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Ann Thorac Surg 1998;65:17-23
© 1998 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Should Angiographically Disease-Free Saphenous Vein Grafts Be Replaced at the Time of Redo Coronary Artery Bypass Grafting?

Section of Cardiothoracic Surgery, Yale University School of Medicine, New Haven, Connecticut, USA
Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut, USA

Dr Elefteriades, 121 FMB, 333 Cedar St, New Haven, CT 06437.

Presented at the Thirty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Feb 3–5, 1997.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Background. Controversy exists regarding the management of angiographically disease-free saphenous vein grafts at the time of redo coronary artery bypass grafting (CABG). Some authorities favor replacement of these disease-free grafts, arguing that occlusion is likely in the near future. Others believe that these grafts are "biologically privileged" and should not be replaced.

Methods. One hundred thirty-two consecutive patients (113 men, 19 women, aged 46 to 88 years, mean 67 years) underwent redo revascularization with one or more angiographically disease-free saphenous vein grafts at the time of redo CABG. Thirty-six patients had the disease-free grafts replaced (R) and 96 did not (NR). The mean interval from the first CABG was 9.25 years.

Results. Surgical mortality was comparable in the NR and R groups (5 of 96 or 5.2% versus 3 of 36 or 8.3%, respectively; p < 0.5). Survival at 1 and 3 years was higher in the NR group than the R group (98% versus 80%, and 95% vs. 66% respectively; p < 0.0001). Late myocardial infarction was less common in the NR group than in the R group (12 of 91 or 12.9% versus 12 of 33 or 36.4%; p < 0.003). Recurrent angina was less common in the NR than in the R group (21 of 91 or 23.1% versus 15 of 33 or 45.5%; p < 0.015). Cardiac hospitalization was required less commonly in the NR than in the R group (11 of 91 or 12.1% versus 12 of 33 or 36.4%; p < 0.002). In nondiseased grafts undergoing angiographic evaluation late after redo CABG, rate of new stenosis was lower in NR grafts than in R grafts (2 of 12 or 16.7% versus 2 of 3 or 66.7%; p < 0.05).

Conclusions. With a conservative approach that does not replace nondiseased saphenous vein grafts at redo CABG (1) there is no increase in operative mortality, (2) good late survival is obtained, (3) clinical ischemia related to the NR saphenous vein grafts is uncommon, and (4) NR grafts continue to be patent. We conclude that disease-free vein grafts may not require routine replacement at redo CABG. A randomized study is required for definitive resolution.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Reoperations for coronary artery bypass grafting (CABG) are an increasingly common clinical problem confronting the cardiac surgeon, currently constituting 9% to 11% of coronary revascularization procedures in major institutions [1][2]. Progression of the arteriosclerotic process in the native coronary circulation or in the previously inserted saphenous vein grafts (SVGs) is responsible for the recurrent symptoms that underlie the presentation for redo CABG. Prior studies indicate that 12% to 20% of vein grafts will close by 1 year. For the next 4 to 5 years, a 2% to 4% annual closure rate is incurred. Between the fifth to tenth year postoperatively, a doubly high yearly closure rate, 4% to 8%, is realized. By the tenth postoperative year, more than 50% of SVGs have become occluded by arteriosclerotic disease [3][4][5][6].

At redo CABG, SVGs that are occluded or severely diseased should be replaced, if feasible. However, controversy exists regarding the management of disease-free SVGs. Some authorities believe that these grafts are likely to occlude and therefore need to be redone [7]. Others suggest that these disease-free grafts patent late after construction are "biologically privileged" and should not be replaced [8]. Very little direct evidence is available in the literature on the natural history of these disease-free SVGs. This controversy remains unanswered.

This report looks at the clinical outcome in a relatively large group of patients who presented for redo CABG with one or more angiographically disease-free SVGs. Clinical results are compared in those patients who had the disease-free grafts replaced and those who did not.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Six hundred fifty patients underwent redo CABG between 1987 and 1995 at Yale-New Haven Hospital. Coronary arteriography had been performed in all patients before redo CABG. One hundred thirty-two patients had at least one angiographically disease-free SVG. "Disease-free SVG" was defined as one having a completely patent lumen without any stenoses or luminal irregularities demonstrated angiographically. Those patients undergoing redo CABG with at least one angiographically disease-free SVG are the subject of the present investigation.

The mean age of these patients was 67 years (range 46 to 88 years). There were 113 men (85.6%) and 19 women (14.4%). The number of grafts placed at the previous operation ranged from 1 to 5 (mean, 3.25). The mean length of time from the prior CABG was 9.25 years (range, 0.5 to 18 years; median, 8.4 years). Recurrent angina pectoris was the indication for operation in the majority of patients. Four patients underwent surgery for mitral valve replacement for mitral regurgitation and 3 patients had redo CABG in conjunction with this procedure. Similarly, 5 patients required reoperation for aortic valve replacement and associated CABG. One patient underwent left ventricular aneurysmectomy in conjunction with redo CABG. For 11 of the patients, the redo CABG studied was their third bypass procedure. Forty-six patients had urgent or emergent operation, one of which was performed after a failed angioplasty procedure. Three patients underwent coronary endarterectomy during the redo CABG procedure (one of the right coronary artery and two of the circumflex). Two patients underwent simultaneous placement of implantable cardioverter-defibrillator hardware for inducible ventricular tachycardia at the time of redo CABG. Of the 132 patients, 20 patients had two disease-free SVGs, 2 patients had three disease-free SVGs, and the remainder had a single disease-free graft at the time of redo CABG.

All redo CABG operations were performed using systemic hypothermia (26° to 30°C) and nonpulsatile cardiopulmonary bypass. Cold hyperkalemic crystalloid or blood cardioplegia was used for myocardial protection in all cases. Retrograde cardioplegia was used in addition to antegrade cardioplegia in many patients who had their redo CABG performed in the 1990s.

Thirty-six patients (27.3%) had the disease-free graft(s) replaced, all with saphenous veins. No specimens of the nondiseased grafts were sent intraoperatively for pathologic analysis. The disease-free grafts in the remaining 96 patients (72.7%) were not replaced. The decision to replace or not to replace was made at the discretion of the operating surgeon. The rate of replacement of nondiseased SVGs by specific surgeons was 5%, 40%, and 44% for the 3 surgeons who performed 20 or more procedures and varied from 0% to 5% in 8 other surgeons who each performed 10 or fewer procedures. In the nonreplaced group, only diseased or occluded SVGs were replaced at redo CABG. The distribution of the nondiseased grafts was as follows: The total number of nondiseased grafts was 156. Twenty-six (16.6%) were in the left anterior descending coronary artery territory, of which 50% were replaced. Fifty-one grafts (32.6%) were in the circumflex artery territory, of which 29.4% were replaced. Fifty-five grafts (35.2%) were in the right coronary artery territory, of which 27.2% were replaced. Twenty-four grafts (15.3%) were on the diagonal branch of the left anterior descending coronary artery and 12.5% were replaced. None of the patients in this study had their nondiseased SVGs replaced with an arterial conduit. However, the internal mammary artery was used to replace the diseased or occluded grafts in other distributions in 64 patients, 19 patients (52.7%) in the replaced group and 45 patients (46.8%) in the nonreplaced group. Eight patients had the internal mammary artery used during primary CABG, of which one internal mammary artery graft was found closed at the time of redo CABG.

Clinical characteristics of the replaced and nonreplaced groups are presented in Table 1. There were no statistically significant differences when these two groups were compared with respect to age, sex, ejection fraction, time to redo CABG, urgency status, angina class, cardiopulmonary bypass time, and the comorbidities of hypertension and diabetes. More patients in the nonreplaced group than in the replaced group underwent associated procedures—mitral valve replacement, aortic valve replacement, left ventricular aneurysmectomy, and coronary endarterectomy. Both patients requiring placement of an implantable cardioverter-defibrillator were also in the nonreplaced group. As would be expected from the definition of the groups, the mean number of new grafts performed was higher in the group that had the nondiseased grafts replaced (2.5 grafts/patient) than in the nonreplaced group (1.8 grafts/patient).

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
The clinical outcome of the replaced and nonreplaced groups was analyzed and compared for the parameters of operative mortality, long-term survival, freedom from angina, freedom from myocardial infarction, and freedom from cardiac readmissions to the hospital (Table 2). In addition, angiographic data on patients who underwent yet another cardiac catheterization late after redo CABG were analyzed to determine patency of the previously disease-free SVG (Table 3).

Survival
Patients were followed up for a mean of 61.2 months after redo CABG (range, 0.5 to 119.2 months). Mean follow-up was 51.1 months for the replaced group and 67.6 months for the nonreplaced group. Examination of the long-term survival in the two groups revealed a significantly better outlook for the nonreplaced versus the replaced group. Survival was 98%, 95%, and 87% at 1, 3, and 5 years for the nonreplaced group and 80%, 66%, and 66% for the replaced group. The difference in survival curves was significant by the log-rank test (p = 0.0001) (Fig 1). Cardiac deaths were related to myocardial infarction (52.6%), arrhythmia (31.6%), and congestive heart failure (15.8%). When noncardiac deaths were excluded, a significantly improved survival was again evident for the nonreplaced group, 98%, 95%, and 92%, respectively at 1, 3, and 5 years, compared with 82%, 69%, and 69% (Fig 2). Multivariate analysis indicated that only sex and replacement versus nonreplacement were found to be significant predictors of survival. Specific results of multivariate analysis are presented in Table 4.

View larger version (14K): [in this window] [in a new window]   Survival of replaced and nonreplaced groups.

View larger version (15K): [in this window] [in a new window]   Survival (excluding noncardiac deaths) comparison of replaced and nonreplaced groups.

Myocardial Infarction
Late myocardial infarction (including both Q-wave and non–Q-wave events) was more common in the replaced than in the nonreplaced group, 36.4% versus 13.2%. This difference was statistically significant (p < 0.003).

Hospital Readmission
When ischemia-related hospitalizations were compared, a significantly higher rate was found in the replaced group (36.4% for the duration of follow-up) compared with the nonreplaced group (12.1%). This difference was statistically significant (p < 0.002). Ischemia-related admissions included patients with angina to rule out myocardial infarction (4 patients), patients with non–Q-wave myocardial infarction (7 patients), and patients with Q-wave myocardial infarction (12 patients). The location of ischemic event could be determined in 12 patients, 7 in the replaced group, (one of which was clearly related to the SVG in question) and 5 in the nonreplaced group, (one of which was clearly related to the SVG in question). There were no additional coronary bypass procedures performed during long-term follow-up on any patients after the bypass procedure evaluated in this report.

Angiography
In addition to the clinical comparisons made above, angiographic follow-up was available in a set of patients catheterized yet again for symptoms late after redo CABG. Fifteen patients underwent such late catheterization. Of the 15 replaced group patients in whom recurrent angina developed, 3 underwent repeat catheterization; two of the three replacement grafts studied (66.7%) at 1 year and 4 years, respectively, after redo CABG manifested severe restenosis. Twelve of the 21 nonreplaced group patients with angina underwent recatheterization at 4 to 84 months (mean 27.8 months) after redo CABG, revealing restenosis in only 2 of the 12 grafts (16.7%) that had been left alone at the time of redo CABG. These two restenoses occurred at 4 and 7 years after redo CABG in the nonreplaced group (Table 3). All other nonreplaced grafts studied continued to be free of disease. These follow-up arteriograms were performed at 12 to 48 months after redo CABG in replaced group patients and 4 to 84 months in nonreplaced group patients.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Whether nondiseased SVGs should be replaced at the time of redo CABG is an important fundamental question. Redo revascularization procedures constitute an increasingly large proportion of coronary artery bypass operations performed [1][2]. Yet, there has been a relative void of scientific information in the literature on the appropriate method of handling disease-free SVGs at the time of redo CABG [8]. The present investigation was undertaken to provide some direct clinical information on this issue.

Research in basic vascular biology has improved our understanding of the etiology and pathogenesis of native arteriosclerotic arterial lesions. However, a unique vascular biology is obtained when a vein graft is used as a conduit to bypass arterial segments [9][10][11]. Research into the unique biology of vein grafts is leading to increased understanding of the accelerated arteriosclerosis of such grafts. The process of disease progression in vein grafts can be divided into somewhat discrete phenomena based on the time since graft placement [12].

Early changes are related to endothelial injury, and can even lead to early graft closure (within 1 month). The endothelium normally maintains a precise balance between anticoagulation and procoagulation and between vasoreactive and vasorelaxant mechanisms, as well as serving an immune function [11]. Endothelial damage can occur during harvesting from direct mechanical trauma or over-distention, from disruption of vasa vasorum, and from prolonged hypothermic storage [9]. Activation of platelets and leukocytes and changes in immune function induced by cardiopulmonary bypass may also contribute to endothelial injury.

Between 1 month and 1 year, vein graft closure has been attributed most commonly to fibrointimal hyperplasia with decreased intimal cellularity, replacement of medial smooth muscle cells by fibrous tissue, and adventitial thickening [4]. These changes, which can continue for up to 5 years postoperatively, render the vein graft rigid and thick [13]. These changes are thought to be related to exposure of the vein wall to arterial pressure. Other etiologic mechanisms postulated include ischemic injury [14], effects of flow velocity [15] and shear stress, vein–artery size mismatch [16], and turbulent flow patterns. Some have suggested that a regulatory process may be active that ideally would terminate the fibrointimal hyperplastic process when the vein lumen matched that of the coronary artery, thus limiting flow turbulence and shear stress [17][18][19].

Arteriosclerosis is a third process that can be observed as early as 3 to 6 months postoperatively. This process then merges with late accelerated vein graft arteriosclerosis. By 3 years, almost one third of SVGs have histopathologic findings of arteriosclerosis, and by 6 years almost 15% [20][21] of patent vein grafts show significant arteriosclerotic change angiographically. By 10 years, 50% of vein grafts that were previously patent have occluded because of accelerated vein graft arteriosclerosis [22]. The accelerated rate of arteriosclerotic disease in vein grafts has been attributed to physiologic factors [23][24][25] like turbulence, flow velocity, and shear stress, as well as to biochemical factors such as changes in lipid metabolism [26][27][28].

Whatever the exact mechanisms of these processes leading to early or late SVG disease, the vein graft that is angiographically disease-free late after coronary bypass grafting has already successfully passed all these hurdles. This is the basis on which proponents of leaving alone disease-free grafts have postulated that these disease-free grafts are in some way biologically privileged. Their replacements, if performed, still need to pass all the biologic vascular hurdles and may not prove to be similarly biologically privileged. In particular, by the time of redo CABG, the patients are older, their saphenous veins are more diseased, and the coronary arteries may present poorer runoff and exacerbate vein–artery mismatch and its biologic consequences.

The present investigation demonstrated that there is no advantage in early surgical mortality attendant to routine replacement of disease-free grafts. The present investigation also demonstrated that in all parameters evaluated—long-term survival, freedom from angina, freedom from myocardial infarction, and freedom from cardiac hospital admission—the advantage lay with the patients who did not have their disease-free grafts replaced. All these differences in follow-up were statistically significant.

We were surprised to find data aligned so strongly against routine replacement of disease-free grafts. These findings may be explained in part by the fact that the old disease-free grafts have already successfully overcome the biologic hurdles that face the new grafts used in routine replacement, including (1) the early technical factors, (2) fibrointimal hyperplasia, (3) the remodeling process, and (4) the late accelerated arteriosclerotic process. That is, the advantages of the nonreplaced group may reflect the biologic privilege of the naturally selected disease-free grafts. The satisfactory graft survival for these old, disease-free grafts realized in (limited) angiographic follow-up also argues in favor of not routinely replacing these grafts.

A limitation of the present study is that it is retrospective and nonrandomized. A prospective, randomized study would be required for definitive resolution of this question. Although a prospective, randomized study would be ideal, it would likely be difficult to dictate to the surgeon his posture on graft replacement in individual patients. Another limitation of the study is the limited number of patients who underwent late angiography after redo CABG. Repeat angiography is costly and not without risk, and its routine performance is difficult to justify for an individual asymptomatic patient. The present study was conceived primarily as a clinical (not angiographic) study, for which its statistical power was adequate to allow multiple statistically significant conclusions. Also, the relatively small number of patients in the replaced group makes possible an exaggeration of the true negative effects of replacement by a small number of adverse events.

Our conclusions are as follows. The information from the present study indicates that not replacing disease-free SVGs at the time of redo CABG confers no disadvantage in terms of operative survival, angina relief, incidence of late myocardial infarction, cardiac readmission, or long-term survival. In fact, for the categories of sustained freedom from angina, incidence of late myocardial infarction or cardiac readmission, and long-term survival, the nonreplacement of disease-free grafts conferred a significant advantage. The limited angiographic follow-up data available late after redo CABG suggests that the nonreplaced grafts satisfactorily stood the test of time and may indeed be biologically privileged in their adaptation as arterial conduits.

The data from the present study suggest that routine replacement of angiographically disease-free SVGs at the time of redo CABG may not be necessary. Randomized studies are warranted.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
This article has been selected for the open discussion forum on the STS Web site: http://www.sts.org/annals

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 

1. Pelletier LC The saphenous vein graft: what have we learned from the past 25 years?. In: Carrier M, Pelletier LC, eds. Conduits for myocardial revascularization. Austin, TX: R. G. Landes, 1993:3-33.
2. Cosgrove DM, Loop FD, Lytle BW, et al. Predictors of reoperation after myocardial revascularization. J Thorac Cardiovasc Surg 1986;92:811-821.[Abstract]
3. Grondin CM, Lesperance J, Dourassa MG, et al. Serial angiographic evaluation in 60 consecutive patients with aortocoronary artery vein grafts, 2 weeks, 1 year and 3 years after operation. J Thorac Cardiovasc Surg 1974;67:1-6.[Medline]
4. FitzGibbon GM, Leach AJ, Keon WJ, Burton JR, Kafka HP Coronary bypass graft fate: angiographic study of 1,179 vein grafts early, one year and five years after operation. J Thorac Cardiovasc Surg 1986;91:773-778.[Abstract]
5. Grondin CM, Lesperance J, Solymoss BC, et al. Atherosclerotic changes in coronary grafts six years after operation. J Thorac Cardiovasc Surgery 1979;77:24-31.[Medline]
6. Grondin CM, Campaeu L, Lesperance J, et al. Comparison of late changes in internal mammary artery and saphenous vein grafts in two consecutive series of patients 10 years after operation. Circulation 1984;70(Suppl 1):208-212.
7. Marshall WG, Jr, Saffitz J, Kouchoukos NT, et al. Management during reoperation of aortocoronary saphenous vein grafts with minimal atherosclerosis by angiography. Ann Thorac Surg 1986;42:163-167.[Abstract]
8. Grondin C The removal of still functioning albeit old grafts: not in our genes. Ann Thorac Surg 1986;42:122-123.[Medline]
9. Cox JL, Chiasson DA, Gotlieb AL Stranger in a strange land: the pathogenesis of saphenous vein graft stenosis with emphasis on structural and functional differences between veins and arteries. Prog Cardiovasc Dis 1991;34:45-68.[Medline]
10. Simionescu M, Simionescu N, Palade GE Sequential differentiation of cell junctions in the vascular endothelium: arteries and veins. J Cell Biol 1976;68:705-723.[Abstract/Free Full Text]
11. Palumbo JD, Blackburn GL, Forse RM Collective review: endothelial cell factors and response to injury. Surg Gynecol Obstet 1991;173:505-518.[Medline]
12. Bourassa MC, Campeau L, Lesperance J, et al. Changes in grafts and coronary arteries after saphenous vein aortocoronary bypass surgery. Results at repeat angiography. Circulation 1982;65(Suppl 2):90-97.[Abstract]
13. Chesebro JM, Fuster V Platelet inhibitor drugs before and after coronary artery bypass surgery and coronary angioplasty. The basis of their use, data from animal studies, clinical trial data and current recommendations. Cardiology 1986;73:292-305.[Medline]
14. Virmani R, Atkinson JB, Forman MB Aortocoronary saphenous vein bypass grafts. Cardiovasc Clin 1988;18:41-59.[Medline]
15. Grondin CM, Lepage A, Castonguay Y, et al. Aortocoronary venous bypass grafts: intimal blood flow through the graft and early post operative patency [Abstract]. Circulation 1970;52(Suppl 3):106.
16. Brody WR, Kosek JC, Angell WW Changes in vein grafts following aortocoronary bypass induced by pressure and ischemia. J Thorac Cardiovasc Surgery 1972;64:846-854.
17. Rittgers SE, Karayannacos PE, Guy JF, et al. Velocity distribution and intimal proliferation in autologous vein grafts in dogs. Circ Res 1978;42:792-801.[Free Full Text]
18. Zwolak RM, Adams MC, Clowes AW Kinetics of vein graft hyperplasia: association with tangential stress. J Vasc Surg 1987;5:126-136.[Medline]
19. Barboriah J, Pintar K, Korns ME Atherosclerosis in aortocoronary vein grafts. Lancet 1974;2:621-624.[Medline]
20. Grondin GM Graft disease in patients with coronary bypass grafting. Why does it start? Where do we stop?. J Thorac Cardiovasc Surg 1986;92:323-329.[Medline]
21. Caro CG, Fitzgerald JM, Schroter RC Atheroma and arterial wall shear: observation, correlation and proposal of a shear dependent mass transfer mechanism for atherogenesis. Proc R Soc Lond (Biol) 1971;177:109-159.[Medline]
22. Fuchs JCA, Mitchner JS, Hagen PO Post-operative changes in autologous vein grafts. Ann Surg 1978;188:1-15.[Medline]
23. Mustard JF, Packham MA, Kinlough-Rathbone RL Platelets, blood flow and the vessel wall. Circulation 1990;81(Suppl 1):124-127.
24. Fox JA, Hugh AE Localization of atheroma: a theory based on boundary layer separation. Br Heart J 1966;28:388-399.[Free Full Text]
25. Stein PO, Sabbah HN Measured turbulence and its effect on thrombus formation. Circ Res 1974;35:608-614.[Abstract/Free Full Text]
26. Cushing GL, Ganbaty JW, Nava ML, et al. Quantitation and localization of apoliproproteins (a) and (b) in coronary artery bypass vein grafts resected at reoperation. Arteriosclerosis 1989;9:593-603.[Abstract/Free Full Text]
27. Fox MH, Grachow HW, Barboriah J, et al. Risk factors among patients undergoing repeat aortocoronary bypass procedures. J Thorac Cardiovasc Surg 1987;93:56-61.[Abstract]
28. Buckley BH, Hutchings GM Acclerated atherosclerosis: a morphologic study of 97 saphenous vein coronary artery bypass grafts. Circulation 1977;55:163-169.[Abstract/Free Full Text]

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