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Significance of new Q waves after bypass grafting: Correlations between graft patency, ventriculogram, and surgical venting technique
Significance of new Q waves after bypass grafting: Correlations between graft patency, ventriculogram, and surgical venting technique Agop Aintabhan, M.D. Robert I. Hamby, M.D. Irwin Hoffman, M.D. Daniel Weisz, M.D. Choudary Voleti, M.D. B. George Wisoff, M.D. New Hyde Park, Jamaica, and Stony Brook, N. Y.
New postoperative electrocardiographic Q waves have been described in eight to 40 per cent of patients undergoing bypass grafting for coronary artery disease.‘-” Various theories have been proposed to explain these new Q waves.6-‘o Correlations of new Q waves to vein bypass occlusion, prolonged pump time or aortic cross-clamping time are controversial.11-*4 Indeed, whether or not the appearance of new postoperative Q waves means real transmural myocardial infarction is not clear.“’ We report herein our experience with postoperative Q waves in 56 patients with vein bypass grafts and the relationship of new Q waves to ventricular venting, graft patency, and the postoperative ventriculogram. Our observations indicate that: (1) Not all Q waves are due to occlusion of the saphenous bypass grafts (as noted by others”. Is. 16). (2) A certain percentage of new Q waves may not reflect true transmural myocardial infarction, especially when all the vein grafts are patent and the postoperative ventriculograms show improvement. (3) Some new Q waves reflect true transmural infarction due to occlusion of grafts or of distal coronary arteries with deteriorated left ~ventriculograms. From the Department of Medicine, Cardiology Division, and the Department of Surgery, Cardiothoracic Division, Long Island Jewish-HiIbdde Medical Center, New Hyde Park, N. Y., Queens Hospital Center Affiliation, Jamaica, N. Y., and the School of Medicine, Health Sciences Center, State University of New York at Stony Brook, N. Y. Received
for publication
Accepted
for publication
Reprint Island
requests: Jewish-Hillside
Agop
Oct. 14, 1976. Dec.
17, 1976.
Aintablian, M.D., Cardiology Division, Long Medical Center, New Hyde Park, N. Y. 11040.
OOOZ-8703/78/0495-0429$01.20/O
0 1978 The
C. V. Mosby
Co.
(4) The high incidence of new Q waves in patients with ventricular vents is probably due to direct myocardial trauma at the apex of the left ventricle. Material
and
methods
Between December, 1970, and February, 1976, 720 patients underwent coronary bypass surgery at Long Island Jewish-Hillside Medical Center. Forty-nine patients were excluded because they also underwent partial ventricular resection, prosthetic valve replacement, or ventricular septal defect closure. Of the remaining 671 patients, 56 patients developed new Q waves making up the case material for the present study. In 621 patients, a saphenous vein graft was utilized for coronary bypass, while in 50 patients the internal mammary artery was anastomosed to the left anterior descending artery. All patients had preoperative left and right heart catheterization and left ventricular and selective coronary angiography using the Judkins** or the Sones and Shirey’? techniques. In quantitating left ventricular dysfunction and the pattern of left ventricular contraction, the same techniques and principles were used as previously reported,‘9 utilizing the descriptive terminology suggested by Herman and associates.*“ Coronary arteries with at least 50 per cent reduction in diameter on coronary angiography were considered significantly stenosed and were bypassed whenever feasible. The severity and the extent of coronary disease was graded according to the criteria of Bruschke and associates.21 Congestive
American
Heart
Journal
429
Aintabiian
et al.
a 1533)
wllhouta (02) No.Pstiatts
With I 104 LEFTVEWTRICULAR VENT116
With 1 567 LEFTATRIA1VEWTIRR
Fig. 1. Comparison of the incidence of new Q waves in patients patients with double or triple vessel disease had higher incidence vessel’ disease.
heart failure and cardiomegaly were defined according to the criteria we used in previous publication. 22 Post-bypass recatheterization and angiography were done 10 to 15 days after surgery in order to assess the patency of the grafts, and any change in left ventricular function. Twelvelead electrocardiograms were performed on each patient on admission, on the day before surgery, then daily for the next four days, and finally one day before discharge. All angiograms and electrocardiograms were reviewed by two different cardiologists in the comparison of pre- and postoperative studies. Electrocardiographic criteria used to evaluate the electrocardiogram were essentially Class I-l and I-2 of the Minnesota code reported by Blackburn and associates.Z3 Cases presenting transient ST segment or T wave changes, but without pathologic Q waves, were not included in the infarction pattern group. One hundred and forty-two of the 671 patients were operated upon for preinfarction angina the same day of the cardiac catheterization as previously reported,24 while 529 had elective surgery for angina. Patients with saphenous vein bypasses to all coronary arteries with luminal narrowing greater than 50 per cent were considered complete revas-
430
with ventricular of new Q waves
or atria1 venting revealed that as compared to those with single
cularizations, while patients vein bypasses could not be more vessels with similar were considered incomplete Operative
in whom saphenous performed. to one or luminal narrowings revascularizations.
technique
All patients had reversed saphenous vein aortocoronary bypass utilizing total cardiopulmonary support. Priming solution was 5 per cent dextrose in one-third normal saline. Flow rates were 40 to 55 ml./Kg. using a bubble oxygenerator with mean arterial pressures of at least 50 mm. Hg. In 104 patients the left ventricle was vented through the apex and in the remaining 567 patients the left ventricle was vented through the right superior pulmonary vein. Moderate hypothermia was achieved by cooling the patient to 32” C. After total cardiopulmonary bypass, the ventricle was occasionally electrically defibrillated and intermittently clamped for the distal anastomosis. Results 1. Effects new Q wave
of surgical incidence.
venting
technique
in
Of 671 operated on, 104 (Group A) had intraoperative ventricular venting, and 567 (Group B) had atria1 venting. The inci-
April,
1978, Vol. 95, No. 4
New Q waves after bypass grafting
dence of new Q waves in Group A was 23/104 (22 per cent) and in Group B 33/567 (5.8 ‘per cent) (p < 0.05).
Table
I. Clinical
profile new Q waves
2. Relation of the clinical profile and underlying coronary disease to the incidence of new Q waves. As seen in Table I, comparison of age, sex,
duration of angina, coronary score, history or location of prior myocardial infarction did not differ in patients with or without new Q waves. Also, there was no difference in the incidence of normal or abnormal left ventricular segmental wall motion between the groups. Although there was a slightly higher incidence of cardiomegaly and congestive heart failure in patients who developed new Q waves, the difference was not statistically significant. Main left coronary stenosis or unstable angina pectoris did not affect the incidence of new Q waves. Patients with double or triple vessel coronary disease had a higher in+dence of new Q waves, as compared to those with single-vessel disease (Fig. 1). 3. Relation grafts placed.
of new
Q waves
to
number
of
In the entire series of 671 operated patients, 56 (8 per cent) had new postoperative Q waves. Of these, 12 (6 per cent) occurred after single bypass in 207 patients, 24 (8 per cent) after double bypass in 287 patients, 18 (11 per cent) after triple bypass in 164 patients, and two (15 per cent) after quadruple bypass in 13 patients. Thirty-one new Q waves appeared on the anterior and septal walls, 23 on the inferior and inferolateral walls, and two on lateral walls (Table II). 4. Relation of new Q waves to ungrafted vessels or to patent grafts with an occluded distsl atiery. New Q waves appeared in the zone
of myocardium supplied by grafted arteries in all except three patients with ventricular venting (Cases No. 6, 7, and 16) (Table III). In the latter three patients, the Q waves occurred within zones of myocardium supplied by diseased, but ungrafted vessels. In all the patients with new Q waves who were restudied, only two (Cases 37 and 40) (with atria1 venting and deteriorated ‘left ventriculograms) demonstrated patent grafts, but an occluded coronary artery beyond the distal anastomotic site (Table IV). 5. Relation of new Q Waves to postoperative alteration of left ventricular function and graft closure. In Group A (ventricular venting), 17
patients
with new Q waves had postoperative
American
Heart
Journal
l-r-l-r With new Q waves
WithOUt
No.
Total number Age (~4 Mean Range
of patients
%
615
No.
%
56
54-c 6 28-84
53 -c 11 32-76
Sex
Male Female Unstable angina History of infarction Documented ECG infarction Septal Anterior Inferior Inferior and anterior Infero-dorsal, infero-lateral and dorsal Normal QRS Enlarged heart Congestive heart failure Normal left ventricular contraction Segmental hypokinesia of one wall Akinesia of one wall Akineaia or segmental hypokinesia of more than one wall Generalized hypokineaia
506 109 132 258
l6 38 >
a2 18 21 42
49
9
2
a7 13 18 43
7 10 24
2 12 3 3
>
7
117 21 12
19 3 2
411 45 25 230
67 7 4 37
11 5 24
43
154
25
13
23
98 103
16 16
9 11
16 20
0
0
3
0.5
34
20
5 5 61 20
9
ventriculograms. Of these (Table III), three (18 per cent) had an improved ventriculogram and O/7 graft closures, 4 (24 per cent) had no change in the ventriculogram with l/7 graft closure, and in 10 patients (58 per cent) with deteriorated postoperative ventriculograms, there were 7116 graft closures (Table III). Of 17 patients in Group A who had postoperative ventriculograms, five had single, 11 had double, and one had triple bypass grafts. In Group B (atria1 venting), 25 patients with new Q waves were studied postoperatively. Of these (Table IV), five (20 per cent) had an improved ventriculogram and O/ 11 graft closures. Fourteen (56 per cent) had an unchanged postoperative ventriculogram and 4/34 graft closures, while six (24 per cent) had a deteriorated postoperative ventriculogram with 6/15 graft closures. Of these 25 patients, four had single, eight had double, 12 had triple, and one had quadruple
431
Aintablian
et al.
Cl Single @ Oouble
T
a
Triple or lluadfupie
100 90
a0 70
a0 50 40 30 20 IO 0
Patients With II CARBIoWLblOwtv
Without lwPm
Fig. 2. Comparison of over-all cardiopulmonary without new Q waves, did not show statistically
a
II. Correlation of graft closure to the new Q waves and location of new Q waves in patients with ventricular and atria1 venting
.~
23
33
56
42 17 8/30
74 27
80 25 9160
76 15
122 42 17/90
75
7
52 31
12 14
36 43
24 21
43 37
2
9
0
1
4
6 13
19
New Q waves Anterior Inferior Infero-lateral Septal Lateral
12
14
0
18
2 7 2
4 12 4
bypass grafts. Although over-all incidence of new Q waves was 22 per cent in patients with ventricular venting, as compared to 5.8 per cent in those with atria1 venting, the graft closure rate in patients with new Q waves was 27 ‘per cent in the ventricular vented group and 15 per cent in those with atria1 Venting. 6. Relation of the location complete versus incomplete
432
of new Q waves revascularization
to
Withsut 9
AORTIC CRgSS CLAMPIIIG TIME
bypass and aortic significant difference.
Table
Patients Grafts Pts. studied Grafts closed
with 0
TIME
cross-clamping
time
in patients
with
and
grafted vessels. All the new Q waves occurred within the zone of myocardium supplied by a grafted artery except for 3156 (5 per cent) of the patients. These three new Q waves appeared in the inferior (Cases 6 and 7) or infero-lateral (Case 16) wall in the group of patients with ventricular venting (Table III). Complete revascularization was performed in 50/104 (48 per cent) of the patients with ventricular venting, in 369/567 (65 per cent) of those with atria1 venting. Patients with ventricular venting and new Q waves had 13/23 (57 per cent) complete revascularization, and those with atria1 venting 21/33 (64 per cent); the difference was,statistically insignificant, indicating that completeness of revascularization did not affect the incidence of new Q waves. and
7. Correlation of new Q waves to the duration of cardiopulmonary bypass, aortic cross-clamping time. In 350 patients with atria1 venting,
there were no significant differences in the overall duration of cardiopulmonary bypass or aortic cross-clamping time in those with or without new Q waves, whether they had single or multiple vessel coronary bypass surgery (Fig. 2). In patients with new Q waves, the incidence of prolonged cardiopulmonary bypass time exceeding 100 minutes for double (30 per cent) and 120
April,
1978, Vo2. 95, No. 4
New Q waves after bypass grafting
III. Correlation Group A patients
of location
Table
of new Q wave, patency
Grafts Patient
LAD
RCA
Patency CX
LAD
RCA
+ +
+ +
X
+
+
X
x x
of graft, and postoperative
Contraction CX
Preop
Postop
ventriculogram
HX MI
Admission ECG Q wave Inferior RBBB + Lateral Inferior (narrow Q)
Anterior Inferior
Septal LAH+ Anterior Inferior Inferior
in
New Q
LVG improved 1.
x
2.
X
X X
3.
X
X
LVG unchanged 4. X 5. X 6. X 7. X LVG Deteriorated a. X
As-Ant As-Ant
Normal Normal
‘1 ‘1
+
As-Ant
Normal
‘1
+ +
0
Normal Normal
Normal Normal
0 0
+ +
+ +
Normal Normal
Normal Normal
0 ‘1
Normal Inferior + Lateral Normal T ll.lll, aVF
‘3
T,.,
Anterior
0 0
Normal Inferior
Anterior Anterior
‘2 0
T”l.“e LAH QRS WNL Anterior
Anterior Anterior
Normal Normal Normal
Inferior Inferior Lateral Inferolateral
X
+
+
AleApic
X
0 0
0
Normal As-Apic
9. 10.
X X
11. 12.
X X
X
0 0
0
Normal As-Ant
. 13.
X
X
+
+
Ak Ant
14. 15. 16. 17.
X
X X
+
+ +
As-Inf Normal Normal As-Inf
X X
0 +
X
Abbreviations: LAD = left anterior As = Segmental hypokineaia.
descending
+ coronary
artery;
RCA = right
minutes for triple or multiple bypass grafts (33 per cent) as compared to those with no Q waves (18 per cent and 13 per cent, respectively), were slightly higher. 8. Disappearance of Q waves. Two of our patients, after coronary bypass surgery, lost longstanding anterior Q waves. Postoperative angiography in these two patients revealed patent saphenous bypass grafts and improved left ventriculogram in one while in the other, the left ventriculogram was unchanged. 9.. Relation
of
mortality
to
graft
patency.
Twelve patients died within one month after bypass surgery (Table V). Three patients died in the operating room. One. of them (Case 2) probably had a myocardial infarction the morning of surgery. Of nine patients who died within two weeks after surgery, two died of noncardiac causes, one died of combined cardiac and
American
Heart
Journal
A~L<~” Ak A;!: AkCA”” Ak-A$!: Ak-Ant As-Ant AkInf + Apic Ah-Inf Ak-Apic Ak-Apic Ak
artery;
‘3 0 0 0 ‘2
CX = circumflex
coronary
Inferior (wide Q)
Inferior
artery;
Ak = Akin&a,
non-cardiac causes, whereas six patients’ deaths were secondary to myocardial infarction. The mortality in two patients, who died after discharge at home, was due to myocardial infarction in one (Case 10) and in the other due to myocardial infarction or ventricular arrhythmia (Case 11). It should be mentioned that 2112 (17 per cent) who died had balloon assist prior to surgery for persistent angina or cardiogenic shock (Cases 6 and 11) and one patient was brought to the operating room after arrest while external cardiac massage was being performed (Case 1). Of 12 patients who died, three (25 per cent) had main left coronary stenosis. Discussion
An 8 per cent incidence of new Q waves in our series is lower than reported by others.“. I5323 Contrary to the report of Williams and asso-
433
Aintablian
et al.
IV. Correlation Group B p&ients
Table
of location
of new Q wave, patency of graft, and postoperative
Grafts Patient L VG improved 18.
Patency
LAD
( RCA
1 CX
LAD
X
X
X
+
Contraction
1 RCA
1 CX
+
+
Preop
HX MI
Postop
**
0
ventriculogram
Admission ECG Q wave
New
T”8.“6
in
Q
Septal
Ap1c
LVG
0
Normal
0
Normal
Inferior
As-Apic A&-Inf As-Ant
As-Apic Ak-Inf As-Ant
1 ‘1 2
Normal Inferior Infero-dorsolateral
Septal Anterior Anterior
Ak-Inf Ak-Apic Normal Normal Normal Normal Normal Ak-Inf Normal Normal Normal Normal
Ak-Inf Ak-Apic Normal Normal Normal Normal Normal Ak-Inf Normal Normal Normal Normal
0 0 ‘1 0 0 0 0 0 0 1 2
Normal Normal TV,-V, T ll.lll aV, Normal Normal T”,.% Normal T ll.lll aV, Normal Anterior + small Q II III aV,
Adterior Inferior Inferior Inferior Inferior Inferior Inferior Inferior Inferior Inferior Inferior
+
Normal As-Ant *k-Basal
Ak-Apic *k-Ant Ak-Basal
0 1
Normal Q II, III,
Septal Anterior
X
+
-I-
21.
X
X
+
+
22.
X
X
X
+
+
+
X
X X
+ -I-
0
+ + 0 + 0
unchanged 23. X 24. X 25. Xt
X X X X X X X X X-l
Ak
+
X X X X X X X X X X X
deteriorated 37. X 38. 0 X
X X X
+ + +
X
+ +
X
+
X X X X
+ + +
X
+* 0 -I-
Normal
As-Apic
Xt X
26. 21. 28. 29. 30. 31. 32. 33. 34. 35. 36. LVG
*’ Inf Normal
Normal Small Q with R V,-V, TV,-V,
+
19. 20.
+ + + + + + 0 + + + +
+ + + + 0 +
Ak
Apic
0 + 1
39.
X
X
X
O
0
0
As-Ant
Inferior
40.
XC
X
X
+
+
+
Normal
Normal
41.
X
X
0
42.
xt
+ *qAnt
X
X
+
+
0
Normal
Apic
Septal
Qs V,-V,
good
Inferior
aV,
+ lateral
Anterior Anterior
Ak-Apid
0
Lateral
Ak-Inf
0
Inferior
Abbreviationa ae in Table III. *Patent grafi, but occluded distal left anterior descending artery (cases 37 and 40). thtemal mammary anaetomoeie to left anterior deecendmg artery.
main left coronary stenosis did not increase the incidence of new Q waves. The age, sex, duration of disease, preinfarction angina, previous myocardial infarction, or abnormal left ventricular wall motion did not affect the incidence of new Q waves. Patients with double or triple vessel disease, as well as those with cardiomegaly or congestive heart failure, had a higher incidence of new Q waves, but this differciaks,’
434
ence was not statistically significant. Of 12 patients who died after doronary bypass surgery, eight died (Table V) of definite acute myocardial infarction, one probably of acute myocardial infarction or ventricular tachyarrhythmia (Case 11, Table V), two of massive pulmonary embolism, and one after an extensive cerebrovascular accident. Of these 12 patients, 25 per cent had significant main left coronary artery disease. The
April,
1978,
Vol.
95, No.
4
New Q waves after bypass grafting mortality rate of only 6 per cent (3/50) (Cases 4, 6, 8, Table V) in the patients developing postbypass new Q waves was much lower than reported mortality rate in CCU’s by different centers, namely 9.8 per cent to 23 per cent.?+?T This suggests that new post-bypass Q waves may not represent true transmural myocardial infarctions. Most of the patients with sudden development of postoperative new Q waves had a benign hospital course and were not clinically different from patients without new Q waves. This has also been noted by others.*O, Is. I6 Patients with presumed true myocardial infarction not only had elevated SGOT and other enzyme levels, but their electrocardiograms demonstrated evolutionary changes of transmural myocardial infarction, usually localized on the anterior wall of the left ventricle. Although Fruehan and associates’” noted that 74 per cent (28/38) of new Q waves were located in the inferior, dorsal, or inferolateral wall in their series of 199 patients, we encountered new Q waves in those locations in only 41 per cent (23/56). Three of 56 patients with new Q waves and a history of previous myocardial infarction (Cases 3,20,36, Tables III and IV) developed significant Q waves in the inferior or anterior wall, sites of previous narrow Q waves. These electrocardiographic changes which suggest “unmasking” of an old myocardial infarction pattern may also be due to a localized conduction disturbance in an area of previous infarction due to redistribution of electrical forces after bypass surgery or to a change of axis secondary to surgery. The left ventriculograms in these patients improved or did not change after the appearance of significant new Q waves. However, none of our patients after coronary bypass surgery manifested the phenomenon of “unmasking of old infarction,” described by Bassan and associates.‘” It is worth mentioning that two of our patients, after coronary bypass surgery and patent grafts, lost longstanding anterior Q waves, which also has been observed by Conde and associates.28 A striking decrease in the incidence of postoperative Q waves (from 22 per cent to 5.8 per cent) occurred when atria1 rather than ventricular venting was adopted. This result may be due, in part, to improved surgical bypass techniques, since the ventricular vented cases were done at the start of the coronary bypass surgery program in our institution. The over-all incidence of saphe-
American Heart Journal
nous bypass graft closure was higher in the early operated group. In the ventricular venting group, the graft closure rate was 22 per cent versus 8. per cent in those patients with atria1 venting. In patients with new Q waves and ventricular venting who had a postoperative study (Table II), the graft closure rate was twice as high, as compared to the atria1 venting group (27 per cent versus 15 per cent). However, the incidence of the new Q waves was much higher in the ventricular venting group (22 per cent), as compared at atria1 venting patients (58 per cent). Thus, improved surgical techniques and fewer graft closures alone cannot explain such a drop in the incidence of new Q waves, The clear implication is that sufficient myocardial trauma results from ventricular venting to result in pathologic Q waves. The anatomic placement of ventricular vents at or near the apex could account for either inferior or anterior wall localization of the postoperative Q waves. Since the ventricular trauma produced by venting is not due to arterial occlusion, there is ‘no wide surrounding ischemic area. Thus, it is ,not surprising that postoperative Q waves attributable to venting are not usually associated with impaired ventricular function in the absence of graft occlusion. Indeed, improved ventricular function may be observed. However, in four patients (Cases 13, 14, 15, and 17), in whom new inferior Q waves developed, new dysfunction of the inferior wall and open grafts to the right coronary artery could be demonstrated. Here we assume that the deterioration in the ventriculogram was probably secondary to the trauma of venting. In contrast are Cases 7, 9, 10, 11, 12, 16, 19,38, and 39, all of whom developed new anterior Q waves and anterior wall dysfunction in the presence of occluded grafts to the left anterior descending artery or its diagonal branch. Here the assumption must be that true infarction secondary to inadequate arterial and graft inflow occurred. The incidence of new Q waves was higher in patients with double, triple, or quadruple bypass surgery, as compared to those with a single bypass, as reported by others.4 Although our patients with atria1 venting .had a higher percentage of complete revascularizations, the incidence of new Q waves was not affected by complete or incomplete revascularization in patients in either the atria1 or ventricular venting groups. All of the new Q waves occurred within
435
Aintablian
et al.
Table V. Circumstances
and causes of death Causes of deuth Died
Patient no.
No. of diseased vessels
Old myocardial infarction
In OR
Within Within 2 wks. 1 month
New Q waves
Infarction
LV VENT. 1
3
Inferior
2
M 3 2
Inferior
4 5 6
3 2 3
0 Anterior Inferior
+ LAH
I 8 9
0 Anterior 0
+ Inferior
10
3 3 M 2 1
11
3
12
M 3
Anterior inferior 0
3
+
-
+
-
+ + +
-
Pulmonary embolism
Cerebrovascular accident
+
Anterior
i-
Interior
LA VENT.
Abbreviations:
-
+ +
Inferior
+ +
0
M = main left coronary
+ LPH
+ RBBB
+ Anterior
+
Anterior
+ + +
Anterior
(3 wks postop)
+
+
+
artery;
LAH
= left anterior
-
hemiblock;
the zone of myocardium supplied by the grafted artery, except three (5 per cent) of the patients in the ventricular vented group in whom the new Q wave appeared in non-grafted vessel zones of inferior or infero-lateral wall. This result is different from the report of Assad-Morel1 and colleagues,” in which 25 per cent of the patients manifested new Q waves in a zone of myocardium supplied by a diseased ungrafted artery, It is worth mentioning that in three patients with atria1 venting and with patent saphenous vein bypass grafts, the coronary artery distal to the anastomosis was closed. This explains the appearance of their new Q waves, as well as the observed deterioration of left ventricular contractility. Although Anderson and associates? noted no direct correlation between ECG evidence of transmural myocardial infarction and graft closure, they did not comment on the corresponding ventriculography. Brewer and associateP confirmed these findings in autopsy studies of
+
+ Probable
+
-
LPH
= left posterior
hemiblock;
RBBB
+
Q right bundle branch
block.
patients dying after coronary bypass surgery. In the present study, new Q waves were noted in patients with deteriorated, unchanged, or even improved ventriculograms. When the data on new Q waves and postoperative ventricular function were correlated, no direct relationship could be seen. However, when graft patency was also considered, a clear relationship emerged. Improved postoperative ventricular function correlated well with graft patency, despite Q waves. Unimproved or deteriorated ventricular function did not predict graft occlusion, since more than half of the vein grafts placed in these patients were patent. Assad-Morel1 and associatesll also noted a lack of correlation between graft closure and electrocardiographic and angioeaphic evidence of myocardial infarction. Half their 32 patients had patent grafts, despite evidence of myocardial infarction in the area of distribution of the grafted vessels. .In our series, only 19 per cent of grafts were closed in patients with new Q waves and only 38
April,
1978, Vol. 95, No. 4
New Q waves after bypass grafting
Comments After cardiac catheterization had chest pain, then arrested. With external cardiac massage was brought to O.R. and double bypass done. Died 4 days later. Autopsy showed patent grafts with recent anterior infarction The morning of surgery had protracted chest pain with ST elevation, Autopsy showed fresh anterior infarction Died 24 hours postop. No autopsy. Postoperative stormy course. No autopsy Autopsy showed pulmonary embolism with patent grafts Balloon assist + nitroprusside for persistent angina. Postop developed anterior Q wave, then LBBB before death No autopsy Developed LBBB + LPH before death No autopsy Expired 3 wks. postop. Autopsy showed fresh anterior infarct and closure of graft Balloon assisted angiograms done. Discharged home after triple patent grafts. Died in his sleep Protracted pleuritic pain. Rat persistent pericardial rub. .Autopsy showed bilateral massive pulmonary emboli + fresh anterior infarct and patent grafts
per cent of left ventriculograms deteriorated, while 43 per cent were unchanged and 19 per cent improved after surgery. Indeed, in the patients without new Q waves, 9 per cent (77/885) of grafts were closed, indicating that graft occlusion can occur without necessarily causing electrocardiographic changes of transmural myocardial infarction. It is important to note that, in our series, patients with single bypass grafts in whom the postoperative left ventriculogram showed deterioration invariably had an occluded bypass graft or a patent graft with occlusion of the coronary artery distal to the anastomosis (Tables III and IV). At least four or five patients developed severe hypotension prior to bypass surgery. These patients most likely sustained myocardial infarction at that moment and electrocardiographic changes of transmural myocardial infarction appeared after completion of the bypass due to reperfusion of the infarcted area, since bypass grafts studied postoperatively were patent in this group. The delayed appearance of new Q waves
American
Heart
Journal
after coronary occlusion in dogs has been explained by Blumenthal and associates.3’ Possible preservation of the sarcolemmal membranes delays the appearance of Q waves in the early phase of infarction, but after reperfusion, disruption of these membranes accelerates the emergency of Q waves. When new Q waves appeared after bypass, using the atria1 venting technique, with ventricular function unimproved or worsened, graft closure or occlusion of the distal coronary artery was common. A compromised arterial inflow and true myocardial infarction must be presumed. Of great interest are those patients with new Q waves following atria1 venting, with improved ventriculograms and patent grafts. The new Q waves must be a consequence of surgical trauma, since aortic cross-clamp and cardiopulmonary bypass times were not significantly prolonged. Two possibilities are suggested. First, direct myocardial damage with muscle necrosis may occur, sufficient to produce Q waves, but nevertheless undetectable by ventriculography. Second, the surgical trauma might result in localized ventricular conduction delays or blocks, affecting the early QRS balance, as postulated by Castellanos and Lemberg.32 They theorized that such local delays in ischemic tissue result in slurring or widening of the QRS, producing “infarct” Qs. It seems reasonable that a similar mechanism in traumatized tissue may account for postoperative Q waves in these patients with improved ventriculograms and patent grafts. Clinical significance and prognosis. Postbypass grafting Q waves, as described and discussed, have a varied pathogenesis. When accompanied by improvement in ventricular function and patent grafts, they are of little significance and do not carry the prognostic importance of myocardial infarction as it occurs in the natural course of arteriosclerotic heart disease. In contrast, when accompanied by graft closure and deteriorated ventricular function, the mechanism may be presumed ischemic and the prognosis must take into account the likelihood of permanent or long-term localized ventricular dysfunction. Summary
New Q waves were observed in 56 (8 per cent) of 671 patients undergoing saphenous vein bypass
437
Aintablian
et al.
Fig. 3. Pre- and postoperative angiographic study surgery developed new septal Q waves (Case No. segment of the left ventricle (urrow) was no more
of a patient with atria1 venting who after triple vein bypass 18). As seen here, segmental hypokinesia of the anteroapical present in the postoperative left ventriculogram.
Fig. 4. Comparison of pre- and postoperative left ventricular contractile pattern of Case ventriculogram did not show any significant change, although postop. he developed new inferior
grafting, with an over-all mortality rate of 1.8 per cent. Forty-two of the 56 (75 per cent) had postoperative ventriculograms and arteriograms and are reported herein. Ventricular venting was used intraoperatively in 17 patients, and atria1 venting in 25. Thirty-one patients had new “ante438
No. 27. Q waves.
Left
rior” and/or “septal” Q waves, while 23 had “inferior” or “infero-lateral” and 2 had “lateral” Q waves. The incidence of new Q waves in patients With ventricular venting was 22 per cent and in those with atria1 venting it was 5.6 per cent (p < 0.05). Age, sex, duration of disease, severity April,
1978, Vol. 95, No. 4
New Q waves after bypass grafting
Fig. 5. Pre- and postoperative left ventriculograms of a patient with atria1 venting and new anterior No. 37). Postoperatively the vein graft was patent with occluded distal left anterior descending hypokinesia of the apical segment of the left ventricle (arrow).
of angina, previous myocardial infarction or main left coronary lesions did not affect the incidence of new Q waves. Although new Q waves were more frequent in patients with preoperative cardiomegaly and congestive heart failure, this difference was not statistically significant. However, there was no significant difference in the over-all cardiopulmonary bypass or aortic crossclamping time in patients with or without new Q waves. Cardiopulmonary bypass time exceeding 100 minutes in patients with double bypasses, and more than 120 minutes with multiple bypasses, were more frequent in patients with new Q waves. Completeness or incompleteness of the revascularization procedure did not affect the incidence of new Q waves. In all but three patients with ventricular venting, new Q waves appeared in a zone of myocardium supplied by a grafted artery. In the three exceptions, the Q waves occurred within the zone of myocardium supplied by diseased but ungrafted vessels. In the ventricular vented group 7 (41 per cent) demonstrated an improved or unchanged postoperative ventriculogram with 7 per cent graft closure and 10 (59 per cent) had deteriorated ventriculograms with 44 per cent graft closure. In 25 patients with atria1 venting, 19 (76 per cent) showed improved or unchanged postoperative ventriculogram with 12 percent graft closure and 6 (14 per cent) had American
Heart
Journal
Q waves (Case artery and new
deteriorated ventriculograms with 40 per cent graft closure. Although over-all incidence of new Q waves was 22 per cent in patients with ventricular venting as compared to 5.8 per cent in those with atria1 venting, the graft closure rate in patients with new Q waves was 27 per cent in ventricular vented group and 15 per cent in those with atria1 venting. These findings indicate a poor correlation between new Q waves and graft closure. Improved postoperative ventriculograms correlated well with graft patency despite new Q waves. The etiology of new post-bypass graft Q waves are varied. They include direct ventricular trauma and conduction delays resulting from surgery or venting, as well as true ischemic infarction. Infarction may be due to compromised arterial inflow either in non-operated diseased vessels, in vessels distal to anastomoses with patent grafts, or due to graft closure. REFERENCES 1.
2.
3.
Williams, D., Iben, A., Jurley, E., Miller, R., Bonanno, J., Massumi, R., Zelis, R., Mason, D. T., and Amsterdam, E. A.: Myocardial infarction during coronary artery bypass surgery (Abstr.), Am. J. Cardiol. 31:164, 1973. Friedberg, D., Zeft, H., Siberman, R., et al.: Myocardial infarction following coronary surgery: Vectorcardiographic assessment (Abstr.), Am. J. Cardiol. 31:132, 1973. Anderson, W. T., Brundage, B. H., and Cheitlin, M. D.:
439
Aintablian
4.
5.
6.
7.
8.
9.
et al.
Vectorcardiographic changes following coronary artery bypass surgery, AM. HEART J. 87:421,1974. Espinoza, J., Lipski, J., Litwak, R., Donoso, E., and Kack, S.: New Q waves after coronary artery bypass surgery for angina pectoris, Am. J. Cardiol. 33:221, 1974. Schrank, J. P., Slabaugh, T. K., and Beckwith, J. R.: The incidence and clinical significance of ECG-VCG changes of myocardial infarction following aortocoronary saphenous-vein bypass surgery, AM. HEART J. 87:46,-1974. Manlev. J. C.. and Johnson. W. D.: Effects of surgery on angina (pre- and postinfarction) and myocardial function (failure), Circulation 48:1208, 1972. Van Heeckeren, D. W., and Ankeney, J. L.: Aortocoronary graft patency related to perioperative myocardial infarction, Circulation 47 (Suppl. IV):IV-226, 1973. Dreifus, L., Cannarozzi, N., and Rabbino, M.: Electrocardiographic alterations following prosthetic valve replacement, Circulation 29 and 30 (Suppl. III):III-70, 1964. Hultgren, H. N., Hubis, H., and Shumway, N.: Cardiac function following prosthetic aortic valve replacement, “I
AM. HEART
”
d. 77:585,
I
percutaneous transfemoral technique, Radiology 89:815, 1967. 19. Hamby, R. I., Tabrah, F., Aintablian, A., Hartstein, M. L., and W&off, G. B.: Left ventricular hemodynamics and contractile pattern after aortocoronary bypass surgery. Factors affecting reversibility of abnormal left ventricular function, AM. HEART J. 88:149, 1974. 20. Herman, M. V., Heinle, R. A., Klein, M. D., and Gorlin, R.: Localized disorders in myocardial contraction. Asynergv and its role in congestive heart failure, N. Engl. J. Med. 279~222, 1967. 21. Bruschke, A. V. G.: The diagnostic significance of the coronary arteriogram. A study of its value in relation to other diagnostic methods, Utrecht. 1970, Kremink en Zovn NY.22. Aintablian, A., Hamby, R. I., and Garsman, J.: Correlation of heart size with clinical and hemodvnamic findines in patients with coronary artery disease; AM. HEART 2. 91:21, 23.
1969.
10. Bassan, M. M., Oatfield, R., Hoffman, I., Matloff, J., and Swan, H. J. C.: New Q waves after aortocoronary bypass surgery. Unmasking of an old infarction, N. Engl. J. Med. 290:349, 1974. 11. Assad-Morell, J. L., Gau, G. T., Frye, R., Connolly, D., Davis, G. D., and Danielson, G. K.: Relation of early postoperative myocardial infarction to patency of aortocoronary bypass grafts and to ungrafted coronary arteries, Am. J. Cardiol. ,35:767, 1975. 12. Morton, B., and March, J.: Myocardial infarction in coronary artery surgery, Circulation 49 and 50 (Suppl. III):III-137, 1974. 13. Codd, J. E., Kaiser, G. E., Barner, H. B., Millman, V. L., and Miens, R. D.: Aortocoronary bypass grafting: incidence of myocardial infarction, Circulation 49 and 50 (Suppl. III): 111-166, 1974. 14. Rose, M. R., Glassman, E., Isom, 0. W., and Spencer, F. C.: Electrocardiographic and serum enzyme changes of myocardial infarction after coronary artery bypass surgery, Am. J. Cardiol. 33:215, 1974. 15. Fruehan, C. T., Johnson, J. W., Potts, J. L., Smulyan, H., Parker, F. B., Jr., and Eich, R. H.: Follow-up catheterization of patients with myocardial infarction during coronary artery bypass surgery, AM. HEART J. 91:186,
24. 25.
26.
27. 28.
29. 30.
31.
1976.
Brewer, D., Bilbro, R. H., and Bartel, A. G.: Myocardial infarction as a complication of coronary bypass surgery, Circulation 47:58, 1973. 17. Sones, F. M. D., and Shirey, E. K.: Cine coronary arteriography, Mod. Concepts. Cardiovasc. Dis. 31:735, 1962. 18. Judkins, M. P.: Selective coronary arteriography. I-A 16.
32.
1976.
Blackburn, H., Keys, A., Simonson, E., et al.: The electrocardiogram in population studies: classification system, Circulation 21:1160, 1960. Wisoff, B. G., Amtablian, A., Hartstein, M. L., and Hambv..- R. I.: Unified diaanostic and surnical annroach to unstable angina, Ann. ?hora&. SUrg. l&412,374. Kanjal, S., Roitman, D., Kouchoukos, N., and Sheffield, L. T.: Ischemic myocardial injury following adrtocoronary bypass surgery, Chest 67:20, 1975. Madias, J. E., Chahine, R. A., Gorlin, R., and Blacklow, D. J.: A comparison of transmural and nontransmural acute myocardia! ‘infarction, Circulation 49:498, 1974. Grace, J. W.: (Editorial) Intermediate coronary care units revisited, Chest 07:510, 1975. Conde, C. A., Meller, I., Espinoza, I., Donoso, E., and Dack, S.: Disappearance of abnormal Q waves after aorto-coronary bypass surgery, Am. J. Cardiol. 36:889, 1975. Zeft, M. J., Friedberg, D., King, F., Manley, C., Huston, J. D.: Reappearance of anterior QRS forces after coronary bypass surgery, Am. J. Cardiol. 36:163, 1975. Stemberg, L., Wisneski, A. J., Ullyot, D. J., and Gertz, W. E.: Significance of new Q waves after aortocoronary bypass surgery: correlation with changee in veritricular wall motion, Circulation S2:1037, 1975. Blumenthal, M. R., Wang, H: H., Pang Liu, L. M.: Experimental coronary artery occlusion and release. Effects of enzymes, electrocardiograms, myocardial contractility and reactive hypere’mia, Am. J. Cardiol. 38:225, 1975. Castellanos, A., Jr., Lemberg, L.: Post infarction conduction disturbances, in Vectorcardiography 1965, by Hoffman, I., and Taymor, R. C., Amsterdam, 1965, NorthHolland Publishing Compdny, pp. 219-225.
April,
1978, Vol. 95, No. 4
New postoperative electrocardiographic Q waves have been described in eight to 40 per cent of patients undergoing bypass grafting for coronary artery disease.‘-” Various theories have been proposed to explain these new Q waves.6-‘o Correlations of new Q waves to vein bypass occlusion, prolonged pump time or aortic cross-clamping time are controversial.11-*4 Indeed, whether or not the appearance of new postoperative Q waves means real transmural myocardial infarction is not clear.“’ We report herein our experience with postoperative Q waves in 56 patients with vein bypass grafts and the relationship of new Q waves to ventricular venting, graft patency, and the postoperative ventriculogram. Our observations indicate that: (1) Not all Q waves are due to occlusion of the saphenous bypass grafts (as noted by others”. Is. 16). (2) A certain percentage of new Q waves may not reflect true transmural myocardial infarction, especially when all the vein grafts are patent and the postoperative ventriculograms show improvement. (3) Some new Q waves reflect true transmural infarction due to occlusion of grafts or of distal coronary arteries with deteriorated left ~ventriculograms. From the Department of Medicine, Cardiology Division, and the Department of Surgery, Cardiothoracic Division, Long Island Jewish-HiIbdde Medical Center, New Hyde Park, N. Y., Queens Hospital Center Affiliation, Jamaica, N. Y., and the School of Medicine, Health Sciences Center, State University of New York at Stony Brook, N. Y. Received
for publication
Accepted
for publication
Reprint Island
requests: Jewish-Hillside
Agop
Oct. 14, 1976. Dec.
17, 1976.
Aintablian, M.D., Cardiology Division, Long Medical Center, New Hyde Park, N. Y. 11040.
OOOZ-8703/78/0495-0429$01.20/O
0 1978 The
C. V. Mosby
Co.
(4) The high incidence of new Q waves in patients with ventricular vents is probably due to direct myocardial trauma at the apex of the left ventricle. Material
and
methods
Between December, 1970, and February, 1976, 720 patients underwent coronary bypass surgery at Long Island Jewish-Hillside Medical Center. Forty-nine patients were excluded because they also underwent partial ventricular resection, prosthetic valve replacement, or ventricular septal defect closure. Of the remaining 671 patients, 56 patients developed new Q waves making up the case material for the present study. In 621 patients, a saphenous vein graft was utilized for coronary bypass, while in 50 patients the internal mammary artery was anastomosed to the left anterior descending artery. All patients had preoperative left and right heart catheterization and left ventricular and selective coronary angiography using the Judkins** or the Sones and Shirey’? techniques. In quantitating left ventricular dysfunction and the pattern of left ventricular contraction, the same techniques and principles were used as previously reported,‘9 utilizing the descriptive terminology suggested by Herman and associates.*“ Coronary arteries with at least 50 per cent reduction in diameter on coronary angiography were considered significantly stenosed and were bypassed whenever feasible. The severity and the extent of coronary disease was graded according to the criteria of Bruschke and associates.21 Congestive
American
Heart
Journal
429
Aintabiian
et al.
a 1533)
wllhouta (02) No.Pstiatts
With I 104 LEFTVEWTRICULAR VENT116
With 1 567 LEFTATRIA1VEWTIRR
Fig. 1. Comparison of the incidence of new Q waves in patients patients with double or triple vessel disease had higher incidence vessel’ disease.
heart failure and cardiomegaly were defined according to the criteria we used in previous publication. 22 Post-bypass recatheterization and angiography were done 10 to 15 days after surgery in order to assess the patency of the grafts, and any change in left ventricular function. Twelvelead electrocardiograms were performed on each patient on admission, on the day before surgery, then daily for the next four days, and finally one day before discharge. All angiograms and electrocardiograms were reviewed by two different cardiologists in the comparison of pre- and postoperative studies. Electrocardiographic criteria used to evaluate the electrocardiogram were essentially Class I-l and I-2 of the Minnesota code reported by Blackburn and associates.Z3 Cases presenting transient ST segment or T wave changes, but without pathologic Q waves, were not included in the infarction pattern group. One hundred and forty-two of the 671 patients were operated upon for preinfarction angina the same day of the cardiac catheterization as previously reported,24 while 529 had elective surgery for angina. Patients with saphenous vein bypasses to all coronary arteries with luminal narrowing greater than 50 per cent were considered complete revas-
430
with ventricular of new Q waves
or atria1 venting revealed that as compared to those with single
cularizations, while patients vein bypasses could not be more vessels with similar were considered incomplete Operative
in whom saphenous performed. to one or luminal narrowings revascularizations.
technique
All patients had reversed saphenous vein aortocoronary bypass utilizing total cardiopulmonary support. Priming solution was 5 per cent dextrose in one-third normal saline. Flow rates were 40 to 55 ml./Kg. using a bubble oxygenerator with mean arterial pressures of at least 50 mm. Hg. In 104 patients the left ventricle was vented through the apex and in the remaining 567 patients the left ventricle was vented through the right superior pulmonary vein. Moderate hypothermia was achieved by cooling the patient to 32” C. After total cardiopulmonary bypass, the ventricle was occasionally electrically defibrillated and intermittently clamped for the distal anastomosis. Results 1. Effects new Q wave
of surgical incidence.
venting
technique
in
Of 671 operated on, 104 (Group A) had intraoperative ventricular venting, and 567 (Group B) had atria1 venting. The inci-
April,
1978, Vol. 95, No. 4
New Q waves after bypass grafting
dence of new Q waves in Group A was 23/104 (22 per cent) and in Group B 33/567 (5.8 ‘per cent) (p < 0.05).
Table
I. Clinical
profile new Q waves
2. Relation of the clinical profile and underlying coronary disease to the incidence of new Q waves. As seen in Table I, comparison of age, sex,
duration of angina, coronary score, history or location of prior myocardial infarction did not differ in patients with or without new Q waves. Also, there was no difference in the incidence of normal or abnormal left ventricular segmental wall motion between the groups. Although there was a slightly higher incidence of cardiomegaly and congestive heart failure in patients who developed new Q waves, the difference was not statistically significant. Main left coronary stenosis or unstable angina pectoris did not affect the incidence of new Q waves. Patients with double or triple vessel coronary disease had a higher in+dence of new Q waves, as compared to those with single-vessel disease (Fig. 1). 3. Relation grafts placed.
of new
Q waves
to
number
of
In the entire series of 671 operated patients, 56 (8 per cent) had new postoperative Q waves. Of these, 12 (6 per cent) occurred after single bypass in 207 patients, 24 (8 per cent) after double bypass in 287 patients, 18 (11 per cent) after triple bypass in 164 patients, and two (15 per cent) after quadruple bypass in 13 patients. Thirty-one new Q waves appeared on the anterior and septal walls, 23 on the inferior and inferolateral walls, and two on lateral walls (Table II). 4. Relation of new Q waves to ungrafted vessels or to patent grafts with an occluded distsl atiery. New Q waves appeared in the zone
of myocardium supplied by grafted arteries in all except three patients with ventricular venting (Cases No. 6, 7, and 16) (Table III). In the latter three patients, the Q waves occurred within zones of myocardium supplied by diseased, but ungrafted vessels. In all the patients with new Q waves who were restudied, only two (Cases 37 and 40) (with atria1 venting and deteriorated ‘left ventriculograms) demonstrated patent grafts, but an occluded coronary artery beyond the distal anastomotic site (Table IV). 5. Relation of new Q Waves to postoperative alteration of left ventricular function and graft closure. In Group A (ventricular venting), 17
patients
with new Q waves had postoperative
American
Heart
Journal
l-r-l-r With new Q waves
WithOUt
No.
Total number Age (~4 Mean Range
of patients
%
615
No.
%
56
54-c 6 28-84
53 -c 11 32-76
Sex
Male Female Unstable angina History of infarction Documented ECG infarction Septal Anterior Inferior Inferior and anterior Infero-dorsal, infero-lateral and dorsal Normal QRS Enlarged heart Congestive heart failure Normal left ventricular contraction Segmental hypokinesia of one wall Akinesia of one wall Akineaia or segmental hypokinesia of more than one wall Generalized hypokineaia
506 109 132 258
l6 38 >
a2 18 21 42
49
9
2
a7 13 18 43
7 10 24
2 12 3 3
>
7
117 21 12
19 3 2
411 45 25 230
67 7 4 37
11 5 24
43
154
25
13
23
98 103
16 16
9 11
16 20
0
0
3
0.5
34
20
5 5 61 20
9
ventriculograms. Of these (Table III), three (18 per cent) had an improved ventriculogram and O/7 graft closures, 4 (24 per cent) had no change in the ventriculogram with l/7 graft closure, and in 10 patients (58 per cent) with deteriorated postoperative ventriculograms, there were 7116 graft closures (Table III). Of 17 patients in Group A who had postoperative ventriculograms, five had single, 11 had double, and one had triple bypass grafts. In Group B (atria1 venting), 25 patients with new Q waves were studied postoperatively. Of these (Table IV), five (20 per cent) had an improved ventriculogram and O/ 11 graft closures. Fourteen (56 per cent) had an unchanged postoperative ventriculogram and 4/34 graft closures, while six (24 per cent) had a deteriorated postoperative ventriculogram with 6/15 graft closures. Of these 25 patients, four had single, eight had double, 12 had triple, and one had quadruple
431
Aintablian
et al.
Cl Single @ Oouble
T
a
Triple or lluadfupie
100 90
a0 70
a0 50 40 30 20 IO 0
Patients With II CARBIoWLblOwtv
Without lwPm
Fig. 2. Comparison of over-all cardiopulmonary without new Q waves, did not show statistically
a
II. Correlation of graft closure to the new Q waves and location of new Q waves in patients with ventricular and atria1 venting
.~
23
33
56
42 17 8/30
74 27
80 25 9160
76 15
122 42 17/90
75
7
52 31
12 14
36 43
24 21
43 37
2
9
0
1
4
6 13
19
New Q waves Anterior Inferior Infero-lateral Septal Lateral
12
14
0
18
2 7 2
4 12 4
bypass grafts. Although over-all incidence of new Q waves was 22 per cent in patients with ventricular venting, as compared to 5.8 per cent in those with atria1 venting, the graft closure rate in patients with new Q waves was 27 ‘per cent in the ventricular vented group and 15 per cent in those with atria1 Venting. 6. Relation of the location complete versus incomplete
432
of new Q waves revascularization
to
Withsut 9
AORTIC CRgSS CLAMPIIIG TIME
bypass and aortic significant difference.
Table
Patients Grafts Pts. studied Grafts closed
with 0
TIME
cross-clamping
time
in patients
with
and
grafted vessels. All the new Q waves occurred within the zone of myocardium supplied by a grafted artery except for 3156 (5 per cent) of the patients. These three new Q waves appeared in the inferior (Cases 6 and 7) or infero-lateral (Case 16) wall in the group of patients with ventricular venting (Table III). Complete revascularization was performed in 50/104 (48 per cent) of the patients with ventricular venting, in 369/567 (65 per cent) of those with atria1 venting. Patients with ventricular venting and new Q waves had 13/23 (57 per cent) complete revascularization, and those with atria1 venting 21/33 (64 per cent); the difference was,statistically insignificant, indicating that completeness of revascularization did not affect the incidence of new Q waves. and
7. Correlation of new Q waves to the duration of cardiopulmonary bypass, aortic cross-clamping time. In 350 patients with atria1 venting,
there were no significant differences in the overall duration of cardiopulmonary bypass or aortic cross-clamping time in those with or without new Q waves, whether they had single or multiple vessel coronary bypass surgery (Fig. 2). In patients with new Q waves, the incidence of prolonged cardiopulmonary bypass time exceeding 100 minutes for double (30 per cent) and 120
April,
1978, Vo2. 95, No. 4
New Q waves after bypass grafting
III. Correlation Group A patients
of location
Table
of new Q wave, patency
Grafts Patient
LAD
RCA
Patency CX
LAD
RCA
+ +
+ +
X
+
+
X
x x
of graft, and postoperative
Contraction CX
Preop
Postop
ventriculogram
HX MI
Admission ECG Q wave Inferior RBBB + Lateral Inferior (narrow Q)
Anterior Inferior
Septal LAH+ Anterior Inferior Inferior
in
New Q
LVG improved 1.
x
2.
X
X X
3.
X
X
LVG unchanged 4. X 5. X 6. X 7. X LVG Deteriorated a. X
As-Ant As-Ant
Normal Normal
‘1 ‘1
+
As-Ant
Normal
‘1
+ +
0
Normal Normal
Normal Normal
0 0
+ +
+ +
Normal Normal
Normal Normal
0 ‘1
Normal Inferior + Lateral Normal T ll.lll, aVF
‘3
T,.,
Anterior
0 0
Normal Inferior
Anterior Anterior
‘2 0
T”l.“e LAH QRS WNL Anterior
Anterior Anterior
Normal Normal Normal
Inferior Inferior Lateral Inferolateral
X
+
+
AleApic
X
0 0
0
Normal As-Apic
9. 10.
X X
11. 12.
X X
X
0 0
0
Normal As-Ant
. 13.
X
X
+
+
Ak Ant
14. 15. 16. 17.
X
X X
+
+ +
As-Inf Normal Normal As-Inf
X X
0 +
X
Abbreviations: LAD = left anterior As = Segmental hypokineaia.
descending
+ coronary
artery;
RCA = right
minutes for triple or multiple bypass grafts (33 per cent) as compared to those with no Q waves (18 per cent and 13 per cent, respectively), were slightly higher. 8. Disappearance of Q waves. Two of our patients, after coronary bypass surgery, lost longstanding anterior Q waves. Postoperative angiography in these two patients revealed patent saphenous bypass grafts and improved left ventriculogram in one while in the other, the left ventriculogram was unchanged. 9.. Relation
of
mortality
to
graft
patency.
Twelve patients died within one month after bypass surgery (Table V). Three patients died in the operating room. One. of them (Case 2) probably had a myocardial infarction the morning of surgery. Of nine patients who died within two weeks after surgery, two died of noncardiac causes, one died of combined cardiac and
American
Heart
Journal
A~L<~” Ak A;!: AkCA”” Ak-A$!: Ak-Ant As-Ant AkInf + Apic Ah-Inf Ak-Apic Ak-Apic Ak
artery;
‘3 0 0 0 ‘2
CX = circumflex
coronary
Inferior (wide Q)
Inferior
artery;
Ak = Akin&a,
non-cardiac causes, whereas six patients’ deaths were secondary to myocardial infarction. The mortality in two patients, who died after discharge at home, was due to myocardial infarction in one (Case 10) and in the other due to myocardial infarction or ventricular arrhythmia (Case 11). It should be mentioned that 2112 (17 per cent) who died had balloon assist prior to surgery for persistent angina or cardiogenic shock (Cases 6 and 11) and one patient was brought to the operating room after arrest while external cardiac massage was being performed (Case 1). Of 12 patients who died, three (25 per cent) had main left coronary stenosis. Discussion
An 8 per cent incidence of new Q waves in our series is lower than reported by others.“. I5323 Contrary to the report of Williams and asso-
433
Aintablian
et al.
IV. Correlation Group B p&ients
Table
of location
of new Q wave, patency of graft, and postoperative
Grafts Patient L VG improved 18.
Patency
LAD
( RCA
1 CX
LAD
X
X
X
+
Contraction
1 RCA
1 CX
+
+
Preop
HX MI
Postop
**
0
ventriculogram
Admission ECG Q wave
New
T”8.“6
in
Q
Septal
Ap1c
LVG
0
Normal
0
Normal
Inferior
As-Apic A&-Inf As-Ant
As-Apic Ak-Inf As-Ant
1 ‘1 2
Normal Inferior Infero-dorsolateral
Septal Anterior Anterior
Ak-Inf Ak-Apic Normal Normal Normal Normal Normal Ak-Inf Normal Normal Normal Normal
Ak-Inf Ak-Apic Normal Normal Normal Normal Normal Ak-Inf Normal Normal Normal Normal
0 0 ‘1 0 0 0 0 0 0 1 2
Normal Normal TV,-V, T ll.lll aV, Normal Normal T”,.% Normal T ll.lll aV, Normal Anterior + small Q II III aV,
Adterior Inferior Inferior Inferior Inferior Inferior Inferior Inferior Inferior Inferior Inferior
+
Normal As-Ant *k-Basal
Ak-Apic *k-Ant Ak-Basal
0 1
Normal Q II, III,
Septal Anterior
X
+
-I-
21.
X
X
+
+
22.
X
X
X
+
+
+
X
X X
+ -I-
0
+ + 0 + 0
unchanged 23. X 24. X 25. Xt
X X X X X X X X X-l
Ak
+
X X X X X X X X X X X
deteriorated 37. X 38. 0 X
X X X
+ + +
X
+ +
X
+
X X X X
+ + +
X
+* 0 -I-
Normal
As-Apic
Xt X
26. 21. 28. 29. 30. 31. 32. 33. 34. 35. 36. LVG
*’ Inf Normal
Normal Small Q with R V,-V, TV,-V,
+
19. 20.
+ + + + + + 0 + + + +
+ + + + 0 +
Ak
Apic
0 + 1
39.
X
X
X
O
0
0
As-Ant
Inferior
40.
XC
X
X
+
+
+
Normal
Normal
41.
X
X
0
42.
xt
+ *qAnt
X
X
+
+
0
Normal
Apic
Septal
Qs V,-V,
good
Inferior
aV,
+ lateral
Anterior Anterior
Ak-Apid
0
Lateral
Ak-Inf
0
Inferior
Abbreviationa ae in Table III. *Patent grafi, but occluded distal left anterior descending artery (cases 37 and 40). thtemal mammary anaetomoeie to left anterior deecendmg artery.
main left coronary stenosis did not increase the incidence of new Q waves. The age, sex, duration of disease, preinfarction angina, previous myocardial infarction, or abnormal left ventricular wall motion did not affect the incidence of new Q waves. Patients with double or triple vessel disease, as well as those with cardiomegaly or congestive heart failure, had a higher incidence of new Q waves, but this differciaks,’
434
ence was not statistically significant. Of 12 patients who died after doronary bypass surgery, eight died (Table V) of definite acute myocardial infarction, one probably of acute myocardial infarction or ventricular tachyarrhythmia (Case 11, Table V), two of massive pulmonary embolism, and one after an extensive cerebrovascular accident. Of these 12 patients, 25 per cent had significant main left coronary artery disease. The
April,
1978,
Vol.
95, No.
4
New Q waves after bypass grafting mortality rate of only 6 per cent (3/50) (Cases 4, 6, 8, Table V) in the patients developing postbypass new Q waves was much lower than reported mortality rate in CCU’s by different centers, namely 9.8 per cent to 23 per cent.?+?T This suggests that new post-bypass Q waves may not represent true transmural myocardial infarctions. Most of the patients with sudden development of postoperative new Q waves had a benign hospital course and were not clinically different from patients without new Q waves. This has also been noted by others.*O, Is. I6 Patients with presumed true myocardial infarction not only had elevated SGOT and other enzyme levels, but their electrocardiograms demonstrated evolutionary changes of transmural myocardial infarction, usually localized on the anterior wall of the left ventricle. Although Fruehan and associates’” noted that 74 per cent (28/38) of new Q waves were located in the inferior, dorsal, or inferolateral wall in their series of 199 patients, we encountered new Q waves in those locations in only 41 per cent (23/56). Three of 56 patients with new Q waves and a history of previous myocardial infarction (Cases 3,20,36, Tables III and IV) developed significant Q waves in the inferior or anterior wall, sites of previous narrow Q waves. These electrocardiographic changes which suggest “unmasking” of an old myocardial infarction pattern may also be due to a localized conduction disturbance in an area of previous infarction due to redistribution of electrical forces after bypass surgery or to a change of axis secondary to surgery. The left ventriculograms in these patients improved or did not change after the appearance of significant new Q waves. However, none of our patients after coronary bypass surgery manifested the phenomenon of “unmasking of old infarction,” described by Bassan and associates.‘” It is worth mentioning that two of our patients, after coronary bypass surgery and patent grafts, lost longstanding anterior Q waves, which also has been observed by Conde and associates.28 A striking decrease in the incidence of postoperative Q waves (from 22 per cent to 5.8 per cent) occurred when atria1 rather than ventricular venting was adopted. This result may be due, in part, to improved surgical bypass techniques, since the ventricular vented cases were done at the start of the coronary bypass surgery program in our institution. The over-all incidence of saphe-
American Heart Journal
nous bypass graft closure was higher in the early operated group. In the ventricular venting group, the graft closure rate was 22 per cent versus 8. per cent in those patients with atria1 venting. In patients with new Q waves and ventricular venting who had a postoperative study (Table II), the graft closure rate was twice as high, as compared to the atria1 venting group (27 per cent versus 15 per cent). However, the incidence of the new Q waves was much higher in the ventricular venting group (22 per cent), as compared at atria1 venting patients (58 per cent). Thus, improved surgical techniques and fewer graft closures alone cannot explain such a drop in the incidence of new Q waves, The clear implication is that sufficient myocardial trauma results from ventricular venting to result in pathologic Q waves. The anatomic placement of ventricular vents at or near the apex could account for either inferior or anterior wall localization of the postoperative Q waves. Since the ventricular trauma produced by venting is not due to arterial occlusion, there is ‘no wide surrounding ischemic area. Thus, it is ,not surprising that postoperative Q waves attributable to venting are not usually associated with impaired ventricular function in the absence of graft occlusion. Indeed, improved ventricular function may be observed. However, in four patients (Cases 13, 14, 15, and 17), in whom new inferior Q waves developed, new dysfunction of the inferior wall and open grafts to the right coronary artery could be demonstrated. Here we assume that the deterioration in the ventriculogram was probably secondary to the trauma of venting. In contrast are Cases 7, 9, 10, 11, 12, 16, 19,38, and 39, all of whom developed new anterior Q waves and anterior wall dysfunction in the presence of occluded grafts to the left anterior descending artery or its diagonal branch. Here the assumption must be that true infarction secondary to inadequate arterial and graft inflow occurred. The incidence of new Q waves was higher in patients with double, triple, or quadruple bypass surgery, as compared to those with a single bypass, as reported by others.4 Although our patients with atria1 venting .had a higher percentage of complete revascularizations, the incidence of new Q waves was not affected by complete or incomplete revascularization in patients in either the atria1 or ventricular venting groups. All of the new Q waves occurred within
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Table V. Circumstances
and causes of death Causes of deuth Died
Patient no.
No. of diseased vessels
Old myocardial infarction
In OR
Within Within 2 wks. 1 month
New Q waves
Infarction
LV VENT. 1
3
Inferior
2
M 3 2
Inferior
4 5 6
3 2 3
0 Anterior Inferior
+ LAH
I 8 9
0 Anterior 0
+ Inferior
10
3 3 M 2 1
11
3
12
M 3
Anterior inferior 0
3
+
-
+
-
+ + +
-
Pulmonary embolism
Cerebrovascular accident
+
Anterior
i-
Interior
LA VENT.
Abbreviations:
-
+ +
Inferior
+ +
0
M = main left coronary
+ LPH
+ RBBB
+ Anterior
+
Anterior
+ + +
Anterior
(3 wks postop)
+
+
+
artery;
LAH
= left anterior
-
hemiblock;
the zone of myocardium supplied by the grafted artery, except three (5 per cent) of the patients in the ventricular vented group in whom the new Q wave appeared in non-grafted vessel zones of inferior or infero-lateral wall. This result is different from the report of Assad-Morel1 and colleagues,” in which 25 per cent of the patients manifested new Q waves in a zone of myocardium supplied by a diseased ungrafted artery, It is worth mentioning that in three patients with atria1 venting and with patent saphenous vein bypass grafts, the coronary artery distal to the anastomosis was closed. This explains the appearance of their new Q waves, as well as the observed deterioration of left ventricular contractility. Although Anderson and associates? noted no direct correlation between ECG evidence of transmural myocardial infarction and graft closure, they did not comment on the corresponding ventriculography. Brewer and associateP confirmed these findings in autopsy studies of
+
+ Probable
+
-
LPH
= left posterior
hemiblock;
RBBB
+
Q right bundle branch
block.
patients dying after coronary bypass surgery. In the present study, new Q waves were noted in patients with deteriorated, unchanged, or even improved ventriculograms. When the data on new Q waves and postoperative ventricular function were correlated, no direct relationship could be seen. However, when graft patency was also considered, a clear relationship emerged. Improved postoperative ventricular function correlated well with graft patency, despite Q waves. Unimproved or deteriorated ventricular function did not predict graft occlusion, since more than half of the vein grafts placed in these patients were patent. Assad-Morel1 and associatesll also noted a lack of correlation between graft closure and electrocardiographic and angioeaphic evidence of myocardial infarction. Half their 32 patients had patent grafts, despite evidence of myocardial infarction in the area of distribution of the grafted vessels. .In our series, only 19 per cent of grafts were closed in patients with new Q waves and only 38
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1978, Vol. 95, No. 4
New Q waves after bypass grafting
Comments After cardiac catheterization had chest pain, then arrested. With external cardiac massage was brought to O.R. and double bypass done. Died 4 days later. Autopsy showed patent grafts with recent anterior infarction The morning of surgery had protracted chest pain with ST elevation, Autopsy showed fresh anterior infarction Died 24 hours postop. No autopsy. Postoperative stormy course. No autopsy Autopsy showed pulmonary embolism with patent grafts Balloon assist + nitroprusside for persistent angina. Postop developed anterior Q wave, then LBBB before death No autopsy Developed LBBB + LPH before death No autopsy Expired 3 wks. postop. Autopsy showed fresh anterior infarct and closure of graft Balloon assisted angiograms done. Discharged home after triple patent grafts. Died in his sleep Protracted pleuritic pain. Rat persistent pericardial rub. .Autopsy showed bilateral massive pulmonary emboli + fresh anterior infarct and patent grafts
per cent of left ventriculograms deteriorated, while 43 per cent were unchanged and 19 per cent improved after surgery. Indeed, in the patients without new Q waves, 9 per cent (77/885) of grafts were closed, indicating that graft occlusion can occur without necessarily causing electrocardiographic changes of transmural myocardial infarction. It is important to note that, in our series, patients with single bypass grafts in whom the postoperative left ventriculogram showed deterioration invariably had an occluded bypass graft or a patent graft with occlusion of the coronary artery distal to the anastomosis (Tables III and IV). At least four or five patients developed severe hypotension prior to bypass surgery. These patients most likely sustained myocardial infarction at that moment and electrocardiographic changes of transmural myocardial infarction appeared after completion of the bypass due to reperfusion of the infarcted area, since bypass grafts studied postoperatively were patent in this group. The delayed appearance of new Q waves
American
Heart
Journal
after coronary occlusion in dogs has been explained by Blumenthal and associates.3’ Possible preservation of the sarcolemmal membranes delays the appearance of Q waves in the early phase of infarction, but after reperfusion, disruption of these membranes accelerates the emergency of Q waves. When new Q waves appeared after bypass, using the atria1 venting technique, with ventricular function unimproved or worsened, graft closure or occlusion of the distal coronary artery was common. A compromised arterial inflow and true myocardial infarction must be presumed. Of great interest are those patients with new Q waves following atria1 venting, with improved ventriculograms and patent grafts. The new Q waves must be a consequence of surgical trauma, since aortic cross-clamp and cardiopulmonary bypass times were not significantly prolonged. Two possibilities are suggested. First, direct myocardial damage with muscle necrosis may occur, sufficient to produce Q waves, but nevertheless undetectable by ventriculography. Second, the surgical trauma might result in localized ventricular conduction delays or blocks, affecting the early QRS balance, as postulated by Castellanos and Lemberg.32 They theorized that such local delays in ischemic tissue result in slurring or widening of the QRS, producing “infarct” Qs. It seems reasonable that a similar mechanism in traumatized tissue may account for postoperative Q waves in these patients with improved ventriculograms and patent grafts. Clinical significance and prognosis. Postbypass grafting Q waves, as described and discussed, have a varied pathogenesis. When accompanied by improvement in ventricular function and patent grafts, they are of little significance and do not carry the prognostic importance of myocardial infarction as it occurs in the natural course of arteriosclerotic heart disease. In contrast, when accompanied by graft closure and deteriorated ventricular function, the mechanism may be presumed ischemic and the prognosis must take into account the likelihood of permanent or long-term localized ventricular dysfunction. Summary
New Q waves were observed in 56 (8 per cent) of 671 patients undergoing saphenous vein bypass
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Fig. 3. Pre- and postoperative angiographic study surgery developed new septal Q waves (Case No. segment of the left ventricle (urrow) was no more
of a patient with atria1 venting who after triple vein bypass 18). As seen here, segmental hypokinesia of the anteroapical present in the postoperative left ventriculogram.
Fig. 4. Comparison of pre- and postoperative left ventricular contractile pattern of Case ventriculogram did not show any significant change, although postop. he developed new inferior
grafting, with an over-all mortality rate of 1.8 per cent. Forty-two of the 56 (75 per cent) had postoperative ventriculograms and arteriograms and are reported herein. Ventricular venting was used intraoperatively in 17 patients, and atria1 venting in 25. Thirty-one patients had new “ante438
No. 27. Q waves.
Left
rior” and/or “septal” Q waves, while 23 had “inferior” or “infero-lateral” and 2 had “lateral” Q waves. The incidence of new Q waves in patients With ventricular venting was 22 per cent and in those with atria1 venting it was 5.6 per cent (p < 0.05). Age, sex, duration of disease, severity April,
1978, Vol. 95, No. 4
New Q waves after bypass grafting
Fig. 5. Pre- and postoperative left ventriculograms of a patient with atria1 venting and new anterior No. 37). Postoperatively the vein graft was patent with occluded distal left anterior descending hypokinesia of the apical segment of the left ventricle (arrow).
of angina, previous myocardial infarction or main left coronary lesions did not affect the incidence of new Q waves. Although new Q waves were more frequent in patients with preoperative cardiomegaly and congestive heart failure, this difference was not statistically significant. However, there was no significant difference in the over-all cardiopulmonary bypass or aortic crossclamping time in patients with or without new Q waves. Cardiopulmonary bypass time exceeding 100 minutes in patients with double bypasses, and more than 120 minutes with multiple bypasses, were more frequent in patients with new Q waves. Completeness or incompleteness of the revascularization procedure did not affect the incidence of new Q waves. In all but three patients with ventricular venting, new Q waves appeared in a zone of myocardium supplied by a grafted artery. In the three exceptions, the Q waves occurred within the zone of myocardium supplied by diseased but ungrafted vessels. In the ventricular vented group 7 (41 per cent) demonstrated an improved or unchanged postoperative ventriculogram with 7 per cent graft closure and 10 (59 per cent) had deteriorated ventriculograms with 44 per cent graft closure. In 25 patients with atria1 venting, 19 (76 per cent) showed improved or unchanged postoperative ventriculogram with 12 percent graft closure and 6 (14 per cent) had American
Heart
Journal
Q waves (Case artery and new
deteriorated ventriculograms with 40 per cent graft closure. Although over-all incidence of new Q waves was 22 per cent in patients with ventricular venting as compared to 5.8 per cent in those with atria1 venting, the graft closure rate in patients with new Q waves was 27 per cent in ventricular vented group and 15 per cent in those with atria1 venting. These findings indicate a poor correlation between new Q waves and graft closure. Improved postoperative ventriculograms correlated well with graft patency despite new Q waves. The etiology of new post-bypass graft Q waves are varied. They include direct ventricular trauma and conduction delays resulting from surgery or venting, as well as true ischemic infarction. Infarction may be due to compromised arterial inflow either in non-operated diseased vessels, in vessels distal to anastomoses with patent grafts, or due to graft closure. REFERENCES 1.
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1978, Vol. 95, No. 4