Coronary artery reoperations are more complicated than primary operations. Patients undergoing reoperations have distinct, more dangerous pathologies; reoperations are technically more difficult to perform; and the risks are greater.^1-12 Vein graft atherosclerosis, present in most reoperative candidates, is a unique and dangerous lesion. Reoperative candidates commonly have severe and diffuse native-vessel distal coronary artery disease (CAD), a problem that has had the time to develop only because these patients did not die from their original proximal coronary artery lesions. Aortic and noncardiac atherosclerosis are also often far advanced in many reoperative candidates. Some technical hazards, including the presence of patent arterial grafts and sternal reentry, are unique to reoperations, and others, such as lack of bypass conduits and difficult coronary artery exposure, are common.

After a primary bypass operation, the likelihood of a patient undergoing a reoperation depends on patient-related variables, primary operation-related variables, adherence to strict medical control of risk factors for disease progression after bypass surgery, the possibility of alternative treatments, physician opinion about the feasibility of reoperation, and time. Studies from the Cleveland Clinic demonstrated a cumulative incidence of reoperation of 3% by 5 years, 10% by 10 years, and 25% by 20 postoperative years¹³ (Fig. 24-1). Factors associated statistically with an increased likelihood of reoperation have been variables predicting a favorable long-term survival (eg, young age, normal left ventricular function [LVF], and single- or double-vessel disease), variables designating an imperfect primary operation (eg, no internal thoracic artery [ITA] graft and incomplete revascularization), and symptom status (eg, class III or IV symptoms at primary operation). Young age at primary operation and incomplete revascularization are also markers of a severe atherogenic diathesis.

Over recent decades the proportion of isolated coronary artery operations that are reoperations has decreased. In 1990, about 37% of coronary artery revascularization operations were reoperative interventions, whereas in 2002 this figure was 30%¹⁴ (Fig. 24-2). Compared to that year, a much more dramatic decrease in reoperative coronary bypass surgery occurred during the most recent decade, with reoperative procedures representing only 4.6% of all isolated coronary bypass operations. This decrease is related in part to the more aggressive use of coronary artery interventions for patients with previous bypass surgery and probably to more effective risk factor control. Also, surgery has changed in directions that will decrease the rate of reoperation. Use of the left internal thoracic artery (LITA) to graft the left anterior descending (LAD) coronary artery decreases the risk of reoperation compared with the strategy of using only vein grafts, and the LITA-LAD graft has become a standard part of operations for coronary artery revascularization.¹⁵ Furthermore, it now appears that use of bilateral ITA grafts decreases the likelihood of death and reoperation when compared with the single LITA-LAD strategy¹⁶ (Fig. 24-3). The use of other arterial conduits such as the radial artery and the gastroepiploic artery in the context of total arterial revascularization may decrease the risk of reoperation further, but as yet the long-term data are insufficient to answer this question.

The patient population of reoperative candidates has evolved. Cleveland Clinic Foundation studies have shown that in the early years of bypass surgery (1967-1978), only 28% of patients underwent reoperation solely because of graft failure, and that graft failure often occurred early after the primary operation (mean postoperative interval of 28 months after primary operation). Reoperation because of the progression of atherosclerosis in nongrafted coronary arteries was common in the 1967 to 1978 time period (55% of patients).^1,2 Between 1988 and 1991, almost all patients had graft failure as at least part of the indication for reoperation (92%), but that graft failure occurred late after the primary operation at a mean interval of 116 months.³ Today, patients undergoing reoperation usually had a successful primary operation at least 10 years previously for the treatment of multivessel CAD, and the angiographic indications for reoperation are progression of native-vessel distal CAD in combination with late graft failure caused by vein graft atherosclerosis.

An understanding of the pathology and causes of saphenous vein graft (SVG) failure is important not only for an understanding of the causes of the need for reoperation, but also for understanding the dangers inherent in either the interventional or the conservative treatment of patients with previous bypass surgery. Saphenous vein to coronary artery grafts exhibit different pathologies at different intervals after operation.^17–20 Within a few months, they often have diffuse endothelial disruptions with associated mural thrombus. The mural thrombus usually is not obstructing, and when grafts do become occluded early after operation owing to thrombosis, it may not be a result of these intimal changes, but rather may be related to hemodynamic factors. Most saphenous vein grafts examined more than 2 to 3 months after operation have developed a proliferative intimal fibroplasia. This is a concentric cellular process, and it is diffuse, extending the entire length of the graft (Fig. 24-4). It evolves with time to a more fibrous lesion. It is not friable, and although intimal fibroplasia involves most vein grafts, it causes stenoses or occlusions of only a few.

Vein graft atherosclerosis is a distinct pathologic process that often is recognized as early as 3 to 4 years after operation and is characterized by lipid infiltration of areas of intimal fibroplasia (Fig. 24-5). The distribution of vein graft atherosclerosis mimics that of intimal fibroplasia in that it is concentric and diffuse, although as vein graft atherosclerosis progresses, stenotic lesions may become eccentric. In addition, vein graft atherosclerosis is a superficial lesion, it is very friable, and it is often associated with overlying mural thrombus. These characteristics make it different from native-vessel coronary atherosclerosis, a process that is segmental and proximal, eccentric, encapsulated, usually not friable, and usually not associated with overlying mural thrombus. Vein graft atherosclerosis is seen in a majority of grafts explanted more than 10 years after surgery whether or not those grafts are stenotic, and atherosclerotic lesions appear to account for almost all late SVG stenoses. The extreme friability of vein graft atherosclerosis creates a substantial risk of distal coronary artery embolization during percutaneous interventions to treat stenotic lesions and during reoperations for patients with atherosclerotic vein grafts. It is also probable that spontaneous coronary artery embolization may occur from atherosclerotic grafts. In addition, atherosclerotic stenoses in vein grafts appear to predispose to graft thrombosis. Vein graft atherosclerosis appears to be an “active” event-producing lesion.

The exact incidence of late SVG stenoses and occlusions is difficult to determine even with prospective studies because death and reoperation are nonrandom events that remove patients from prospective populations available for late coronary artery angiography. However, it appears that by 10 years after operation, approximately 30% of vein grafts are totally occluded, and 30% of patent grafts exhibit some degree of stenosis or intimal irregularities characteristic of vein graft atherosclerosis.^21,22 Although vein graft atherosclerosis is not the only factor related to late SVG occlusion, it is an important one. Native-vessel stenoses distal to the insertion site of vein grafts may decrease SVG graft outflow and contribute to graft failure, but late graft occlusion usually occurs in the presence of vein graft atherosclerosis. Furthermore, when stenotic vein grafts are replaced at reoperation, the late patency rate of the new vein grafts is good.²

Progress has been made toward decreasing the rate of vein graft failure. The early patency rates of SVGs have been improved by the use of perioperative and long-term platelet inhibitors,^23–25 but the best data involving patients receiving platelet inhibitors indicate that the 10-year vein graft failure rate is approximately 35%. Some studies now indicate that lipid-lowering regimens decrease late vein graft disease and the risk of late cardiac events.^26,27 However, the overall level of improvement has been small.^26,27 So far, the only way known to avoid vein graft atherosclerosis is to avoid using vein grafts.

ITA grafts rarely develop late atherosclerosis, and the late attrition rate of patent ITA grafts is extremely low. Left ITA to LAD grafts have a very high late (20 years) patency rate, and for most patients, the LAD is a profoundly important coronary artery.^21,28 These factors account for the impact of the LITA-LAD graft not only in decreasing the rate of late death after primary bypass surgery, but also in decreasing the rate of reoperation.¹⁵ Multiple ITA grafts provide incremental benefit in decreasing the risk of reoperation.¹⁶ It is also important that ITA grafts do not develop graft atherosclerosis, and therefore do not create the risk of coronary artery embolization during reoperation. The presence of patent arterial grafts may create other technical problems during repeat surgery, but embolization is not among them.

The randomized trials of bypass surgery versus medical management that were initiated in the 1970s provided a framework of information concerning the indications for bypass surgery, and subsequent observational studies have added substance to that framework. However, no randomized trials of medical versus surgical management pertain to patients with prior surgery. The coronary pathology of patients with previous bypass surgery is different from that of patients with only native-vessel stenoses, and we cannot assume that the natural history of, for example, triple-vessel disease based on atherosclerotic vein grafts, is equivalent to that of triple-native-vessel disease.

Two nonrandomized, retrospective studies of patients who had angiograms after bypass surgery addressed the issue of late survival.^29,30 One study showed that patients with early (fewer than 5 years after operation) stenoses in vein grafts and patients with no stenotic vein grafts had approximately the same outcomes and that these outcomes were relatively good.²⁹ However, the presence of late (5 years or more after operation) stenoses in vein grafts predicted poor long-term outcomes, particularly if a stenotic vein graft supplied the LAD coronary artery. When late stenoses in LAD vein grafts were combined with other high-risk characteristics, the late survival rate was particularly dismal. For example, patients with a 50 to 99% stenosis in an LAD vein graft combined with abnormal LVF and triple-vessel or left main stenoses had only a 46% 2-year survival without reoperation. Patients with late stenoses in an LAD vein graft had significantly worse long-term outcomes than did patients with the LAD jeopardized by a native lesion (see Fig. 24-5). This study showed that the difference in the pathology of early (intimal fibroplasia) and late (vein graft atherosclerosis) vein graft stenoses is associated with a difference in clinical outcome and that late stenoses in vein grafts are dangerous lesions.

A second study compared the outcomes of patients with stenotic vein grafts treated with reoperation (REOP group) versus those treated with medical treatment (MED group).³⁰ Again, this was a nonrandomized, retrospective study, and the patients in the REOP group were older and more symptomatic, had worse LVF, and had fewer patent grafts than the patients in the MED group.

The survival of patients with early (fewer than 5 years) SVG stenoses was not different in the two groups. The operative risk for the REOP group was low (no deaths among the 59 patients) and the long-term survival was good, but late survival was just as good for the patients treated medically (Fig. 24-6). It is important to note that the patients in the REOP group were more symptomatic to start with, and at late follow-up, they were less symptomatic than the patients in the MED group. Thus, reoperation for patients with early vein graft stenosis was an effective way of relieving symptoms of angina, but it appears that patients without symptoms can be treated medically with safety, at least over the short term.

However, the overall outcomes were worse for patients with late stenoses in vein grafts, and many subgroups had improved survival rates with reoperation. By multivariate testing (Table 24-1), a stenotic (20-99%) LAD vein graft predicted late death, and performing a reoperation increased late survival for these patients. Multivariate testing of smaller subgroups showed that the survival advantage for the REOP group was true even for patients with only class I or class II symptoms, and that reoperation still improved survival for the remaining patients when patients with stenoses in LAD vein grafts were excluded from the analysis.

Univariate comparisons for the REOP and MED subgroups of patients with stenotic LAD grafts are shown in Fig. 24-7, demonstrating the improved survival for the REOP group. When patients with stenotic LAD vein grafts were subgrouped on the basis of severity of the stenotic lesions (Fig. 24-8), the patients with severely stenotic (50-99%) vein grafts obviously benefited from surgery, exhibiting a decreased risk of death even early in the follow-up period. For patients with moderate stenoses (20-49%) in LAD vein grafts, the survivals of the MED and REOP groups were equivalent for about 2 years, but after that point survival of the patients in the MED group became rapidly worse, so that by 3 to 4 years of follow-up, the survival benefit of reoperation became apparent. Although the patients in these studies did not have consistent functional testing, there is evidence that myocardial perfusion and functional studies can help to identify patients likely to benefit from reoperation. Lauer and colleagues studied 873 symptom-free postoperative patients with symptom-limited exercise thallium-201 studies and found that patients with reversible perfusion defects were more likely to die or experience major cardiac events during a 3-year follow-up.³¹ Impaired exercise capacity also was strongly predictive of unfavorable outcomes.

Anatomical indications for reoperation to improve survival prognosis include: (1) atherosclerotic (late) stenoses in vein grafts that supply the LAD artery; (2) multiple stenotic vein grafts that supply large areas of myocardium; and (3) multivessel disease with a proximal LAD lesion and/or abnormal LVF based on either native-vessel lesions or stenotic vein grafts or a combination of the two pathologies. Reoperation is also effective in other anatomical situations in which severe symptoms are the indication for invasive treatment, including patients with a patent ITA to LAD graft combined with other ischemia-producing pathology and multiple early vein graft stenoses. The combination of the anatomical characteristics just noted and reversible ischemia and/or worsening LVF during stress constitutes a particularly strong indication for reoperation.

Percutaneous treatments (PCTs) represent alternative anatomical treatments for postoperative patients and often are useful. The effectiveness of PCTs is related to the vascular pathology to be treated and the clinical implications of treatment failure. Today, native coronary artery stenoses often can be treated with a low restenosis rate as long as those vessels are large enough to allow intracoronary stenting. Unfortunately, many postoperative patients have very diffuse native coronary atherosclerosis that makes PCT difficult or ineffective. Also, PCT has not been as effective in the treatment of diabetic native CAD.

The rate of technologic change in interventional cardiology has been rapid, and multiple percutaneous technologies have been used to treat stenotic vein grafts. Balloon angioplasty, first-generation PCT, was relatively dangerous to perform and produced ineffective long-term revascularization, particularly when used to treat older (atherosclerotic) vein grafts.³² Direct coronary atherectomy (DCA) increased the risk of coronary embolization at the time of the procedure without improving the restenosis rate.³³ It has been hoped that the use of intracoronary stents, particularly covered stents and drug-eluting stents (DESs), in stenotic vein grafts might provide better outcomes, and stenting does represent an improvement over balloon angioplasty.³² The Randomized Evaluation of Polytetrafluoroethylene Covered Stent in Saphenous Vein Grafts (RECOVERS) trial, a randomized study designed to compare rates of SVG restenosis between coronary artery bypass graft (CABG) patients treated with covered stents and with bare stents, showed identical restenosis rates at 6 months of follow-up (24.2 vs 24.8%; p = .24).³⁴ In a nonrandomized retrospective study comparing the effects of DESs with those of bare metal stents in treating SVG stenosis, Ge and colleagues reported significant differences in in-stent stenosis between groups at 6 months of follow-up (10 vs 26%; p = .03).³⁵ However, other reports comparing DES with bare metal stents showed that the use of DES lowered the rate of restenosis but increased the risk of death.³⁶

The kinetics of treatment failure after PCT for vein grafts are different from those for native coronary vessels. Restenosis and new stenotic lesions in vein grafts continue to appear with time, and the shoulder on the adverse outcome curve that appears at 6 months to 1 year after PCT for native vessels does not appear for vein grafts. Thus, there is still some uncertainty about the clinical impact of PCTs of stenotic vein grafts. Patients with previous bypass surgery are an extremely heterogeneous group; some subgroups are at low risk without any anatomical treatment at all, and some subgroups are at high risk without effective therapy. To date, the reported studies of PCT of SVG lesions have not included clinical risk stratifications that would allow comparison of patient survival rates.

Despite persistently high restenosis rates after percutaneous interventions, there are still many indications for their use in the treatment of patients with previous bypass surgery. Realistically, the ideal uses of PCTs are in situations in which failure of the anatomical treatment is not likely to be catastrophic as the impact of stenting on survival is unclear. These situations include symptomatic patients with: (1) early vein graft stenoses; (2) native coronary stenoses; or (3) focal late SVG stenoses in vein grafts not supplying the LAD artery. There are many patients with previous surgery who will fall into a middle ground where it is not clear whether percutaneous transluminal coronary angioplasty (PTCA) or reoperation is likely to yield the best outcome, and judgments must be made on the specific advantages and disadvantages of the treatments for those particular patients. Factors making PTCA more attractive than reoperation are listed in Table 24-2.

There are patients with postsurgical repeat ischemic syndromes and very unfavorable coronary anatomy for whom good options for anatomical treatment do not exist. For reoperative coronary surgery to be of benefit there must be bypass conduits available to construct new grafts to graftable coronary arteries that subtend substantial areas of ischemic but viable myocardium. If these conditions do not exist, surgery may not be in the interest of even a symptomatic patient. Studies of diabetic patients undergoing postsurgical repeat revascularization with PCT or surgery have shown unfavorable 10-year-survival rates.³⁷ Unless good coronary targets to receive bypass grafts are available, PCT may be the best choice for marginal candidates because of lower initial costs and, in some settings, lower initial mortality.

Reoperations are more complicated than primary operations. The specific technical challenges that surgeons must recognize and solve that are unique to or more common during coronary reoperation are:

1. 
   

   Sternal reentry

   
   
2. 
   

   Stenotic or patent vein or arterial bypass grafts

   
   
3. 
   

   Aortic atherosclerosis

   
   
4. 
   

   Diffuse native-vessel coronary artery disease

   
   
5. 
   

   Coronary arteries located amid old grafts and epicardial scarring

   
   
6. 
   

   Lack of bypass conduits

The overall problem of myocardial protection is more difficult during reoperations, with perioperative myocardial infarction still being the most common cause of in-hospital death.^3,6 The metabolic concepts of myocardial protection in use today are valid, but the reasons that myocardial protection sometimes fails during reoperation are related to anatomical causes of myocardial infarction. These anatomical causes of perioperative myocardial infarction include injury to bypass grafts, atherosclerotic embolization from vein grafts or the aorta to distal coronary arteries, myocardial devascularization secondary to graft removal, hypoperfusion through new grafts, failure to deliver cardioplegic solution, early vein graft thrombosis, incomplete revascularization, diffuse air embolization, and technical error.^3,38–42 To be consistently successful, coronary reoperations must be designed to avoid these causes of myocardial infarction.

Preoperative Assessment