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Myocardial infarction in patients with previous coronary artery bypass surgery
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JACC Vol. 3, No.4 April 1984:909-15
Myocardial Infarction in Patients With Previous Coronary Artery Bypass Surgery DAVID D. WATERS, MD, FACC, GUY B. PELLETIER, MD, FACC, MARILYN HACHE, RN, PIERRE THEROUX MD, FACC, LUCIEN CAMPEAU, MD, FACC Montreal, Quebec. Canada
An increasing proportion of patients hospitalized with myocardial infarction have previously undergone coronary artery bypass surgery. To define this subgroup, 77 patients with acute infarction occurring 2 or more months (mean 52.8) after bypass surgery were compared with 77 control patients with infarction. Baseline characteristics of the groups were similar except that post-bypass patients were more often men (p 0.02) and more likely to have had a previous infarction (37 versus 21, p 0.008). Infarct size was smaller in the post-bypass group as assessed by peak creatine kinase (CK), peak CK-MB, maximal number of electrocardiographic leads with ST elevation, maximal summed ST elevation and QRS score measured 7 to 10 days after admission (p < 0.001 for each variable). Five control patients but none ofthe postbypass patients died in the hospital (p = 0.06). Serious
=
=
The clinical manifestations of acute myocardial infarction are determined by the extent (1) and location (2) of the infarction. Myocardial infarction is caused by acute coronary artery obstruction (3) and the most important determinant of infarct size and location is the severity, extent and location of coronary obstructive disease (4.5), Because coronary artery bypass surgery produces important functional changes in the coronary circulation, patients with previous surgery who sustain a new infarction might be expected to have a smaller infarct and fewer complications than others. Perioperative infarction has been investigated in detail (6-11); however, the features of myo-
complications (death, acute heart failure, ventricular fibrillation, second or third degree atrioventricular block) occurred in 24 control patients but in only 5 post-bypass patients (p < 0.001). Angiography was performed after infarction in 45 of the 77 post-bypass patients. Occlusion of both a native coronary artery and its graft was found in 24 of the 45; these patients had had higher peak CK 0.008) than the other 21 patients who had levels (p angiography. The probable causes of infarction in these 21 were disease progression in nonbypassed arteries or graft occlusion with arterial stenosis, or vice versa, and disease progression distal to a patent graft. Thus, patients with previous bypass surgery tend to have a smaller myocardial infarction with fewer complications due to underlying differences in coronary circulation compared with patients without previous surgery.
=
cardial infarction occurring later after surgery have not been studied in a large series of patients. Among 2,000 consecutive patients with acute myocardial infarction treated in our coronary care unit between 1977 and 1982, 77 (3.8%) had undergone coronary bypass surgery at least 2 months before admission, This group increased from 2.3 to 6,7% of our patients with infarction during this period (probability [p] < 0.001). The purpose of this study is to compare these patients with a control group of patients with acute infarction and to investigate the causes of any observed differences between the groups.
Methods From the Department of Medicine, Montreal Heart Institute. and the University of Montreal Medical School, Montreal. Quebec, Canada. This study was supported in part by grants from the Jean-Louis Levesque Foundation, Montreal, Quebec, the Montreal Heart Institute Research Fund and Alcan Company. Montreal, Quebec, Canada. Manuscript received August 10, 1983; revised manuscript received November 7. 1983, accepted November 11,1983. Address for reprints: David D. Waters, MD. Montreal Heart Institute. 5000 East Belanger Street, Montreal, Quebec, HIT IC8, Canada. © 1984 by the American College of Cardiology
Patients. For the purposes of this study, acute myocardial infarction was diagnosed in patients with at least two of the following three criteria: I) a recent episode of retrosternal chest pain characteristic of myocardial ischemia lasting for at least 30 minutes, 2) a transient increase above normal limits of both total creatine kinase (CK) and its MB fraction (12) with the appropriate temporal relation to the 0735-1097/84/$3.00
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WATERS EL AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
episode of prolonged pain, and 3) Minnesota code criteria (13,14) for definite or probable myocardial infarction accompanied by increasing or decreasing ST elevation, ST depression or T wave inversions. Among 2,000 consecutive patients hospitalized with acute myocardial infarction in the coronary care unit of the Montreal Heart Institute between 1977 and 1982, 77 had undergone coronary artery bypass surgery at least 2 months before admission. Excluded from this study group were three additional patients who had valve replacement or aneurysmectomy in association with bypass grafting. For each study patient, the preceding patient admitted to the coronary care unit with acute myocardial infarction was selected for inclusion in the control group. Identical criteria for the diagnosis of myocardial infarction were used in the control patients and the post-bypass group. Patient management. Cardiac catheterization. Selective coronary arteriography was performed by a percutaneous femoral approach using preformed catheters as previously described (15). Views with cranial angulation were routinely filmed (16). The left ventricular angiogram was filmed in the 30° right anterior oblique view before coronary arteriography. Surgical management. The study patients had undergone bypass surgery between 1970 and 1982, in all but five cases at our hospital. During this 13 year period 4,630 coronary bypass operations were done at our institution. As in other large North American centers, patient selection criteria, anesthetic management and surgical techniques evolved during this time interval. In general, symptomatic patients with stenoses reducing coronary artery diameter by 70% or greater were considered for surgery and all lesions 50% or greater with adequate distal runoff were bypassed. Among the 77 study patients, 33 had triple vessel disease, 22 double vessel disease, 20 single vessel disease and 2 had stenoses less than 70%. The average number of grafts per study patient was 2.4 ± 1.0. Before 1977, anoxic cardiac arrest with intermittent aortic cross-clamping under moderate systemic hypothermia was used; thereafter, standard practice included cold cardioplegic solution, topical and systemic hypothermia. Management in the coronary care unit. Management of patients with suspected myocardial infarction was not influenced by the presence of previous bypass surgery. The electrocardiograms of all patients were recorded at least three times within 24 hours of admission, on days 2 and 3 and at least once between days 7 and 10. In all cases, serum levels of CK and its isoenzymes were measured at regular intervals within the first 72 hours of admission. All patients did not have the same number of serum enzyme determinations due to changes in our standardized protocol during the study period; however, the number of measurements per patient, 5.4 within 72 hours, was similar in the post-bypass and control groups.
lACC Vol. 3. NO.4 April 1984:909-15
Follow-up. All patients were followed up regularly after hospital discharge. Forty-five of the 77 post-bypass patients had coronary arteriography after myocardial infarction, at I month in 23 and later in 22. The mean interval from infarction to arteriography was 4.9 months (range I to 24). Those undergoing arteriography were more likely to have postinfarction angina and less likely to have severe heart failure and were thus not representative of the entire study group. Quantification of infarct size. For each patient peak CK and peak isoenzyme CK-MB were tabulated as enzymatic indexes of infarct size (17). The electrocardiogram showing the most ST elevation in the absence of conduction disturbances was selected to count the number of leads with ST elevation 0.1 mV (I mm) or greater and the sum of the ST elevation in these leads. ST elevation was measured between 0.04 and 0.08 second after the J point, depending on heart rate so as not to impinge on the T wave, and averaged over at least 3 beats for each lead. If ST elevation from a previous infarction persisted, it was not included in the measurement. The limitations of ST segment analysis to quantitate ischemic damage, particularly in relation to therapeutic interventions designed to reduce infarct size, have been described (18). In this study ST elevation was used only as an index of infarct size to compare post-bypass and control groups. A QRS scoring system that estimates infarct size from a standard 12 lead electrocardiogram, as refined by Wagner et al. (19), has been shown to correlate well with both the anatomic extent of infarction (20), postinfarction ejection fraction and infarct size as assessed by thallium-20 I defect (21). The QRS score for all patients was calculated from the electrocardiogram recorded between 7 and 10 days after admission, excluding residual abnormalities from previous infarctions. Statistical analysis. Differences between the post-bypass and control groups were assessed statistically in two ways: I) a matched pair analysis using McNemar's test (22) and the Wilcoxon matched-pairs signed-ranks test (23), and 2) intergroup comparisons using the Student's t test, the Fisher exact test or the chi-square test with Yates' correction where appropriate. All indexes of infarct size were significantly higher (p < 0.000 I) in the control group using either method. However, more intergroup differences in baseline variables attained statistical significance using the chi-square test than McNemar's test. Because these baseline differences may have influenced the results, the p values using the chi-square test are displayed in Table I and in text.
Results The mean interval between coronary bypass surgery and myocardial infarction was 52.8 ± 33.1 months (range 2 to 123). The clinical features of post-bypass patients and the
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WATERS ET AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
Table 1. Comparison of Post-Bypass and Control Groups Post-Bypass Patients Clinical characteristics Number of patients Age (mean ± SD) Male/female Previous infarction History of angina History of hypertension Preadmission medication Beta-blocking agents Digitalis Diuretic drugs Long-acting nitrates Assessment of infarct size Maximal CK (IU/liter) Maximal CK-MB Leads with ST elevation Maximal summed ST elevation (mm) QRS score (19) Total patients with old Q waves Developing new Q waves Without new Q waves Total patients without old Q waves Developing new Q waves Without new Q waves
77 53.7 69/8 37 30 19
1.075 175 1.58 3.44 1.64 34
=
atrioventricular; CK
=
creatine kinase; ECG
± 867 ± 198 ± 1.81 ± 482 ± 2.86
21 5 15 15
NS NS NS NS
1.829 342 3.39 8.92 4.43 21 12 9 56 42 14
43 20 23
± ± ± ± ±
1.300 341 2.61 9.57 4.49
< < < < <
13 14
o o
0.004
<
2 2 2 5
13 24
electrocardiographic; NS
=
not significant; p
=
0.001 NS
5 II 10 6
4
0.001 0.001 0.001 0.001 0.001 0.D3 0.006
54 30 21 3
27
control group are compared in Table 1. Control patients were slightly but not significantly older. The control group contained more women (19 versus 8, p = 0.02) than the post-bypass group, probably because only 16% of the patients undergoing bypass surgery at our hospital are women. A previous myocardial infarction had been documented in 21 control patients (27%) compared with 37 post-bypass patients (48%, p = 0.008). The prevalence of angina, hypertension and the use of drugs that might influence infarct size were similar in the two groups before infarction. Assessment of infarct size. By both enzymatic and electrocardiographic criteria, patients with previous bypass surgery had smaller infarcts than control patients. Mean maximal CK in the post-bypass group was 1,075 ± 867 international units (lV)/liter compared with 1,829 ± 1,300 IV/liter in the control group (p < 0.001). Mean maximal CK-MB was 175 ± 198 versus 342 ± 341 IV/liter (p <
28
NS 0.02 0.008 NS NS
27
7 27
=
p Value
77 56.5 ± 9.9 58/19 21
± 8.2
27 8 13 17
Total developing new Q waves Anterior ECG leads Inferior ECG leads Both anterior and inferior Complications Death in hospital Death within 1 year Acute heart failure in hospital Ventricular fibrillation 2nd or 3rd degree A V block Total complications in hospital (no. of patients) AV
Control Patients
< probability; SD
=
0.06 0.06 0.04 NS 0.007 0.001
standard deviation.
0.001). The maximal number of electrocardiographic leads with ST elevation was lower in the post-bypass group, 1.58 ± l.81 compared with 3.39 ± 2.61 (p < 0.001), and maximal summed ST elevation was also lower, 3.44 ± 4.82 versus 8.92 ± 9.57 mm (p < 0.001). The QRS score measured 7 to 10 days after infarction was 1.64 ± 2.86 in the post-bypass group and 4.43 ± 4.49 in the control group (p < 0.001), providing further evidence that post-bypass patients had smaller infarcts. Both groups exhibited a broad range of values for each of these indexes of infarct size and thus overlap widely, despite the highly significant intergroup differences (Fig. I). Role of previous myocardial infarction. More patients in the post-bypass group had preexisting Q waves (34 versus 21, P = 0.03) and patients with preexisting Q waves were less likely to develop new ones (p < 0.00 I). Therefore, subgroups were analyzed to eliminate the possibility that
WATERS EL AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
912
CK max
JACe Vol. 3, No.4 April 1%4:909-15
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Figure 1. Patients with previous bypass surgery (POST-BYPASS) had a smaller infarct than control patients, as assessed by peak (max) creatine kinase (CK) and CK-MB (lUlliter) (A), number of leads with ST elevation ( t ) and maximal summed ST elevation (E t ST max) (B) and QRS score as measured on a standard electrocardiogram 7 to 10 days after infarction (C) (19). The black squares indicate the mean value for each group .
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CONTROL
the observed differences in infarct size were related to the higher prevalence of previous infarction in the post-bypass group. Both in patients with and without preexisting Q waves, new Q waves developed more often in the control group than in the post-bypass group, Only 7 of 34 post-bypass patients with old Q waves developed new ones, compared with 12 of21 control patients with old Q waves (p = 0.006). Among patients without old Q waves, only 20 of 43 in the post-bypass group compared with 42 of 56 control patients developed new Q waves (p = 0.004). Patients with old Q waves had lower serum peak CK values than those without Q waves in the control group (p = 0,005) but not in the post-bypass group (p > 0,1), In patients with old Q waves, maximal CK value was higher in control than in post-bypass patients, 1,318 ± 686 versus 910 ± 662 IU/liter (p = 0.03). Similarly, in those without preexisting Q waves, maximal CK value was higher in control patients (2,020 ± 1,424 versus 1,206 ± 987 IV/liter,
POST-BYPASS
p = 0.001). Thus, the higher prevalence of previous infarction in the post-bypass group does not account for the observed differences in infarct size between the two groups. Subgroup analysis also showed that the higher proportion of women in the control group was not related to the differences. The site of new Q waves, anterior versus inferior, was not significantly different in the two groups. Complications. Post-bypass patients might have been expected to have more complications because more of them had had a previous infarction; however, the opposite occurred (Table I). Five control patients but none of the postbypass patients died in the hospital (p = 0.06). Within I year of admission 11 control patients and 4 post-bypass patients had died (p = 0.06). Acute heart failure in the hospital, defined as heart failure severe enough to require intravenous vasodilator or inotropic drugs, occurred in 10 control and 2 post-bypass patients (p = 0.04). Thirteen control and two post-bypass patients had second or third degree atrioventricular (AV) block (p = 0.007). Overall,
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WATERS ET AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
24 control and 5 post-bypass patients experienced complications (death, acute heart failure, ventricular fibrillation, second or third degree AV block) in the hospital (p < 0.001). Angiographic findings after infarction. After myocardial infarction, 45 of the 77 post-bypass patients underwent coronary arteriography. Although these 45 patients were not representative of the entire group, their angiographic data were examined in search of potential explanations for smaller infarct size in the post-bypass patients. All grafts were occluded in 10 cases, all grafts were patent in 14 and both patent and occluded grafts were present in 21. The site of infarction could be localized from the electrocardiogram in 27 of the 45 cases; in the other 18 neither ST elevation nor new Q waves were recorded and the electrocardiographic site of infarction was classified as unknown. Probable causes ofmyocardial infarction (Table 2). Both the bypass graft and the coronary artery that it supplied were totally occluded in 24 cases. In 16 of these 24 patients, the distribution of this vessel corresponded to the electrocardiographic site of infarction and in the other 8 patients the infarct could not be localized electrocardiographically. In six patients, either the bypass graft was occluded and the native artery was stenotic or the artery was occluded and the graft stenotic. In nine cases, either an occlusion or progression of a less than 50% lesion to 70% or greater had developed in an artery that had not been bypassed. Infarction was caused by disease progression distal to a patent graft in three cases. Finally, in three patients whose infarct could not be localized electrocardiographically, more than one of these three situations were present (graft or artery occluded with the other stenotic, progression in a nonbypassed artery, progression distal to a patent graft) and the likeliest cause of infarction could not be ascertained.
Table 2, Angiographic Findings After Infarction in Post-Bypass Group Infarct Site Probable Cause of Infarction
Known
Unknown
Total
A. Graft and bypassed artery occluded B. Graft or bypassed artery occluded C. Progression* in nonbypassed artery D. Progression* distal to patent graft E. > I of mechanisms B to D possible Total
16
8
24
4 5
2 4
6 9
2
1 3
3
0
27
18
45
3
*Progression is defined as an increase in a lesion to 100% or from less than 50% to 70% or greater in a nonbypassed artery or distal to the anastomosis in a bypassed artery.
913
Patients with an occluded graft and artery to the infarct zone might be expected to have a larger infarct than patients with other causes for post-bypass infarction. Thus, mean maximal CK level in the 24 patients with graft and arterial occlusion was 1,288 ± 1,084 versus 598 ± 506 IU/liter in the 21 patients with other causes (p = 0.008). A similar difference was found for CK-MB isoenzyme (p = 0.009) but the differences for the electrocardiographic indexes of infarct size did not attain statistical significance, probably because many of these patients had only minimal electrocardiographic changes. Control group. After myocardial infarction, 35 patients in the control group underwent coronary arteriography. As with the bypass group, the patients undergoing arteriography are unrepresentative of the entire sample. One of the 35 patients had no coronary lesions 70% or greater, 12 had one vessel disease, 15 had double vessel and 7 had triple vessel disease. All but two patients had segmental left ventricular contraction abnormalities corresponding to the territory of infarction.
Discussion Among patients hospitalized with acute myocardial infarction, those who have previously undergone coronary bypass surgery represent a small but rapidly growing subgroup whose characteristics have not been defined. This study compared a group of post-bypass and control patients with acute myocardial infarction; the post-bypass group contained fewer women and more patients with previous infarction. The interval from surgery to myocardial infarction ranged from 2 months to 12 years, averaging about 41f2 years. Patients with infarction within 2 months of surgery were prospectively excluded so that the acute effects of surgery would not be a complicating factor. Both enzymatic and electrocardiographic assessments of infarct size consistently demonstrated statistically significant differences: post-bypass patients had a smaller infarct than control patients. Subgroup analysis showed that this finding was not due to baseline clinical differences in the two groups. Postbypass patients had fewer complications. Five of the 77 control patients but none of the 77 post-bypass patients died in the hospital. Limitations of the study. Bias in the surgical group. Do post-bypass patients really have a smaller infarct with fewer complications, or could other factors account for the results of this study? Myocardial infarction may be silent, unrecognized or cause death before admission to a coronary care unit. Because of their previous medical experience, postbypass patients with a small infarct may have been more likely to seek medical attention and gain admission than patients without previous surgery, thus biasing our results. Although we admit all patients with suspected or proven infarction irrespective of their medical history, we cannot
914
WATERS EL AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
eliminate the possibility that patient self-selection influenced our results. Methods of estimating infarct size. A second limitation of this study involves the methods used to estimate infarct size (17-19). To calculate total serum CK release accurately in an individual patient requires more samples than were obtained in this study. However, peak CK correlates well with total CK release, the number of samples per patient were similar in the two groups, the size of the groups was large and the mean difference in peak CK between the groups was also large; thus, the conclusion that CK infarct size was smaller in the post-bypass group is most likely valid. Serum CK may originate from noncardiac sources; however, measurements of the cardiac MB isoenzyme yielded similar results. The electrocardiographic assessment of infarct size presents theoretical and practical difficulties (J8). The number of leads with ST elevation and maximal summed ST elevation on a standard 12 lead electrocardiogram are insensitive and inaccurate indexes of myocardial ischemia. However, these data were gathered and measured in both groups in an identical way and yielded results that are both internally consistent and consistent with the CK and CK-MB results. Other techniques to estimate infarct size were not used in this study. For example, if patients with previous infarction were excluded, radionuclide or contrast ventriculography could have provided an accurate comparison of the extent of segmental left ventricular dysfunction in the two groups. Absence of complete angiographic data. A final limitation of the study is the absence of angiographic data after infarction in 1J:J of the post-bypass patients. In addition, the delay between infarction and angiography allows for recanalization of arteries that may have been totally occluded during the acute phase (3); thus, the reason for infarction may not always be apparent after reviewing the angiogram, particularly if the site of infarction could not be localized by electrocardiographic or other methods. Causes of infarction in post-bypass patients. During the early phase of acute myocardial infarction most patients will exhibit complete coronary occlusion at arteriography; for example, in the study of DeWood et al. (3), this finding was present in 110 of 126 patients evaluated within 4 hours of the onset of symptoms. In contrast, perioperative myocardial infarction is often associated with a patent graft to the infarct zone as assessed by angiography (8) or at autopsy (9). Reperfusion injury (9) or coronary spasm (24) may account for some of these infarcts. In this study, angiographic data are available for 45 patients with infarction at least 2 months after bypass surgery. In 24 of the 45 patients, both the artery and bypass graft to the infarct zone were occluded. This situation may be analogous to a complete arterial obstruction in a patient without
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coronary bypass, but several circumstances can be envisaged where the surgically treated patient would have an advantage in terms of infarct size. A completely occluded artery proximal to a small infarct, often with good collateral vessels, is frequently bypassed, in part, to preserve residual myocardial function; in such a case, subsequent graft occlusion would be likely to produce only a minimal amount of new necrosis. Second, if coronary occlusion is an abrupt event, a patient who had coronary bypass may be more likely to have time to develop collateral vessels because the occlusion occurs in two stages (graft and artery). Third, a patient with two conduits to a myocardial segment may be more likely to have two small infarcts instead of one large one; for example, a proximal left anterior descending coronary occlusion might obstruct a septal or diagonal branch and produce a small infarct despite a patent graft to the distal artery. Subsequently, the graft might become blocked leading to complete infarction of the left anterior descending niyocardial territory. This study provides no firm data to support these speculations. Peak serum CK was higher in control patients (l,829 ± 1,300 IU/liter), than in the 24 patients with graft and arterial occlusion (l,288 ± 1,084 IU/liter) (p = 0.04), but such a comparison may be biased because not all postbypass patients underwent arteriography. The other 2 J post-bypass patients who underwent arteriography could be classified into three groups: I) those with an occluded graft and stenotic artery, or vice-versa, 2) those with disease progression in a nonbypassed artery, and 3) those with disease progression distal to a graft. Peak CK and CK-MB levels were significantly lower in these 21 patients than in the 24 with a completely obstructed graft and artery. The smaller infarcts in these subgroups may result from different mechanisms. In patients with either the native artery or graft incompletely obstructed, infarct size may have been limited by residual perfusion (unless complete obstruction had been present and recanalization later occurred). Arteries that are small or perfuse akinetic areas are often not bypassed; infarcts due to disease in such vessels would tend to be small. Similarly, obstruction distal to the site of a graft anastomosis would cause less necrosis than if the artery were blocked more proximally. Implications. Progressive disease in nonbypassed coronary arteries, distal to anastomoses and within bypass grafts themselves are commonly observed from 5 to 12 years after surgery (25,26). These changes correlate with the recurrence of angina and often cause no myocardial necrosis (25,26). The patterns of coronary perfusion in patients with angina or myocardial infarction after bypass surgery are complex and difficult to classify because many variables are involved (the site, severity and number of lesions in each native artery and graft, the number of grafts, the sites of anastomoses and the relation between the sites of graft and arterial dis-
WATERS ET AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
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ease). Despite this diversity, this study indicates that in patients with previous bypass surgery, myocardial infarcts tends to be smaller and associated with fewer complications. The reasons for this difference will be better understood when coronary arteriography is performed soon after infarction in a large series of patients with previous bypass surgery and of control patients.
915
infarction: late clinical course after coronary artery bypass surgery Circulation 1982;66: 1185-9. 12. Delva E. Maille IG, Solymoss BC, Chabot M, Grondin CM, Bourassa MG. Evaluation of myocardial damage during coronary artery grafting with serial determinations of serum CPK-MB isoenzyme. 1 Thorac Cardiovasc Surg 1978;75:467-75. 13. Blackburn H. Keys A, Simonson E. Rautaharju P, Punsar S. The electrocardiogram in population studies. A classification system. Circulation 1960:21:1160-75. 14. Rose GA. Blackburn H. Cardiovascular Survey Methods. Geneva: World Health Organization Monograph 56, 1968.
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3. DeWood MA, Spores 1, Notske R, et a!. Prevalence of total coronary occlusion during the eady hours of transmural myocardial infarction. N Engll Med 1980;303:897-902.
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6. Brewer DL, Bilbro RH, Bartel AG. Myocardial infarction as a complication of coronary bypass surgery. Circulation 1973;47:58-64. 7. Espinoza 1, Lipski 1, Litwak R, Donoso E, Dack S. New Q waves after coronary artery bypass surgery for angina pectoris. Am 1 Cardiol 1974;33:221-4. 8. Assad-Morell lL, Frye RL, Connolly DC, et al. Relation of intraoperative or eady postoperative transmural myocardial infarction to patency of aortocoronary bypass grafts and to diseased ungrafted coronary arteries. Am 1 Cardiol 1975;35:767-73. 9. Bulkley BH, Hutchins GM. Myocardial consequences of coronary artery bypass graft surgery. The paradox of necrosis in areas of revascularization. Circulation 1977;56:906-13. 10. Namay DL, Hammermeister KE, Zia MS, DeRouen TA. Dodge HT. Namay K. Effect of perioperative myocardial infarction on late survival in patients undergoing coronary artery bypass surgery. Circulation 1982;65: 1066-71. II. Gray Rl, Matloff 1M, Conklin CM, et a!. Perioperative myocardial
21. DePace NL. Iskandrian AS. Hakki A, Kane SA, Segal BL. Use of QRS scoring and thallium-20 I scintigraphy to assess left ventricular function after myocardial infarction. Am 1 Cardiol 1982;50: 1262-8. 22. McNemar Q. Note on the sampling error of the difference between correlated proportions or percentages. Psychometrika 1947; 12: 153-7. 23. Siegel S. Non-parametric statistics for the behavioral sciences. New York: McGraw-Hili. 1956:75-81. 24. Buxton AE. Hirshfeld lW Jr. Untereker W1. et a!. Perioperative coronary arterial spasm: long-term follow-up. Am 1 Cardiol 1982;50:444-51. 25. Campeau L. Lesperance 1. Hermann 1, Corbara F, Grondin CM, Bourassa MG. Loss of improvement of angina between I and 7 years after aortocoronary bypass surgery. Correlations with changes in vein grafts and in coronary arteries. Circulation 1979;60(suppl 1):1-1-5. 26. Bourassa MG. Campeau L. Lesperance 1, Grondin CM. Changes in grafts and coronary arteries after saphenous vein aortocoronary bypass surgcry: rcsults at repeat angiography. Circulation 1982:65(suppl 11):1190-7.
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Myocardial Infarction in Patients With Previous Coronary Artery Bypass Surgery DAVID D. WATERS, MD, FACC, GUY B. PELLETIER, MD, FACC, MARILYN HACHE, RN, PIERRE THEROUX MD, FACC, LUCIEN CAMPEAU, MD, FACC Montreal, Quebec. Canada
An increasing proportion of patients hospitalized with myocardial infarction have previously undergone coronary artery bypass surgery. To define this subgroup, 77 patients with acute infarction occurring 2 or more months (mean 52.8) after bypass surgery were compared with 77 control patients with infarction. Baseline characteristics of the groups were similar except that post-bypass patients were more often men (p 0.02) and more likely to have had a previous infarction (37 versus 21, p 0.008). Infarct size was smaller in the post-bypass group as assessed by peak creatine kinase (CK), peak CK-MB, maximal number of electrocardiographic leads with ST elevation, maximal summed ST elevation and QRS score measured 7 to 10 days after admission (p < 0.001 for each variable). Five control patients but none ofthe postbypass patients died in the hospital (p = 0.06). Serious
=
=
The clinical manifestations of acute myocardial infarction are determined by the extent (1) and location (2) of the infarction. Myocardial infarction is caused by acute coronary artery obstruction (3) and the most important determinant of infarct size and location is the severity, extent and location of coronary obstructive disease (4.5), Because coronary artery bypass surgery produces important functional changes in the coronary circulation, patients with previous surgery who sustain a new infarction might be expected to have a smaller infarct and fewer complications than others. Perioperative infarction has been investigated in detail (6-11); however, the features of myo-
complications (death, acute heart failure, ventricular fibrillation, second or third degree atrioventricular block) occurred in 24 control patients but in only 5 post-bypass patients (p < 0.001). Angiography was performed after infarction in 45 of the 77 post-bypass patients. Occlusion of both a native coronary artery and its graft was found in 24 of the 45; these patients had had higher peak CK 0.008) than the other 21 patients who had levels (p angiography. The probable causes of infarction in these 21 were disease progression in nonbypassed arteries or graft occlusion with arterial stenosis, or vice versa, and disease progression distal to a patent graft. Thus, patients with previous bypass surgery tend to have a smaller myocardial infarction with fewer complications due to underlying differences in coronary circulation compared with patients without previous surgery.
=
cardial infarction occurring later after surgery have not been studied in a large series of patients. Among 2,000 consecutive patients with acute myocardial infarction treated in our coronary care unit between 1977 and 1982, 77 (3.8%) had undergone coronary bypass surgery at least 2 months before admission, This group increased from 2.3 to 6,7% of our patients with infarction during this period (probability [p] < 0.001). The purpose of this study is to compare these patients with a control group of patients with acute infarction and to investigate the causes of any observed differences between the groups.
Methods From the Department of Medicine, Montreal Heart Institute. and the University of Montreal Medical School, Montreal. Quebec, Canada. This study was supported in part by grants from the Jean-Louis Levesque Foundation, Montreal, Quebec, the Montreal Heart Institute Research Fund and Alcan Company. Montreal, Quebec, Canada. Manuscript received August 10, 1983; revised manuscript received November 7. 1983, accepted November 11,1983. Address for reprints: David D. Waters, MD. Montreal Heart Institute. 5000 East Belanger Street, Montreal, Quebec, HIT IC8, Canada. © 1984 by the American College of Cardiology
Patients. For the purposes of this study, acute myocardial infarction was diagnosed in patients with at least two of the following three criteria: I) a recent episode of retrosternal chest pain characteristic of myocardial ischemia lasting for at least 30 minutes, 2) a transient increase above normal limits of both total creatine kinase (CK) and its MB fraction (12) with the appropriate temporal relation to the 0735-1097/84/$3.00
910
WATERS EL AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
episode of prolonged pain, and 3) Minnesota code criteria (13,14) for definite or probable myocardial infarction accompanied by increasing or decreasing ST elevation, ST depression or T wave inversions. Among 2,000 consecutive patients hospitalized with acute myocardial infarction in the coronary care unit of the Montreal Heart Institute between 1977 and 1982, 77 had undergone coronary artery bypass surgery at least 2 months before admission. Excluded from this study group were three additional patients who had valve replacement or aneurysmectomy in association with bypass grafting. For each study patient, the preceding patient admitted to the coronary care unit with acute myocardial infarction was selected for inclusion in the control group. Identical criteria for the diagnosis of myocardial infarction were used in the control patients and the post-bypass group. Patient management. Cardiac catheterization. Selective coronary arteriography was performed by a percutaneous femoral approach using preformed catheters as previously described (15). Views with cranial angulation were routinely filmed (16). The left ventricular angiogram was filmed in the 30° right anterior oblique view before coronary arteriography. Surgical management. The study patients had undergone bypass surgery between 1970 and 1982, in all but five cases at our hospital. During this 13 year period 4,630 coronary bypass operations were done at our institution. As in other large North American centers, patient selection criteria, anesthetic management and surgical techniques evolved during this time interval. In general, symptomatic patients with stenoses reducing coronary artery diameter by 70% or greater were considered for surgery and all lesions 50% or greater with adequate distal runoff were bypassed. Among the 77 study patients, 33 had triple vessel disease, 22 double vessel disease, 20 single vessel disease and 2 had stenoses less than 70%. The average number of grafts per study patient was 2.4 ± 1.0. Before 1977, anoxic cardiac arrest with intermittent aortic cross-clamping under moderate systemic hypothermia was used; thereafter, standard practice included cold cardioplegic solution, topical and systemic hypothermia. Management in the coronary care unit. Management of patients with suspected myocardial infarction was not influenced by the presence of previous bypass surgery. The electrocardiograms of all patients were recorded at least three times within 24 hours of admission, on days 2 and 3 and at least once between days 7 and 10. In all cases, serum levels of CK and its isoenzymes were measured at regular intervals within the first 72 hours of admission. All patients did not have the same number of serum enzyme determinations due to changes in our standardized protocol during the study period; however, the number of measurements per patient, 5.4 within 72 hours, was similar in the post-bypass and control groups.
lACC Vol. 3. NO.4 April 1984:909-15
Follow-up. All patients were followed up regularly after hospital discharge. Forty-five of the 77 post-bypass patients had coronary arteriography after myocardial infarction, at I month in 23 and later in 22. The mean interval from infarction to arteriography was 4.9 months (range I to 24). Those undergoing arteriography were more likely to have postinfarction angina and less likely to have severe heart failure and were thus not representative of the entire study group. Quantification of infarct size. For each patient peak CK and peak isoenzyme CK-MB were tabulated as enzymatic indexes of infarct size (17). The electrocardiogram showing the most ST elevation in the absence of conduction disturbances was selected to count the number of leads with ST elevation 0.1 mV (I mm) or greater and the sum of the ST elevation in these leads. ST elevation was measured between 0.04 and 0.08 second after the J point, depending on heart rate so as not to impinge on the T wave, and averaged over at least 3 beats for each lead. If ST elevation from a previous infarction persisted, it was not included in the measurement. The limitations of ST segment analysis to quantitate ischemic damage, particularly in relation to therapeutic interventions designed to reduce infarct size, have been described (18). In this study ST elevation was used only as an index of infarct size to compare post-bypass and control groups. A QRS scoring system that estimates infarct size from a standard 12 lead electrocardiogram, as refined by Wagner et al. (19), has been shown to correlate well with both the anatomic extent of infarction (20), postinfarction ejection fraction and infarct size as assessed by thallium-20 I defect (21). The QRS score for all patients was calculated from the electrocardiogram recorded between 7 and 10 days after admission, excluding residual abnormalities from previous infarctions. Statistical analysis. Differences between the post-bypass and control groups were assessed statistically in two ways: I) a matched pair analysis using McNemar's test (22) and the Wilcoxon matched-pairs signed-ranks test (23), and 2) intergroup comparisons using the Student's t test, the Fisher exact test or the chi-square test with Yates' correction where appropriate. All indexes of infarct size were significantly higher (p < 0.000 I) in the control group using either method. However, more intergroup differences in baseline variables attained statistical significance using the chi-square test than McNemar's test. Because these baseline differences may have influenced the results, the p values using the chi-square test are displayed in Table I and in text.
Results The mean interval between coronary bypass surgery and myocardial infarction was 52.8 ± 33.1 months (range 2 to 123). The clinical features of post-bypass patients and the
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911
WATERS ET AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
Table 1. Comparison of Post-Bypass and Control Groups Post-Bypass Patients Clinical characteristics Number of patients Age (mean ± SD) Male/female Previous infarction History of angina History of hypertension Preadmission medication Beta-blocking agents Digitalis Diuretic drugs Long-acting nitrates Assessment of infarct size Maximal CK (IU/liter) Maximal CK-MB Leads with ST elevation Maximal summed ST elevation (mm) QRS score (19) Total patients with old Q waves Developing new Q waves Without new Q waves Total patients without old Q waves Developing new Q waves Without new Q waves
77 53.7 69/8 37 30 19
1.075 175 1.58 3.44 1.64 34
=
atrioventricular; CK
=
creatine kinase; ECG
± 867 ± 198 ± 1.81 ± 482 ± 2.86
21 5 15 15
NS NS NS NS
1.829 342 3.39 8.92 4.43 21 12 9 56 42 14
43 20 23
± ± ± ± ±
1.300 341 2.61 9.57 4.49
< < < < <
13 14
o o
0.004
<
2 2 2 5
13 24
electrocardiographic; NS
=
not significant; p
=
0.001 NS
5 II 10 6
4
0.001 0.001 0.001 0.001 0.001 0.D3 0.006
54 30 21 3
27
control group are compared in Table 1. Control patients were slightly but not significantly older. The control group contained more women (19 versus 8, p = 0.02) than the post-bypass group, probably because only 16% of the patients undergoing bypass surgery at our hospital are women. A previous myocardial infarction had been documented in 21 control patients (27%) compared with 37 post-bypass patients (48%, p = 0.008). The prevalence of angina, hypertension and the use of drugs that might influence infarct size were similar in the two groups before infarction. Assessment of infarct size. By both enzymatic and electrocardiographic criteria, patients with previous bypass surgery had smaller infarcts than control patients. Mean maximal CK in the post-bypass group was 1,075 ± 867 international units (lV)/liter compared with 1,829 ± 1,300 IV/liter in the control group (p < 0.001). Mean maximal CK-MB was 175 ± 198 versus 342 ± 341 IV/liter (p <
28
NS 0.02 0.008 NS NS
27
7 27
=
p Value
77 56.5 ± 9.9 58/19 21
± 8.2
27 8 13 17
Total developing new Q waves Anterior ECG leads Inferior ECG leads Both anterior and inferior Complications Death in hospital Death within 1 year Acute heart failure in hospital Ventricular fibrillation 2nd or 3rd degree A V block Total complications in hospital (no. of patients) AV
Control Patients
< probability; SD
=
0.06 0.06 0.04 NS 0.007 0.001
standard deviation.
0.001). The maximal number of electrocardiographic leads with ST elevation was lower in the post-bypass group, 1.58 ± l.81 compared with 3.39 ± 2.61 (p < 0.001), and maximal summed ST elevation was also lower, 3.44 ± 4.82 versus 8.92 ± 9.57 mm (p < 0.001). The QRS score measured 7 to 10 days after infarction was 1.64 ± 2.86 in the post-bypass group and 4.43 ± 4.49 in the control group (p < 0.001), providing further evidence that post-bypass patients had smaller infarcts. Both groups exhibited a broad range of values for each of these indexes of infarct size and thus overlap widely, despite the highly significant intergroup differences (Fig. I). Role of previous myocardial infarction. More patients in the post-bypass group had preexisting Q waves (34 versus 21, P = 0.03) and patients with preexisting Q waves were less likely to develop new ones (p < 0.00 I). Therefore, subgroups were analyzed to eliminate the possibility that
WATERS EL AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
912
CK max
JACe Vol. 3, No.4 April 1%4:909-15
CK-MB max
8000
QRS SCORE
2000 p< 000 1
20
p
6000
1500
4000
1000
15
10
;.
500
1':' .,
....
.. -. .:1t
",f.' • ...y c.
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• ~,yo
A
CONTROL
POST-BYPASS
CONTROL
POST-BYPASS
.
.. o
c
........,
- - w.::::.:.\:.::s=:I
CONTROL
I
POST-BYPASS
50 p
p
8
40
6
30
20
•
2
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£ +STmax
10
o
.."
5
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4
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• ................. I
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-000:::::::::::::::..I
POST-BYPASS
10
o
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. ......:::. M" ..... 000
·....·::i~·......·-
Figure 1. Patients with previous bypass surgery (POST-BYPASS) had a smaller infarct than control patients, as assessed by peak (max) creatine kinase (CK) and CK-MB (lUlliter) (A), number of leads with ST elevation ( t ) and maximal summed ST elevation (E t ST max) (B) and QRS score as measured on a standard electrocardiogram 7 to 10 days after infarction (C) (19). The black squares indicate the mean value for each group .
.... ....
...
...:::.
-"WN·::fiNA'lo"'-
CONTROL
the observed differences in infarct size were related to the higher prevalence of previous infarction in the post-bypass group. Both in patients with and without preexisting Q waves, new Q waves developed more often in the control group than in the post-bypass group, Only 7 of 34 post-bypass patients with old Q waves developed new ones, compared with 12 of21 control patients with old Q waves (p = 0.006). Among patients without old Q waves, only 20 of 43 in the post-bypass group compared with 42 of 56 control patients developed new Q waves (p = 0.004). Patients with old Q waves had lower serum peak CK values than those without Q waves in the control group (p = 0,005) but not in the post-bypass group (p > 0,1), In patients with old Q waves, maximal CK value was higher in control than in post-bypass patients, 1,318 ± 686 versus 910 ± 662 IU/liter (p = 0.03). Similarly, in those without preexisting Q waves, maximal CK value was higher in control patients (2,020 ± 1,424 versus 1,206 ± 987 IV/liter,
POST-BYPASS
p = 0.001). Thus, the higher prevalence of previous infarction in the post-bypass group does not account for the observed differences in infarct size between the two groups. Subgroup analysis also showed that the higher proportion of women in the control group was not related to the differences. The site of new Q waves, anterior versus inferior, was not significantly different in the two groups. Complications. Post-bypass patients might have been expected to have more complications because more of them had had a previous infarction; however, the opposite occurred (Table I). Five control patients but none of the postbypass patients died in the hospital (p = 0.06). Within I year of admission 11 control patients and 4 post-bypass patients had died (p = 0.06). Acute heart failure in the hospital, defined as heart failure severe enough to require intravenous vasodilator or inotropic drugs, occurred in 10 control and 2 post-bypass patients (p = 0.04). Thirteen control and two post-bypass patients had second or third degree atrioventricular (AV) block (p = 0.007). Overall,
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WATERS ET AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
24 control and 5 post-bypass patients experienced complications (death, acute heart failure, ventricular fibrillation, second or third degree AV block) in the hospital (p < 0.001). Angiographic findings after infarction. After myocardial infarction, 45 of the 77 post-bypass patients underwent coronary arteriography. Although these 45 patients were not representative of the entire group, their angiographic data were examined in search of potential explanations for smaller infarct size in the post-bypass patients. All grafts were occluded in 10 cases, all grafts were patent in 14 and both patent and occluded grafts were present in 21. The site of infarction could be localized from the electrocardiogram in 27 of the 45 cases; in the other 18 neither ST elevation nor new Q waves were recorded and the electrocardiographic site of infarction was classified as unknown. Probable causes ofmyocardial infarction (Table 2). Both the bypass graft and the coronary artery that it supplied were totally occluded in 24 cases. In 16 of these 24 patients, the distribution of this vessel corresponded to the electrocardiographic site of infarction and in the other 8 patients the infarct could not be localized electrocardiographically. In six patients, either the bypass graft was occluded and the native artery was stenotic or the artery was occluded and the graft stenotic. In nine cases, either an occlusion or progression of a less than 50% lesion to 70% or greater had developed in an artery that had not been bypassed. Infarction was caused by disease progression distal to a patent graft in three cases. Finally, in three patients whose infarct could not be localized electrocardiographically, more than one of these three situations were present (graft or artery occluded with the other stenotic, progression in a nonbypassed artery, progression distal to a patent graft) and the likeliest cause of infarction could not be ascertained.
Table 2, Angiographic Findings After Infarction in Post-Bypass Group Infarct Site Probable Cause of Infarction
Known
Unknown
Total
A. Graft and bypassed artery occluded B. Graft or bypassed artery occluded C. Progression* in nonbypassed artery D. Progression* distal to patent graft E. > I of mechanisms B to D possible Total
16
8
24
4 5
2 4
6 9
2
1 3
3
0
27
18
45
3
*Progression is defined as an increase in a lesion to 100% or from less than 50% to 70% or greater in a nonbypassed artery or distal to the anastomosis in a bypassed artery.
913
Patients with an occluded graft and artery to the infarct zone might be expected to have a larger infarct than patients with other causes for post-bypass infarction. Thus, mean maximal CK level in the 24 patients with graft and arterial occlusion was 1,288 ± 1,084 versus 598 ± 506 IU/liter in the 21 patients with other causes (p = 0.008). A similar difference was found for CK-MB isoenzyme (p = 0.009) but the differences for the electrocardiographic indexes of infarct size did not attain statistical significance, probably because many of these patients had only minimal electrocardiographic changes. Control group. After myocardial infarction, 35 patients in the control group underwent coronary arteriography. As with the bypass group, the patients undergoing arteriography are unrepresentative of the entire sample. One of the 35 patients had no coronary lesions 70% or greater, 12 had one vessel disease, 15 had double vessel and 7 had triple vessel disease. All but two patients had segmental left ventricular contraction abnormalities corresponding to the territory of infarction.
Discussion Among patients hospitalized with acute myocardial infarction, those who have previously undergone coronary bypass surgery represent a small but rapidly growing subgroup whose characteristics have not been defined. This study compared a group of post-bypass and control patients with acute myocardial infarction; the post-bypass group contained fewer women and more patients with previous infarction. The interval from surgery to myocardial infarction ranged from 2 months to 12 years, averaging about 41f2 years. Patients with infarction within 2 months of surgery were prospectively excluded so that the acute effects of surgery would not be a complicating factor. Both enzymatic and electrocardiographic assessments of infarct size consistently demonstrated statistically significant differences: post-bypass patients had a smaller infarct than control patients. Subgroup analysis showed that this finding was not due to baseline clinical differences in the two groups. Postbypass patients had fewer complications. Five of the 77 control patients but none of the 77 post-bypass patients died in the hospital. Limitations of the study. Bias in the surgical group. Do post-bypass patients really have a smaller infarct with fewer complications, or could other factors account for the results of this study? Myocardial infarction may be silent, unrecognized or cause death before admission to a coronary care unit. Because of their previous medical experience, postbypass patients with a small infarct may have been more likely to seek medical attention and gain admission than patients without previous surgery, thus biasing our results. Although we admit all patients with suspected or proven infarction irrespective of their medical history, we cannot
914
WATERS EL AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
eliminate the possibility that patient self-selection influenced our results. Methods of estimating infarct size. A second limitation of this study involves the methods used to estimate infarct size (17-19). To calculate total serum CK release accurately in an individual patient requires more samples than were obtained in this study. However, peak CK correlates well with total CK release, the number of samples per patient were similar in the two groups, the size of the groups was large and the mean difference in peak CK between the groups was also large; thus, the conclusion that CK infarct size was smaller in the post-bypass group is most likely valid. Serum CK may originate from noncardiac sources; however, measurements of the cardiac MB isoenzyme yielded similar results. The electrocardiographic assessment of infarct size presents theoretical and practical difficulties (J8). The number of leads with ST elevation and maximal summed ST elevation on a standard 12 lead electrocardiogram are insensitive and inaccurate indexes of myocardial ischemia. However, these data were gathered and measured in both groups in an identical way and yielded results that are both internally consistent and consistent with the CK and CK-MB results. Other techniques to estimate infarct size were not used in this study. For example, if patients with previous infarction were excluded, radionuclide or contrast ventriculography could have provided an accurate comparison of the extent of segmental left ventricular dysfunction in the two groups. Absence of complete angiographic data. A final limitation of the study is the absence of angiographic data after infarction in 1J:J of the post-bypass patients. In addition, the delay between infarction and angiography allows for recanalization of arteries that may have been totally occluded during the acute phase (3); thus, the reason for infarction may not always be apparent after reviewing the angiogram, particularly if the site of infarction could not be localized by electrocardiographic or other methods. Causes of infarction in post-bypass patients. During the early phase of acute myocardial infarction most patients will exhibit complete coronary occlusion at arteriography; for example, in the study of DeWood et al. (3), this finding was present in 110 of 126 patients evaluated within 4 hours of the onset of symptoms. In contrast, perioperative myocardial infarction is often associated with a patent graft to the infarct zone as assessed by angiography (8) or at autopsy (9). Reperfusion injury (9) or coronary spasm (24) may account for some of these infarcts. In this study, angiographic data are available for 45 patients with infarction at least 2 months after bypass surgery. In 24 of the 45 patients, both the artery and bypass graft to the infarct zone were occluded. This situation may be analogous to a complete arterial obstruction in a patient without
lACC Vol. 3. No.4 April J984:909- J5
coronary bypass, but several circumstances can be envisaged where the surgically treated patient would have an advantage in terms of infarct size. A completely occluded artery proximal to a small infarct, often with good collateral vessels, is frequently bypassed, in part, to preserve residual myocardial function; in such a case, subsequent graft occlusion would be likely to produce only a minimal amount of new necrosis. Second, if coronary occlusion is an abrupt event, a patient who had coronary bypass may be more likely to have time to develop collateral vessels because the occlusion occurs in two stages (graft and artery). Third, a patient with two conduits to a myocardial segment may be more likely to have two small infarcts instead of one large one; for example, a proximal left anterior descending coronary occlusion might obstruct a septal or diagonal branch and produce a small infarct despite a patent graft to the distal artery. Subsequently, the graft might become blocked leading to complete infarction of the left anterior descending niyocardial territory. This study provides no firm data to support these speculations. Peak serum CK was higher in control patients (l,829 ± 1,300 IU/liter), than in the 24 patients with graft and arterial occlusion (l,288 ± 1,084 IU/liter) (p = 0.04), but such a comparison may be biased because not all postbypass patients underwent arteriography. The other 2 J post-bypass patients who underwent arteriography could be classified into three groups: I) those with an occluded graft and stenotic artery, or vice-versa, 2) those with disease progression in a nonbypassed artery, and 3) those with disease progression distal to a graft. Peak CK and CK-MB levels were significantly lower in these 21 patients than in the 24 with a completely obstructed graft and artery. The smaller infarcts in these subgroups may result from different mechanisms. In patients with either the native artery or graft incompletely obstructed, infarct size may have been limited by residual perfusion (unless complete obstruction had been present and recanalization later occurred). Arteries that are small or perfuse akinetic areas are often not bypassed; infarcts due to disease in such vessels would tend to be small. Similarly, obstruction distal to the site of a graft anastomosis would cause less necrosis than if the artery were blocked more proximally. Implications. Progressive disease in nonbypassed coronary arteries, distal to anastomoses and within bypass grafts themselves are commonly observed from 5 to 12 years after surgery (25,26). These changes correlate with the recurrence of angina and often cause no myocardial necrosis (25,26). The patterns of coronary perfusion in patients with angina or myocardial infarction after bypass surgery are complex and difficult to classify because many variables are involved (the site, severity and number of lesions in each native artery and graft, the number of grafts, the sites of anastomoses and the relation between the sites of graft and arterial dis-
WATERS ET AL. MYOCARDIAL INFARCTION AFTER BYPASS SURGERY
lACC Vol. 3. No.4 April 1984:909-15
ease). Despite this diversity, this study indicates that in patients with previous bypass surgery, myocardial infarcts tends to be smaller and associated with fewer complications. The reasons for this difference will be better understood when coronary arteriography is performed soon after infarction in a large series of patients with previous bypass surgery and of control patients.
915
infarction: late clinical course after coronary artery bypass surgery Circulation 1982;66: 1185-9. 12. Delva E. Maille IG, Solymoss BC, Chabot M, Grondin CM, Bourassa MG. Evaluation of myocardial damage during coronary artery grafting with serial determinations of serum CPK-MB isoenzyme. 1 Thorac Cardiovasc Surg 1978;75:467-75. 13. Blackburn H. Keys A, Simonson E. Rautaharju P, Punsar S. The electrocardiogram in population studies. A classification system. Circulation 1960:21:1160-75. 14. Rose GA. Blackburn H. Cardiovascular Survey Methods. Geneva: World Health Organization Monograph 56, 1968.
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21. DePace NL. Iskandrian AS. Hakki A, Kane SA, Segal BL. Use of QRS scoring and thallium-20 I scintigraphy to assess left ventricular function after myocardial infarction. Am 1 Cardiol 1982;50: 1262-8. 22. McNemar Q. Note on the sampling error of the difference between correlated proportions or percentages. Psychometrika 1947; 12: 153-7. 23. Siegel S. Non-parametric statistics for the behavioral sciences. New York: McGraw-Hili. 1956:75-81. 24. Buxton AE. Hirshfeld lW Jr. Untereker W1. et a!. Perioperative coronary arterial spasm: long-term follow-up. Am 1 Cardiol 1982;50:444-51. 25. Campeau L. Lesperance 1. Hermann 1, Corbara F, Grondin CM, Bourassa MG. Loss of improvement of angina between I and 7 years after aortocoronary bypass surgery. Correlations with changes in vein grafts and in coronary arteries. Circulation 1979;60(suppl 1):1-1-5. 26. Bourassa MG. Campeau L. Lesperance 1, Grondin CM. Changes in grafts and coronary arteries after saphenous vein aortocoronary bypass surgcry: rcsults at repeat angiography. Circulation 1982:65(suppl 11):1190-7.