Perioperative Myocardial Infarction: Late ClinicalCourse After Coronary Artery Bypass SurgeryRICHARD J. GRAY, M.D., JACK M. MATLOFF, M.D., CAROLYN M. CONKLIN, R.N.,

WILLIAM GANZ, M.D. , YZHAR CHARUZI, M.D., RALPH WOLFSTEIN, M.D. AND

H.J.C. SWAN, M.D., PH.D.

SUMMARY The effects of perioperative myocardial infarction (MI) on long-term survival and sympto-matic status after coronary bypass surgery was assessed by a 64.9-month follow-up of the survivors (225) ofall isolated coronary bypass surgery (227) performed at our institution from November 1975 to July 1976.

Patients were separated into three groups: group 1 (111 patients) showed no postoperative ECG changes;group 2 (31 patients) showed appearance and persistence of new or enlarged Q waves with localized STelevation; and group 3 (83 patients) showed less specific ECG changes. Group 2 had greater technetiumpyrophosphate scan positivity (eight of 19 vs one of 35, p < 0.0005) and higher peak MB-CK activity (8320 vs 20 + 3 IU/I (mean + SEM) (p < 0.01) than group 1. Using the ECG criteria of group 2, the incidence ofperioperative MI was 13.7% (31 of 227 patients).

Groups 1 and 2, compared according to age, prior infarction, number of diseased vessels, left mainstenosis, coronary collaterals, left ventricular ejection fraction and number of grafts inserted, were notsignificantly different. However, both ischemic (aortic cross-clamp) time and total pump time were greaterin group 2 than in group 1 (65 + 3 vs 51 2 minutes and 166 + 7 vs 132 ± 3 minutes, respectively, p <0.05).There were no perioperative (30-day) deaths in group 1, whereas group 2 had a perioperative mortality

rate of 3.2% (one of 31). The 5-year survival rates ofgroup 1 (94.3%), group 2 (96.8%) and group 3 (91.1 %)were not significantly different. Late postoperative status regarding relief of angina, dyspnea, level ofphysical activity, and use of cardiac medications were not different between the groups. In all patients andin those age 55 years or younger, work status was not different.

Although perioperative MI may be associated with a higher operative mortality, late survival and cardiacstatus were not affected by it in 5 years of follow-up.

THE GOALS of therapy for coronary atherosclerosisinclude relief of angina pectoris, modification of theincidence of myocardial infarction, protection againstsudden death and increased longevity. Considerabledebate has centered on the relative merits of medicaland surgical therapy in achieving these goals. Theoccurrence of perioperative myocardial infarction hasbeen cited as a significant limitation to surgicaltherapy.

This attitude has largely been influenced by thelong-term result of naturally occurring myocardial in-farction, which is associated with serious morbidityand mortality, especially in subsets of patients withventricular ectopy.'-3 Further, variable reports of theincidence and significance (mortality) of perioperativemyocardial infarction in regard to early and intermedi-ate implications have added to the confusion over thisissue. Some of these differences have been an expres-sion of the variable criteria used to make the diagnosis.Recent reports have focused on the relative diagnosticmerits of electrocardiography, quantitative MB-CK re-lease and technetium pyrophosphate scintigraphy.4-7To test the hypothesis that perioperative myocardial

infarction may adversely affect the outcome of coro-

From the Divisions of Thoracic and Cardiovascular Surgery andCardiology, Cedars-Sinai Medical Center, and the Department of Medi-cine, University of California, Los Angeles, Los Angeles, California.

Supported in part by NIH SCOR grant 2-P50-HL17651, the Hal &Lois Haytin Foundation, and the United Hostesses.

Address for correspondence: Richard J. Gray, M.D., Department ofThoracic and Cardiovascular Surgery, Cedars-Sinai Medical Center,8700 Beverly Boulevard, Los Angeles, California 90048.

Received February 4, 1982; revision accepted May 27, 1982.Circulation 66, No. 6, 1982.

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nary artery bypass surgery, we performed a long-termfollow-up study. Electrocardiographic, enzymatic andscintigraphic criteria were used to diagnose periopera-tive myocardial infarction.

Patients and MethodsFrom November 1975 to July 1976, 227 patients

(197 male and 30 female) had isolated coronary arterybypass graft surgery and form the basis for this study.The mean age of this group was 57 years. Based onpreoperative historical and ECG findings, 104 (46%)had evidence of previous (more than 2 weeks earlier)myocardial infarction. Coronary arteriography re-vealed significant coronary disease (50% or greaterdiameter reduction) in 2.4 vessels per patient; 24 pa-tients (11%) had left main stenosis. The mean Frie-singer coronary score (maximum score of 15 pointsrepresents total occlusion of all three major vessels)was 11 for our patients.8 The mean ejection fractioncalculated from the right anterior oblique ventriculo-gram was 62%.

Anesthesia was induced and maintained using i.v.morphine sulfate and diazepam. Supplementation witha mixture of nitrous oxide (50%) and oxygen (50%)was occasionally used. Nitroprusside by i.v. infusionand small doses of i.v. propranolol (0.5-2.0 mg) wereused to blunt the hypertension and tachycardia oc-casionally seen with endotracheal intubation andstemotomy.The surgical technique at that time included cardio-

pulmonary bypass with a bubble oxygenator, hemodi-lution and intermittent aortic cross-clamping, withmild-to-moderate systemic hypothermia. The coldest

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temperature reached varied from 28° to 32°C. Nochemical cardioplegia was used. All distal anasto-moses were done using aortic cross-clamping on car-diopulmonary bypass; proximal anastomoses weredone with a side-gripping forceps. A mean of 3.1grafts per patient was inserted. The mean cardiopul-monary bypass and total ischemic times were 139 and57 minutes, respectively. Two patients died becausethey could not be weaned from cardiopulmonarybypass.

Three independent observers unfamiliar with the pa-tient's clinical status compared postoperative ECGs(for 10.6 3.8 days, mean SD) and assigned themto one of three categories based upon ECG criteria tobe described below. Differences in interpretation wereresolved by consensus. Each ECG was evaluatedbased upon specific features thought to represent myo-cardial infarction. Twenty-eight of 31 abnormalities(90%) first appeared within 24 hours of surgery; butthose appearing at any time during the postoperativehospitalization were included. Group 1 consisted of111 patients who had unchanged postoperative ECGsand were considered to have no evidence of periopera-tive myocardial infarction. Group 2 consisted of 31patients who had persistent, pathologic, new or en-larged Q waves with localized ST elevation (D 1

mm). Group 3 consisted of patients with persistent newpathologic Q waves but without ST elevation (22 pa-tients). patients with only transient Q-wave develop-ment or enlargement without ST elevation (17 pa-tients), and patients with isolated nonspecific ST- andT-wave changes or localized diminished R waveheight (44 patients). Because our intention was to com-pare patients who had more traditional ECG signs ofperioperative myocardial infarction with those whoseECGs were normal, we expected that certain patientswith equivocal criteria or some with subendocardialinfarction would be assigned to group 3.

Six patients had postoperative left bundle branchblock. In three in whom it was present before surgery,it was associated with no further ECG changes or en-zyme abnormalities; these patients were assigned togroup 1. Three patients had new left bundle branchblock. In two it was transient (< 24 hours) and al-lowed traditional ECG evaluation; one of these twopatients was assigned to group 2 and the other to group3. The remaining patient developed asymptomatic leftbundle branch block 5 days postoperatively, but beforethat he had been assigned to group 3.

Serial MB-CK data obtained 0, 8, 16, 24 and 48hours after surgery was available in 183 patients. Somedata were missing because of an oversight in obtainingproperly timed samples or misplacement of laboratoryresults. A mean peak value within 16 hours is reportedfor each ECG group (mean + SEM). To demonstratewhich of the ECG groups may be different from group1 and thus represent perioperative myocardial infarc-tion, statistical comparison of peak 16-hour postoper-ative MB-CK was performed using the Kruskall-Wal-lis analysis of variance9 (table 1). Patients in group 2had the highest MB-CK values, which were statistical-

TABLE 1. Postoperative MB-CK (within 16 hours) -Correla-tion with ECG Groups

MB-CKGroup (IU/I)

1 20±32 83 ± 20*

3 37±5*t*p <0.01 vs group 1.tp = 0.09 vs group 2.

ly different from group 1 (p < 0.05), but not fromgroup 3 (p < 0.09).

Postoperative technetium pyrophosphate scintigra-phy was performed in 97 patients using multiple-viewimages obtained 1-2 hours after the injection of 15mCi of technetium-99m pyrophosphate. We obtainedas many pyrophosphate scintigrams as possible; butthis study was initiated when such studies were notavailable on a portable basis. Consequently, scanswere not obtained unless the patient was stable enoughto leave the intensive care area for the required time.This often necessitated waiting beyond the optimaltime for imaging. The results were considered positivewhen uptake was interpreted as discrete and of 2 + orgreater intensity. The incidence of scan positivity ingroup 1 was compared with that in each of the otherECG groups. This comparison, done with a Fisherexact test,'0 was used to determine which patients devi-ate from the normal group, further establishing a groupwith unequivocal perioperative myocardial infarction(table 2). Group 2 had the highest incidence, statisti-cally different from group 1 (p < 0.0005), but notfrom group 3 (p = 0.281).The ECG criteria in group 2 (persistent, pathologic,

new or enlarged Q waves with localized ST elevation)are similar to those used by others."I Based on thesecriteria and strengthened by the correlation with MB-CK and technetium pyrophosphate scan data, we con-sidered only those 31 patients in group 2 to have sus-tained a definite perioperative myocardial infarction.All such patients had either a positive scan or peakMB-CK of > 40 IU/l in addition to the described ECGcriteria. In our clinical experience and in that of oth-ers,5 a peak MB-CK of 40 IU/l or greater correlateswell with other indicators of perioperative myocardialinfarction. In this report, these patients will be con-trasted repeatedly to those in groups 1 and 3 to high-light any differences between the group with the defi-nite perioperative myocardial infarction, the normalgroup and all patients with less certain electrocardio-graphic findings (group 3).

TABLE 2. Technetium Pyrophosphate Myocardial InfarctionScan Results

Group Incidence of positivity1 1/35 (3%)2 8/19 (42%)*3 7/30 (23%)t

*p < 0.0005 vs group 1.tp = 0.281 vs group 1.

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Long-term follow-up was completed on all 225 sur-vivors of surgery and was obtained through telephoneinterview of the patient. Data on postoperative tread-mill or angiographic studies were not available.

ResultsThere were two operative deaths (0.9%) in the entire

cohort. Since these patients had no postoperativeECGs, they could not be classified into a group, andthe remainder of the study involved the 225 surgicalsurvivors.The contribution of age, presence of previous myo-

cardial infarction, number of diseased coronary ves-sels, Friesinger coronary score, left main disease,coronary collateral formation, preoperative ejectionfraction, number of grafts inserted, and the number ofpostoperative hospital days are shown in table 3. Com-parison between groups 1, 2 and 3 show that none ofthese variables had any significant relationship to per-ioperative myocardial infarction. Total cardiopulmo-nary bypass time and total ischemic time (aortic cross-clamp time), however, were significantly longer ingroup 2 than group 1, 166 + 7 vs 132 + 3 minutes and65 ± 3 vs 51 ± 2 minutes (p <0.05).The 30-day mortality rate for the total group was

four of 227 (1.8%), including the two surgical deaths.One patient in group 2 (3.2%) died 5 days postopera-tively due to cardiac arrest from which he could not beresuscitated. One patient in group 3 (1.2%) died 10days postoperatively from severe neurologic sequelaeof sudden massive postoperative hemorrhage. Of the31 patients in group 2, the infarction was anterior (in-cluding anteroseptal) in 12 (39%), inferior in 15 (48%)and posterior in four ( 13%). In six ( 19%), the perioper-ative myocardial infarction represented an extension inthe same site as a previous myocardial infarction (en-largement of Q waves).The long-term follow-up extended to 64.9 months

(average 59.5 ± 0.2 months). There have been 12 late

TABLE 3. Factors Analyzed for Contribution to PerioperativeMyocardial Infarction

Group 1 Group 2 Group 3(n = lll) (n= 31) (n = 83)

Age 57 55 57Male 89 29 76Female 22 2 7

Previous myocardialinfarction 48% 45% 45%

No. of diseased vessels 2.3 2.5 2.5

Friesinger score 10 11 11

Left main disease 9% 16% 10%Coronary collaterals 41% 42% 36%Ejection fraction 61% 64% 62%No. of grafts/patient 3.1 3.3 3.1

Days in hospital 12 12 13Pump time (minutes) 132±3 * 166±7 138±4.2Ischemic time (minutes) 51±2 * 65±3 58±2.2

*p < 0.05 vs group 1.

100

>

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m

0

a-0o

A -.

o---O---o---o-- -0- --O---0--0

- A

90

POSTOPERATIVE MONTHS

FIGURE 1. Long-term survival afterperioperative myocardialinfarction comparing the likelihood of survival of the normalgroup (group 1, triangles) to perioperative infarction (group 2,circles) and the intermediate group (group 3, diamonds).

deaths (six in group 1, none in group 2, and six ingroup 3). The causes of late death include suddencardiac death in six (three in group 1 and three in group3), congestive heart failure in two (one in group 1, onein group 3), cancer in two and hepatitis in two.

Figure illustrates the probability of survival up to65 months after coronary bypass surgery for group 1(93.9%), group 2 (96.8%), and group 3 (91.1%). Nosignificant differences between groups can be demon-strated after 5 years of follow-up. There have been nolate deaths in the group with perioperative myocardialinfarction. The annualized mortality rate of the 225operative survivors is 1.3%.

Symptomatic outcome is shown in table 4. Sincecoronary bypass surgery is expected to alleviate angina(and not traditionally done for relief of dyspnea), pa-tients who continue postoperatively to have angina(unchanged, symptomatic) were included with thosewhose angina worsened after surgery, whereas thosewho continue to have dyspnea (unchanged, symptom-atic) are included with those who had no dyspnea be-fore or after surgery (unchanged, asymptomatic). Theincidence of angina or dyspnea (and current level ofphysical activity) is not different between groups 1, 2and 3.

In groups 1, 2 and 3, respectively, 17%, 23% and14% of the patients were using nitrates, 31%, 13% and

TABLE 4. Symptomatic Outcome

Current symptoms Group 1 Group 2 Group 3

Angina pectorisImproved 73% 60% 67%

Unchanged(asymptomatic) 22% 23% 20%

Worse 5% 17% 13%

DyspneaImproved 53% 57% 59%

Unchanged (sympto-matic and asympto-matic) 38% 37% 36%

Worse 9% 7% 5%

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I I I I I0 3 6 12 18 24 30 36 42 48 54 60 66

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26% 13 blockers, 16%, 13% and 17% antiarrhythmicmedication, 24%, 23% and 29% diuretics, and 23%,13% and 13% digoxin. The proportions are not signifi-cantly different between the groups.The employment status of our patients is shown in

table 5. Patients were considered improved if theywere working only after surgery; unchanged if theyreturned to their preoperative work (or were unem-ployed both before and after surgery); and worsened ifworking before surgery but currently unemployed.Sixty percent of the patients are employed. No signifi-cant differences were found between the proportion ofpatients in any group in any of these categories. Sincepatients approaching retirement age might be expectedto ask for early retirement after surgery, not necessar-ily for health reasons, all persons age 55 years oryounger (at the time of surgery) were analyzed sepa-rately. Again, no significant differences were foundbetween groups in this age category.

DiscussionBecause patients were recruited during a relatively

short period (9 months) and all consecutive coronarybypass patients were included in the study, majorchanges in patient selection, surgical technique andpostoperative management during the study wereminimized. This was apparent from analysis of theclinical variables.

Although the diagnostic criteria for perioperativemyocardial infarction may never be uniform, there isagreement that electrocardiography, cardiac-specificenzyme determination and scintigraphy are all useful.The analysis of this patient cohort began with appli-

cation of several descriptive ECG criteria to try todefine a "normal" postoperative group and a definiteinfarction group. Then, the enzymatic and scinti-graphic characteristics of each group were contrastedstatistically. In this manner, group 2 patients wereisolated as statistically different from group 1. Sincelocalized ST elevation was required in addition to per-sistent Q-wave development, we undoubtedly ex-cluded from our perioperative myocardial infarction

TABLE 5. Employment Status*

Group 1 Group 2 Group 3(n = 105) (n = 30) (n = 76)

All agesTotal currently employed 64% 63% 53%

Improved 12% 10% 12%Unchanged 65% 77% 53%Worse 23% 13% 35%

S 55 years (n=S1) (n =15) (n=35)Total currently employed 71% 100% 67%

Improved 4% 0% 8%Unchanged 74% 100% 63%Worse 22% 0% 29%*Improved = now working full- or part-time, not employed

preoperatively; unchanged = no postoperative change in employ-ment status; worse = employed preoperatively, not employed now.

cohort some patients likely to have been included inother studies. " 12, 13 Group 3 was created for thosewho had ECG evidence of acute ischemic injury diag-nosed by ST- or T-wave abnormalities without Q-waveappearance or enlargement. Some of these patientsmay have had myocardial necrosis, presumably suben-docardial. The separation of this intermediate groupwas designed to allow another group of patients withsingularly diagnostic ECG, enzyme and scintigraphiccriteria (group 2) to be contrasted with a selected groupof patients with no such abnormalities (group l).

Specifically, group 3 may well contain patientswhose ECG or MB-CK response indicates a small-to-moderate perioperative myocardial infarction, such aswith subendocardial necrosis. If these patients wereincluded in group 2, our incidence of perioperativemyocardial infarction would increase, but because pa-tients in group 3 may well have smaller amounts ofmyocardial damage, they would not be representativeof patients with signs of clear-cut transmural perioper-ative myocardial infarction. The need for a separate,intermediate classification of such patients has beenrecognized.6 Three patients in group 1 had MB-CK>40 IU/i, but none had positive ECG or scintigraphicfindings; similarly, none of the patients in group 3 withabnormal MB-CK had positive scintigraphic results,making it unlikely that any patients in this group haveextensive myocardial damage.

In our patients, perioperative transmural myocardialinfarction as defined by new or enlarged Q waves withlocalized ST elevation, carried no additional risk ofmortality or morbidity during long-term follow-up, incontrast to naturally occurring myocardial infarction.The electrocardiographic changes in our patients areidentical to those of nonsurgical infarction, except thatQ waves often mark the appearance of infarction fromthe beginning with the usual later resolution of ST andT changes. Our long-term survival results are similarto those in other studies with a somewhat shorter peri-od of follow-up.6'11,14 The rate offreedom from anginaat 64.9 months (95% group 1, 83% group 2, and 87%group 3) is the same with or without a perioperativemyocardial infarction. The proportion of our patientswho worked after surgery was high and unrelated tothe presence or absence of perioperative myocardialinfarction even in patients younger than 55 years.These findings are similar to those reported by Fennelland co-workers.6

Although the surgical (30-day) mortality in our per-ioperative myocardial infarction patients (3.2%) isabove that for the entire cohort (1.8%), these figurescompare favorably to those reported by others.6' 12While the operative mortality may be higher, no otherfactors distinguish the remainder of the postoperativeand long-term course with perioperative myocardialinfarction, suggesting that the amount of involvedmyocardium may be quite limited. Support for thisassertion is speculative, but several factors should beconsidered. First, the intraoperative occurrence ofmost of these events suggests that perioperative myo-cardial infarction is due not to bypass graft failure,'2' 13

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but to other factors, such as inadequate myocardialpreservation in the presence of a low threshold forsegmental myocardial ischemia. In this manner, thearea affected by the perioperative myocardial infarc-tion participates in any benefits of early reperfusion.Also, residual cardiac and systemic hypothermia maylast for several hours after cardiopulmonary bypassand confer some measure of protection to any areas ofreversibly damaged myocardium.An important consideration is that of estimating the

actual amount of injured or necrotic myocardium. Al-though such estimates have been made,7 further insightinto certain of the apparently benign features of periop-erative myocardial infarction will come when the areasof injury are quantified in large groups of such pa-tients. One may then be able to establish, for instance,that perioperative myocardial infarction is commonlyassociated with a small area of necrosis and that otherfactors tend to exaggerate the resulting level of MB-CK enzyme activity. Such factors might include thepresence of good local myocardial perfusion capableof washing out all released MB-CK or other physical-and chemical factors that may act to enhance the en-zyme activity of CK. Hypocalcemia, hypermagnese-mia, hyperglycemia, hemodilution, hypothermia, res-piratory alkalosis, anemia and diminished urea levels,all of which are seen during or after cardiopulmo-nary bypass, should be studied to determine if theyaffect the chemical activity of MB-CK. Other factorsthat may decrease the clearance of MB-CK, such asmorphine sulfate and pentobarbital, must also beconsidered.

During surgery, we have found progressively ele-vated MB-CK levels, beginning from the time of aorticcross-clamping,7 in patients with and without perioper-ative infarction. Preceding this release is a uniformfinding of myocardial ischemia as evidenced by myo-cardial lactate release.15

Rucker et al.5 studied release of MB-CK after coro-nary bypass. They found that for the group mean (nor-mal vs abnormal), the peak MB-CK release occursimmediately after surgery with or without periopera-tive myocardial infarction. As expected, continuedslow release persisted for as long as 36 hours withperioperative myocardial infarction. Thus, MB-CKoccurs early such that the peak level is seen within the16-hour period of our routine sampling.While the amount of myocardium affected by peri-

operative myocardial infarction may be small, as arule, a large infarction can have very serious effects.Presumably, many of the patients with adequate cardi-ac function preoperatively who die in surgery due tocardiac pump failure have severe myocardial necrosis.We believe that efforts should continue to evaluate

old and develop new methods of myocardial preserva-tion and safer methods of anesthesia. We believe that

the widespread use of hypothermic cardioplegia willresult in a lower incidence of myocardial damage dur-ing myocardial revascularization. Using contemporarymyocardial preservation techniques, the incidence ofperioperative myocardial infarction may be as lowas 6%.16

AcknowledgmentThe authors gratefully acknowledge the assistance of JoAnn Prause,

Elaine Marcus, Helen Schamroth and Lance LaForteza.

References1. The Coronary Drug Project Research Group: The Coronary Drug

Project. Design, Methods, and Baseline Results. Circulation 47:(suppl 1): 1-1, 1971

2. Oliver GC, Nolle FM, Tiefenbrunn AJ, Kleiger RE, Martin TF,Krone RJ, Miller JP, Cox JR: Ventricular arrhythmias associatedwith sudden death in survivors of acute myocardial infarction. AmJ Cardiol 33: 160, 1974

3. Vismara LA, Amsterdam EA, Mason DT: Relation of ventriculararrhythmias in the late hospital phase of acute myocardial infarc-tion to sudden death after hospital discharge. Am J Med 59: 6,1975

4. Moore CH, Gordon FT, Allums JA, Reeves TJ, Lombardo TA,Barclay GW, Brady AB, Sweet RL: Diagnosis of perioperativemyocardial infarction after coronary artery bypass. Ann ThoracSurg 24: 323, 1977

5. Rucker CH, Dugall JC, Ganter EL, Kartub MG: The detection ofperioperative myocardial infarction in aorto-coronary bypass sur-gery. Chest 75: 300, 1979

6. Fennell WH, Chua KG, Cohen L, Mortan J, Karunaratne HB,Resnekov L, Al-Sadir J, Lin CY, Lamberti JJ, AnagnostopoulosCE: Detection, prediction, and significance of perioperative myo-cardial infarction following aorto-coronary bypass. J Thorac Car-diovasc Surg 78: 244, 1979

7. Gray RJ, Shell WE, Conklin C, Ganz W, Shah PK, Miyamoto AT,MatloffJM, Swan HJC: Quantification of myocardial injury duringcoronary bypass graft. Circulation 58 (suppl I): 1-38, 1978

8. Friesinger GC, Page EE, Ross RS: Prognostic significance of coro-nary arteriography. Trans Assoc Am Phys 83: 78, 1970

9. Winkler RL: Statistics: Probability, Inference and Decision, 2nded. New York, Holt, Rinehart & Winston, 1975, pp 862-864

10. Reynolds HT: Analysis of Cross-Classifications. New York, Mac-Millan, 1977, pp 9-1 1

11. Codd JE, Wiens RD, Kaiser GC, Barner HB, Tyras DH, Mudd JG,Willman LV: Late sequelae of perioperative myocardial infarction.Ann Thorac Surg 26: 208, 1978

12. Lim JS, Proudfit WL, Sheldon WC, Alosilla C, Phillips DF, LoopFD: Perioperative myocardial infarction related to coronary bypasssurgery. Am Heart J 96: 463, 1978

13. Assad-Morell JL, Frye RL, Connolly DC, Gau GT, Pluth JR,Barnhorst DA, Wallace RN, Davis GD, Elveback LR, DanielsonGK: Relation of intraoperative or early postoperative transmuralmyocardial infarction to patency of aortocoronary bypass graftsand to diseased ungrafted coronary arteries. Am J Cardiol 35: 767,1975

14. Hultgren HN, Miyagawa M, Buck W, Angell WW: Ischemic myo-cardial injury during coronary artery surgery. Am Heart J 82: 624,1971

15. Gray RJ, Harris WS, Shah PK, Miyamoto ATM, Matloff JM,Swan HJC: Coronary sinus blood flow and sampling for detectionof unrecognized myocardial ischemia and injury. Circulation 56(suppl II): 11-58, 1976

16. Conti VR, Bertranou EG, Blackstone EH, Kirklin VW, DigemessSB: Cold cardioplegia versus hypothermnia for myocardial protec-tion. J Thorac Cardiovasc Surg 76: 577, 1978

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R J Gray, J M Matloff, C M Conklin, W Ganz, Y Charuzi, R Wolfstein and H J Swansurgery.

Perioperative myocardial infarction: late clinical course after coronary artery bypass

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1982 American Heart Association, Inc. All rights reserved.

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