This would suggest t h a t the loss of m y o c a r dium due to infarction m a y occur w h e n the native circulation occludes even t h o u g h a p a t e n t graft m a y be present distal to the occlusion. C o m p a r ison of groups with a n d w i t h o u t E C G evidence of m y o c a r d i a l infarction (L a n d M) was n o t as discriminating as changes in native circulation. This m a y be related to the insensitivity of E C G to recognize new m y o c a r d i a l d a m a g e in the postoperative period. Vectorcardiographic 14 a n d enz y m e 1~ techniques suggest t h a t the incidence of perioperative infarction m a y be quite high in this operation. T h e incidence of perioperative infarction by E C G was u n u s u a l l y high (40 per cent) in the group of p a t i e n t s restudied. This m a y well bias t h e entire group t o w a r d worse postoperative v e n t r i c u l a r function. However, the purpose of this s t u d y was to determine factors t h a t influence v e n t r i c u l a r function following b y p a s s surgery. Perioperative infarction b y E C G criteria is only one factor t h a t affects p o s t o p e r a t i v e function and comparison of Groups L and M indicates t h a t it is not the m o s t differentiating. T h e p a t i e n t s who h a d either angina, a positive stress test, or b o t h p o s t o p e r a t i v e l y (Group S) had an increased ejection fraction and a reduction in L V E D P postoperatively. T h i s could be interpreted as a n i m p r o v e m e n t in v e n t r i c u l a r function in a group of p a t i e n t s in w h o m deterioration m i g h t well be expected. However, this group also h a d a significant drop in resting aortic m e a n pressure and decreased a f t e r l o a d is k n o w n to improve ejection fraction a n d L V E D P . 1~ Stroke work indices, however, were depressed postoperatively in these patients. T h e s e observations p r o m p t e d us to f u r t h e r investigate the relationship of postoperative changes in resting aortic m e a n pressure on changes in ejection fraction. I t was found t h a t the p a t i e n t s w i t h improved p o s t o p e r a t i v e ejection fractions as a group had a significant decrease in baseline aortic m e a n pressure (Table II). T h e cause of the lower p o s t o p e r a t i v e aortic m e a n pressures in our patients is u n k n o w n . I t is possible
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Function after aorto-coronary bypass
t h a t this represents a c o m p e n s a t o r y m e c h a n i s m to preserve cardiac o u t p u t in a group of p a t i e n t s who h a v e f u r t h e r depression of v e n t r i c u l a r function a f t e r b y p a s s surgery. A n o t h e r u n e x p l a i n e d o b s e r v a t i o n in our p a t i e n t s is t h e increased resting h e a r t r a t e postoperatively. T h i s has been r e p o r t e d b y others. 12-14 T h e e x p l a n a t i o n t h a t it is due to a high c a t e c h o l a m i n e s t a t e f r o m the stress of operation does n o t seem plausible in a group of p a t i e n t s studied an average of 5 m o n t h s a f t e r surgery and this increase in h e a r t r a t e has been observed by others as late as 1 y e a r p o s t o p e r a t i v e ly. TM T h i s could r e p r e s e n t a b a r o r e c e p t o r reflex because of lower aortic pressure. T h e observation t h a t a drop in p o s t o p e r a t i v e aortic m e a n pressure correlates with i m p r o v e d ejection fraction m a k e s it i m p e r a t i v e t h a t this h e m o d y n a m i c p a r a m e t e r be k n o w n before i n t e r p r e t i n g increased ejection fractions a f t e r surgery as i m p r o v e d v e n t r i c u l a r function. Since our p a t i e n t s often h a d increases in posto p e r a t i v e h e a r t r a t e with c o n c o m i t a n t decreases in stroke v o l u m e a n d often with decreases in blood pressure it is a p p a r e n t t h a t the decreases in stroke work index would occur. However, these changes should h a v e produced an a p p r o p r i a t e decrease in L V E D P according to the F r a n k S t a r l i n g m e c h a n i s m unless there h a d been alterations in v e n t r i c u l a r function or compliance. T h e fact t h a t L V E D P did not decrease postoperatively explains t h e p o s t o p e r a t i v e depression of v e n t r i c u l a r function curves seen in m a n y of our patients.
Conclusion M a n y of the p a t i e n t s in this s t u d y d e m o n s t r a t e d depressed v e n t r i c u l a r function a f t e r c o r o n a r y a r t e r y b y p a s s surgery. T h e m o s t import a n t d e t e r m i n a n t of deterioration was a new occlusion in the native circulation, even t h o u g h the m a j o r i t y of p a t i e n t s h a d a p a t e n t graft distal to t h e new occlusion. P a t i e n t s with very ischemic ventricles p r e o p e r a t i v e l y a p p e a r to h a v e the best c h a n c e of showing m a i n t e n a n c e or i m p r o v e m e n t in p o s t o p e r a t i v e v e n t r i c u l a r function. C a u t i o n m u s t be used in i n t e r p r e t i n g increases in postoperative ejection fraction as i m p r o v e m e n t in v e n t r i c u l a r function, because of t h e often seen decrease in p o s t o p e r a t i v e aortic m e a n pressure. T h i s decrease in aortic pressure m a y explain t h e increased p o s t o p e r a t i v e h e a r t r a t e observed by us a n d others. ~
American Heart Journal
Summary V e n t r i c u l a r function was e v a l u a t e d b y the d e v e l o p m e n t of v e n t r i c u l a r function curves f r o m the v o l u m e stress of angiographic c o n t r a s t m e d i a in 30 p a t i e n t s before a n d a n average of 5 m o n t h s a f t e r c o r o n a r y b y p a s s surgery. P a t i e n t s were grouped according to p r e o p e r a t i v e operative indications, perioperative events, and p o s t o p e r a t i v e s t a t u s to d e t e r m i n e the m o s t i m p o r t a n t factors affecting p o s t o p e r a t i v e v e n t r i c u l a r function. Pro: gression of lesions in t h e n a t i v e c o r o n a r y circulation correlated m o s t significantly with a decrease in p o s t o p e r a t i v e v e n t r i c u l a r function. In 18 of 19 p a t i e n t s t h e changes in n a t i v e c o r o n a r y circulation were progression to c o m p l e t e occlusion. S e v e n t y - t h r e e per cent of these changes were associated with a p a t e n t graft distal to the change. P a t i e n t s with v e r y ischemic ventricles as evidenced b y a m a r k e d l y positive stress test ( > 2 m m . S T depression) a n d / o r m a i n left c o r o n a r y obstruction m a i n t a i n e d or i m p r o v e d p o s t o p e r a tively v e n t r i c u l a r function. Increase in p o s t o p e r a tive ejection fraction was often associated with decrease in aortic m e a n pressure, m a k i n g it difficult to use this p a r a m e t e r to e v a l u a t e p o s t o p e r a tive v e n t r i c u l a r function.
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