Follow-up catheterization of patients with myocardial infarction during coronary artery bypass surgery C. Thomas Fruehan, M.D. Lewis W. Johnson, M.D. James L. Potts, M.D. Harold Smulyan, M.D. Frederick B. Parker, Jr., M.D. Robert H. Eich, M.D, Syracuse, N.Y.
Coronary bypass surgery has become an accepted and common surgical procedure. To assess properly the benefits and role of aortocoronary bypass surgery, its risks and problems should be better understood. One of these problem areas is the development of intraoperative myocardial infarction, which has been reported to occur with 'an incidence as high as 29 per cent. 1 The purpose of this report is to review a series of patients with electrocardiographic evidence of intraoperative myocardial infarction which occurred during aortocoronary bypass surgery, and to review the results of postoperative coronary arteriography and left ventriculography of these patients. Materials and methods
During a 30 month period, from October, 1971, through April, 1974, 239 patients had aortocoronary bypass surgery at State University Hospital, Upstate Medical Center, Syracuse, N.Y. Excluded from the study group were 42 patients who had other concomitant cardiac surgical procedures, such as resection of ventricular aneuFrom the Departments of Medicine and Surgery, State University of New York Upstate Medical CenteL Syracuse, N. Y. Received for publication Feb. 12, 1975. Reprint requests: C. Thomas Fruehan. M.D.. State University Hospital of the Upstate Medical Center. College of Medicine, Department of Medicine. Cardiology Section, 750 E. Adams St., Syracuse, N. Y. 13210.
186
rysm, valvular surgery, ventricular septal defect closure, or internal mammary implantations. The remaining 197 patients in the study group had aortocoronary bypass grafts only. All patients were evaluated preoperatively by left heart catheterization, left ventriculography, and selective coronary cineangiography by the Sones and Shirey 2 or Judkins 3 technique. All of the aortocoronary bypass operations were performed by the same team of surgeons. All procedures were carried out under cardiopulmonary bypass with modified hypothermia at 32 ~ C. and with controlled ventricular fibrillation. Grafts placed to the left coronary system were performed with intermittent aortic occlusion for brief periods not exceeding 10 minutes. Right coronary grafts were performed by localized occlusion of the right coronary artery at the area of anastomosis. An electrocardiogram (ECG) was obtained on all patients within 48 hours before surgery. Serial postoperative ECG's of all patients undergoing aortocoronary bypass were reviewed independently by three cardiologists. Patients were considered to have had myocardial infarction only with unanimous opinion of the reviewers. The diagnosis of myocardial infarction was made only in the presence of: (1) characteristic change in QRS complexes from the preoperative ECG and (2) evolutionary changes in the ST-T deflections in the same leads as the changed QRS
February, 1976, Vol. 91, No. 2, pp. 186-190
Myocardial infarction during coronary artery bypass surgery complexes. ST-T abnormalities alone were considered nondiagnostic. The characteristic change of the QRS complexes was nearly/always the appearance of new Q waves, essentially the classes I-1 and I-2 of the Minnesota Code of Blackburn and associates2 There was one exception to this requirement for new Q waves. True posterior wall infarction was diagnosed when all the following findings were present in ECG leads V1_3: (1) R / S ratio over 1.0 for the first time in the postoperative ECG's; (2) increase in R / S ratio of over 100 per cent; (3) appropriate ST-T evolution; and (4) absence of an intraventricular conduction defect. Serum enzymes (creatinine phosphokinase, serum glutamic oxalacetic transaminase, lactic dehydrogenase [CPK, SGOT, LDH]) were obtained preoperatively and on the first, second, and third postoperative days. Upper limits of normal in our laboratory are: CPK, 139 units; SGOT, 40 units; and LDH, 207 units. Serum enzyme levels suggesting myocardial infarction after single-vessel surgery were selected as: CPK, more than four times normal ( > 556 units); SGOT, more than twice normal ( > 80 units); and LDH, more than 360 units. For multi, pie-graft surgery, these levels were CPK, more than 9 times normal ( > 1,251 units); SGOT, more than 3.5 times normal ( > 140 units); and LDH, more than 560 units. These levels are similar to the ninetieth percentile levels described by Alderman and co-workers ~ as correlating with myocardial infarction following coronary artery surgery. We have been able to obtain follow-up catheterization studies on 11 survivors of intraoperatire myocardial infarction. Restudies have included standard left heart catheterizations with left ventriculography in both right and left anterior oblique projections, selective coronary cineangiography, and selective injection of the bypass graft(s). Results
Intraoperative myocardial infarction was diagnosed by serial postoperative ECG's in 38 (19 per cent) of the 197 patients undergoing aortocoronary bypass procedures. Eighty-one per cent of patients diagnosed as having had myocardial infarction by ECG also had an elevation of at least one serum enzyme level (CPK, SGOT,
American Heart Journal
Table I.
Wall involvement of intraoperative myocardial infarctions
Location Inferior Anterior True posterior Anterior-lateral Anterior,inferior Inferior-lateral Inferior-true posterior Anterio~-lateraI-inferior Total
]
No. of patients 22 6 3 1 1 1 2 2 38
LDH) sufficient to suggest myocardial infarction. Thirty-one of the 38 (82 per cent) infarctions involved a single wall; the other seven (18 per cent) involved multiple walls (Table I). Twentytwo of the intraoperative infarcts were of the inferior wall and another six involved the inferior wall and another wall. Anterior, lateral, and true posterior wall infarctions were less frequent. Patients having multiple grafts were more likely to have intraoperative myocardial infarction. Of the 197 patients of the study group, 30 (15 per cent) had three or more grafts and 13 (43 per cent) of these 30 patients had intraoperative infarction. In contrast, 104 (53 per cent) patients had a single graft; there were only eight (7 per cent) intraoperative infarctions in this group. Correlation of infarct location with graft site. Thirty-four of the 38 intraoperative infarctions occurred in a cardiac location supplied by the grafted coronary artery (Table II). For example, four of five infarctions occurring in patients receiving only right coronary artery grafts involved the inferior wall. Four of the intraoperative infarcts occurred in walls not perfused by the coronary artery which was grafted. All four of these patients had occlusive disease, not suitable for bypass, in the arterial supply of the wall which infarcted. It is notable that most of the infarctions involved the inferior or true posterior wall, even when multiple vessels were grafted. In patients receiving grafts to all three major coronary arteries, there were 10 infarctions; eight occurred in the inferior wall alone, one was posterior, and one was inferior and lateral.
187
F r u e h a n et al.
Table II. graft site
J__t
Seven of the 11 patients had all grafts p a t e n t . Of these seven, three had a new area of hypokinesis in the area of infarction; the other four had ventriculograms which were n o r m a l or unchanged from the preoperative ventriculogram. Four of the 11 patients h a d at least one occluded graft; three of these four had a new area of hypokinesis corresponding to t h e m y o c a r d i a l infarct. Two of these three new hypokinetic areas were supplied by an occluded graft; the third was supplied by a p a t e n t graft. T h e f o u r t h p a t i e n t with a closed graft had a n o r m a l ventriculogram. In all cases the area of hypokinesis, when present, corresponded to the ECG location of the intraoperative infarction. The graft p a t e n c y rate of patients r e c a t h e t e r ized after intraoperative infarction was 68 per cent (15 of 22). If the two patients who died (with all grafts occluded) are included, the graft patency rate of these 13 patients is 54 per cent (15 of 28). This is in contrast to the 83 per cent graft patency rate of all patients restudied an average of 1 year after a o r t o c o r o n a r y bypass surgery at this institution. This difference is statistically significant (p < 0.01).
4
Discussion
Correlation of infarct location with
Coronary artery grafted
LAD + LCA + RCA*
Infarct location
I
No. of infarcts
INF
8
POST INF-LAT
1
LAD + RCA
INF INF-POST ANT-INF ANT
LAD + LCA
INF ANT ANT-LAT ANT-LATINF
RCA + LCA
INF POST
LAD
ANT-LATINF POST
1 10 9 2 2 1 14 2t 1 1 1 5 1 1 2 1 2
RCA Total
INF ANT
1~ 38
*LAD,left anteriordescendingcoronary artery; LCA,left circumflex coronaryartery;RCA,rightcoronaryartery;ANT,anteriorwall; INF, inferiorwall; LAT,lateral wall; POST,true posterior wall. "Hnfarction in wall not supplied by grafted coronary.
Hospital course following intraoperative infarction. T h e m a j o r i t y of patients with intraoperative myocardial infarction had a postoperative course not appreciably different from t h a t of bypass patients w i t h o u t infarction; however, six of the 38 patients with intraoperative infarction developed severe and prolonged left v e n t r i c u l a r failure. Two of these patients died; a n o t h e r four who developed cardiogenic shock required intraa o r t i c balloon c o u n t e r - p u l s a t i o n , and survived. Follow-up catheterization studies. Eleven of the patients who survived intraoperative m y o c a r dial infarction have been recatheterized. T h e average time between surgery and recatheterization was 10 m o n t h s (range, 2 weeks to 22 months).
188
T h e incidence of intraoperative m y o c a r d i a l infarction in this series is similar to t h a t of previous reports2 -s T h e high incidence of inferior wall involvement of such infarctions has not been described previously. ECG diagnosis of myocardial infarction in patients undergoing cardiac surgery has been demonstrated to err on the side of underdiagnosis. Brewer and associates 6 reported no false-positive ECG diagnoses in a series of patients who h a d both ECG evidence of intraoperative m y o c a r d i a l infarction and autopsy confirmation. Several patients in t h a t report, with a u t o p s y evidence of myocardial infarction, did not show diagnostic ECG evidence of infarction. The apparent discrepancy between p a t i e n t s showing E C G evidence of m y o c a r d i a l infarction without a diagnostic level of serum enzymes has been previously discussed by Alderman and associates, ~ who has pointed out t h a t the use of ninetieth percentile e n z y m e levels yielded a substantial n u m b e r of false-negative a n d falsepositive results as compared with E C G diagnosis.
February, 1976, Vol. 91, No. 2
Myocardial infarction during coronary artery bypass surgery
Bonchek and associates' described a group of patients with occluded bypass grafts. In their series of 205 patients, 52 (25 per cent) patients had at least one graft which occluded between the time of surgery and recatheterization. Eight of these 52 patients had intraoperative myocardial infarction; 44 of the 52 (85 per cent) had one or more occluded grafts without evidence of infarction. This indicates t h a t graft occlusion can occur without necessarily causing clinically recognizable infarction. Van Heeckeren and Ankeney reported 9 on eight patients recatheterized after intraoperative infarction; one of these patients had all grafts patent and seven had occlusion of one or more grafts. Those authors did not report on the ventricu!ograms of patients with intraoperative infarctions. Our data differ from van Heeckeren's, in t h a t we found a larger proportion of intraoperative infarctions in the presence of patent grafts to the areas involved. The finding of hypokinesis in the infarcted wall, which was not present in the preoperative ventriculogram, supports the fact that myocardial infarction did indeed occur. The occurrence of myocardial infarction in areas with patent grafts does not support previously published opinion 7 t h a t the major threat to patients having bypass grafts is residual coronary disease which is not bypassed; in this series, most of the infarcts occurred in areas supplied by vessels which were bypassed, and with patent grafts. There are many etiologic factors pertinent to intraoperative infarction in coronary bypass surgery. Early graft occlusion appeared to have been a factor in some of these patients, as demonstrated by the follow-up cineangiograms. Prolonged cardiopulmonary bypass, with less than optimal perfusion of ischemic areas unable to be revascularized, appears to be a likely factor in those patients with infarction in areas not perfused by the bypass grafts. There remains a group of patients with patent grafts and electrocardiographic evidence of infarction in the area perfused by the graft. To date, we have no satisfactory explanation for these infarctions. We have no good explanation for the failure to find hypokinesis in five of the eleven patients with presumed intraoperative infarction. It is possible that the infarction was not large enough
American Heart Journal
to affect gross patterns of ventricular contraction. We conclude that intraoperative myocardial infarction is a fairly common problem of aortocoronary bypass surgery, often involves an area supplied by a grafted vessel, and is not necessarily related to graft closure. Summary
Of 197 consecutive patients having aortocoronary bypass grafts over a 30 month period, 38 (19 per cent) had ECG evidence of myocardial infarction. The infarctions occurred more commonly in patients receiving multiple grafts. The infarctions were usually in areas supplied by grafted vessels. The infarctions occurred most often in the inferior wall, even when multiple vessels were grafted. Eleven patients with intraoperative infarction have had repeat postoperative coronary arteriograms. Seven had all grafts patent; three of these patients had hypokinesis of the infarcted wall. Four of the 11 patients had one or more occluded grafts; three of these patients had an area of hypokinesis. We conclude t h a t intraoperative myocardial infarction is a common problem in aortocoronary bypass surgery and is not necessarily caused by graft occlusion. Addendum
During the twelve months following the study period of this report, 87 aortocoronary bypass procedures were done at this institution, with an intraoperative infarction rate of 4.5 per cent (four infarcts). No single factor has been identified as a cause for the lower incidence. The improvement is likely due to a combination of: shorter periods of aortic occlusion; increased aortic perfusion pressure; improved surgical exposure; use of combined grafts; and increased surgical experience.
REFERENCES
1 Ellis, R., Kligfield,P., Gay, W., and Ebert, P.: Distal coronary artery bypass; local occlusionversus ischemic arrest technique,Circulation49 (Suppl. III):136, 1974. 2. Sones, F. M. J., and Shirey, E. K.: Cine coronary arteriography, Mod. Conc. Cardiovasc. Dis. 31:735, 1962. 3. Judkins, M. P.: Selective coronary arteriography, I. A percutaneoustransfemoraltechnique,Radiology89:815, 1967. 4. Blackburn,H., Keys, A., Simonson, E., Rautaharju, P., and Punsar, S.: The electrocardiogram in population
189
F r u e h a n et al.
studies: A classification system, Circulation 21:1160, 1960. 5. Alderman, E. L., Matlof, H. J., Shumway, N. E., and Harrison, D. C.: Evaluation of enzyme testing for the detection of myocardial infarction following direct coronary surgery, Circulation 48:135, 1973. 6. Brewer, D. L., Bilbro, R. H., and Bartel, A. G.: Myocardial infarction as a complication of coronary bypass surgery, Circulation 47:58, 1973. 7. Bonchek, L. I., Rahimtoola, S. H., Chaitman, B. R.,
190
Rosch, J., Anderson, R. P., and Starr, A.: Vein graft occlusion: Immediate and late consequences and therapeutic implications, Circulation 49(Suppl. II):84, 1974. 8. Hultgren, H. N., Miyagawa, M., Buck, W., and Angell, W. W.: Ischemic myocardial injury during coronary artery surgery, AM. HEART J. 82:624, 1971. 9. Van Heeckeren, D. W., and Ankeney, J. L.: Aortocoronary graft patency related to peri-operative myocardial infarction, Circulation 47(Suppl. IV):226, 1973.
February, 1976, Vol. 91, No, 2
Coronary bypass surgery has become an accepted and common surgical procedure. To assess properly the benefits and role of aortocoronary bypass surgery, its risks and problems should be better understood. One of these problem areas is the development of intraoperative myocardial infarction, which has been reported to occur with 'an incidence as high as 29 per cent. 1 The purpose of this report is to review a series of patients with electrocardiographic evidence of intraoperative myocardial infarction which occurred during aortocoronary bypass surgery, and to review the results of postoperative coronary arteriography and left ventriculography of these patients. Materials and methods
During a 30 month period, from October, 1971, through April, 1974, 239 patients had aortocoronary bypass surgery at State University Hospital, Upstate Medical Center, Syracuse, N.Y. Excluded from the study group were 42 patients who had other concomitant cardiac surgical procedures, such as resection of ventricular aneuFrom the Departments of Medicine and Surgery, State University of New York Upstate Medical CenteL Syracuse, N. Y. Received for publication Feb. 12, 1975. Reprint requests: C. Thomas Fruehan. M.D.. State University Hospital of the Upstate Medical Center. College of Medicine, Department of Medicine. Cardiology Section, 750 E. Adams St., Syracuse, N. Y. 13210.
186
rysm, valvular surgery, ventricular septal defect closure, or internal mammary implantations. The remaining 197 patients in the study group had aortocoronary bypass grafts only. All patients were evaluated preoperatively by left heart catheterization, left ventriculography, and selective coronary cineangiography by the Sones and Shirey 2 or Judkins 3 technique. All of the aortocoronary bypass operations were performed by the same team of surgeons. All procedures were carried out under cardiopulmonary bypass with modified hypothermia at 32 ~ C. and with controlled ventricular fibrillation. Grafts placed to the left coronary system were performed with intermittent aortic occlusion for brief periods not exceeding 10 minutes. Right coronary grafts were performed by localized occlusion of the right coronary artery at the area of anastomosis. An electrocardiogram (ECG) was obtained on all patients within 48 hours before surgery. Serial postoperative ECG's of all patients undergoing aortocoronary bypass were reviewed independently by three cardiologists. Patients were considered to have had myocardial infarction only with unanimous opinion of the reviewers. The diagnosis of myocardial infarction was made only in the presence of: (1) characteristic change in QRS complexes from the preoperative ECG and (2) evolutionary changes in the ST-T deflections in the same leads as the changed QRS
February, 1976, Vol. 91, No. 2, pp. 186-190
Myocardial infarction during coronary artery bypass surgery complexes. ST-T abnormalities alone were considered nondiagnostic. The characteristic change of the QRS complexes was nearly/always the appearance of new Q waves, essentially the classes I-1 and I-2 of the Minnesota Code of Blackburn and associates2 There was one exception to this requirement for new Q waves. True posterior wall infarction was diagnosed when all the following findings were present in ECG leads V1_3: (1) R / S ratio over 1.0 for the first time in the postoperative ECG's; (2) increase in R / S ratio of over 100 per cent; (3) appropriate ST-T evolution; and (4) absence of an intraventricular conduction defect. Serum enzymes (creatinine phosphokinase, serum glutamic oxalacetic transaminase, lactic dehydrogenase [CPK, SGOT, LDH]) were obtained preoperatively and on the first, second, and third postoperative days. Upper limits of normal in our laboratory are: CPK, 139 units; SGOT, 40 units; and LDH, 207 units. Serum enzyme levels suggesting myocardial infarction after single-vessel surgery were selected as: CPK, more than four times normal ( > 556 units); SGOT, more than twice normal ( > 80 units); and LDH, more than 360 units. For multi, pie-graft surgery, these levels were CPK, more than 9 times normal ( > 1,251 units); SGOT, more than 3.5 times normal ( > 140 units); and LDH, more than 560 units. These levels are similar to the ninetieth percentile levels described by Alderman and co-workers ~ as correlating with myocardial infarction following coronary artery surgery. We have been able to obtain follow-up catheterization studies on 11 survivors of intraoperatire myocardial infarction. Restudies have included standard left heart catheterizations with left ventriculography in both right and left anterior oblique projections, selective coronary cineangiography, and selective injection of the bypass graft(s). Results
Intraoperative myocardial infarction was diagnosed by serial postoperative ECG's in 38 (19 per cent) of the 197 patients undergoing aortocoronary bypass procedures. Eighty-one per cent of patients diagnosed as having had myocardial infarction by ECG also had an elevation of at least one serum enzyme level (CPK, SGOT,
American Heart Journal
Table I.
Wall involvement of intraoperative myocardial infarctions
Location Inferior Anterior True posterior Anterior-lateral Anterior,inferior Inferior-lateral Inferior-true posterior Anterio~-lateraI-inferior Total
]
No. of patients 22 6 3 1 1 1 2 2 38
LDH) sufficient to suggest myocardial infarction. Thirty-one of the 38 (82 per cent) infarctions involved a single wall; the other seven (18 per cent) involved multiple walls (Table I). Twentytwo of the intraoperative infarcts were of the inferior wall and another six involved the inferior wall and another wall. Anterior, lateral, and true posterior wall infarctions were less frequent. Patients having multiple grafts were more likely to have intraoperative myocardial infarction. Of the 197 patients of the study group, 30 (15 per cent) had three or more grafts and 13 (43 per cent) of these 30 patients had intraoperative infarction. In contrast, 104 (53 per cent) patients had a single graft; there were only eight (7 per cent) intraoperative infarctions in this group. Correlation of infarct location with graft site. Thirty-four of the 38 intraoperative infarctions occurred in a cardiac location supplied by the grafted coronary artery (Table II). For example, four of five infarctions occurring in patients receiving only right coronary artery grafts involved the inferior wall. Four of the intraoperative infarcts occurred in walls not perfused by the coronary artery which was grafted. All four of these patients had occlusive disease, not suitable for bypass, in the arterial supply of the wall which infarcted. It is notable that most of the infarctions involved the inferior or true posterior wall, even when multiple vessels were grafted. In patients receiving grafts to all three major coronary arteries, there were 10 infarctions; eight occurred in the inferior wall alone, one was posterior, and one was inferior and lateral.
187
F r u e h a n et al.
Table II. graft site
J__t
Seven of the 11 patients had all grafts p a t e n t . Of these seven, three had a new area of hypokinesis in the area of infarction; the other four had ventriculograms which were n o r m a l or unchanged from the preoperative ventriculogram. Four of the 11 patients h a d at least one occluded graft; three of these four had a new area of hypokinesis corresponding to t h e m y o c a r d i a l infarct. Two of these three new hypokinetic areas were supplied by an occluded graft; the third was supplied by a p a t e n t graft. T h e f o u r t h p a t i e n t with a closed graft had a n o r m a l ventriculogram. In all cases the area of hypokinesis, when present, corresponded to the ECG location of the intraoperative infarction. The graft p a t e n c y rate of patients r e c a t h e t e r ized after intraoperative infarction was 68 per cent (15 of 22). If the two patients who died (with all grafts occluded) are included, the graft patency rate of these 13 patients is 54 per cent (15 of 28). This is in contrast to the 83 per cent graft patency rate of all patients restudied an average of 1 year after a o r t o c o r o n a r y bypass surgery at this institution. This difference is statistically significant (p < 0.01).
4
Discussion
Correlation of infarct location with
Coronary artery grafted
LAD + LCA + RCA*
Infarct location
I
No. of infarcts
INF
8
POST INF-LAT
1
LAD + RCA
INF INF-POST ANT-INF ANT
LAD + LCA
INF ANT ANT-LAT ANT-LATINF
RCA + LCA
INF POST
LAD
ANT-LATINF POST
1 10 9 2 2 1 14 2t 1 1 1 5 1 1 2 1 2
RCA Total
INF ANT
1~ 38
*LAD,left anteriordescendingcoronary artery; LCA,left circumflex coronaryartery;RCA,rightcoronaryartery;ANT,anteriorwall; INF, inferiorwall; LAT,lateral wall; POST,true posterior wall. "Hnfarction in wall not supplied by grafted coronary.
Hospital course following intraoperative infarction. T h e m a j o r i t y of patients with intraoperative myocardial infarction had a postoperative course not appreciably different from t h a t of bypass patients w i t h o u t infarction; however, six of the 38 patients with intraoperative infarction developed severe and prolonged left v e n t r i c u l a r failure. Two of these patients died; a n o t h e r four who developed cardiogenic shock required intraa o r t i c balloon c o u n t e r - p u l s a t i o n , and survived. Follow-up catheterization studies. Eleven of the patients who survived intraoperative m y o c a r dial infarction have been recatheterized. T h e average time between surgery and recatheterization was 10 m o n t h s (range, 2 weeks to 22 months).
188
T h e incidence of intraoperative m y o c a r d i a l infarction in this series is similar to t h a t of previous reports2 -s T h e high incidence of inferior wall involvement of such infarctions has not been described previously. ECG diagnosis of myocardial infarction in patients undergoing cardiac surgery has been demonstrated to err on the side of underdiagnosis. Brewer and associates 6 reported no false-positive ECG diagnoses in a series of patients who h a d both ECG evidence of intraoperative m y o c a r d i a l infarction and autopsy confirmation. Several patients in t h a t report, with a u t o p s y evidence of myocardial infarction, did not show diagnostic ECG evidence of infarction. The apparent discrepancy between p a t i e n t s showing E C G evidence of m y o c a r d i a l infarction without a diagnostic level of serum enzymes has been previously discussed by Alderman and associates, ~ who has pointed out t h a t the use of ninetieth percentile e n z y m e levels yielded a substantial n u m b e r of false-negative a n d falsepositive results as compared with E C G diagnosis.
February, 1976, Vol. 91, No. 2
Myocardial infarction during coronary artery bypass surgery
Bonchek and associates' described a group of patients with occluded bypass grafts. In their series of 205 patients, 52 (25 per cent) patients had at least one graft which occluded between the time of surgery and recatheterization. Eight of these 52 patients had intraoperative myocardial infarction; 44 of the 52 (85 per cent) had one or more occluded grafts without evidence of infarction. This indicates t h a t graft occlusion can occur without necessarily causing clinically recognizable infarction. Van Heeckeren and Ankeney reported 9 on eight patients recatheterized after intraoperative infarction; one of these patients had all grafts patent and seven had occlusion of one or more grafts. Those authors did not report on the ventricu!ograms of patients with intraoperative infarctions. Our data differ from van Heeckeren's, in t h a t we found a larger proportion of intraoperative infarctions in the presence of patent grafts to the areas involved. The finding of hypokinesis in the infarcted wall, which was not present in the preoperative ventriculogram, supports the fact that myocardial infarction did indeed occur. The occurrence of myocardial infarction in areas with patent grafts does not support previously published opinion 7 t h a t the major threat to patients having bypass grafts is residual coronary disease which is not bypassed; in this series, most of the infarcts occurred in areas supplied by vessels which were bypassed, and with patent grafts. There are many etiologic factors pertinent to intraoperative infarction in coronary bypass surgery. Early graft occlusion appeared to have been a factor in some of these patients, as demonstrated by the follow-up cineangiograms. Prolonged cardiopulmonary bypass, with less than optimal perfusion of ischemic areas unable to be revascularized, appears to be a likely factor in those patients with infarction in areas not perfused by the bypass grafts. There remains a group of patients with patent grafts and electrocardiographic evidence of infarction in the area perfused by the graft. To date, we have no satisfactory explanation for these infarctions. We have no good explanation for the failure to find hypokinesis in five of the eleven patients with presumed intraoperative infarction. It is possible that the infarction was not large enough
American Heart Journal
to affect gross patterns of ventricular contraction. We conclude that intraoperative myocardial infarction is a fairly common problem of aortocoronary bypass surgery, often involves an area supplied by a grafted vessel, and is not necessarily related to graft closure. Summary
Of 197 consecutive patients having aortocoronary bypass grafts over a 30 month period, 38 (19 per cent) had ECG evidence of myocardial infarction. The infarctions occurred more commonly in patients receiving multiple grafts. The infarctions were usually in areas supplied by grafted vessels. The infarctions occurred most often in the inferior wall, even when multiple vessels were grafted. Eleven patients with intraoperative infarction have had repeat postoperative coronary arteriograms. Seven had all grafts patent; three of these patients had hypokinesis of the infarcted wall. Four of the 11 patients had one or more occluded grafts; three of these patients had an area of hypokinesis. We conclude t h a t intraoperative myocardial infarction is a common problem in aortocoronary bypass surgery and is not necessarily caused by graft occlusion. Addendum
During the twelve months following the study period of this report, 87 aortocoronary bypass procedures were done at this institution, with an intraoperative infarction rate of 4.5 per cent (four infarcts). No single factor has been identified as a cause for the lower incidence. The improvement is likely due to a combination of: shorter periods of aortic occlusion; increased aortic perfusion pressure; improved surgical exposure; use of combined grafts; and increased surgical experience.
REFERENCES
1 Ellis, R., Kligfield,P., Gay, W., and Ebert, P.: Distal coronary artery bypass; local occlusionversus ischemic arrest technique,Circulation49 (Suppl. III):136, 1974. 2. Sones, F. M. J., and Shirey, E. K.: Cine coronary arteriography, Mod. Conc. Cardiovasc. Dis. 31:735, 1962. 3. Judkins, M. P.: Selective coronary arteriography, I. A percutaneoustransfemoraltechnique,Radiology89:815, 1967. 4. Blackburn,H., Keys, A., Simonson, E., Rautaharju, P., and Punsar, S.: The electrocardiogram in population
189
F r u e h a n et al.
studies: A classification system, Circulation 21:1160, 1960. 5. Alderman, E. L., Matlof, H. J., Shumway, N. E., and Harrison, D. C.: Evaluation of enzyme testing for the detection of myocardial infarction following direct coronary surgery, Circulation 48:135, 1973. 6. Brewer, D. L., Bilbro, R. H., and Bartel, A. G.: Myocardial infarction as a complication of coronary bypass surgery, Circulation 47:58, 1973. 7. Bonchek, L. I., Rahimtoola, S. H., Chaitman, B. R.,
190
Rosch, J., Anderson, R. P., and Starr, A.: Vein graft occlusion: Immediate and late consequences and therapeutic implications, Circulation 49(Suppl. II):84, 1974. 8. Hultgren, H. N., Miyagawa, M., Buck, W., and Angell, W. W.: Ischemic myocardial injury during coronary artery surgery, AM. HEART J. 82:624, 1971. 9. Van Heeckeren, D. W., and Ankeney, J. L.: Aortocoronary graft patency related to peri-operative myocardial infarction, Circulation 47(Suppl. IV):226, 1973.
February, 1976, Vol. 91, No, 2
