Abstract
Repeat myocardial revascularization procedures are markedly different from de novo interventions, with increased procedural risk and technical-demanding complexity.
However the number of patients previously treated with coronary artery bypass graft (CABG) that need a repeat revascularization due to graft failure is increasing consistently. Late graft failure, usually caused by saphenous vein grafts (SVG) attrition, is certainly not uncommon. However PCI on degenerated SVG presents higher complication rate and worse clinical outcome compared with native arteries interventions.
In acute graft failure setting, PCI represents a valuable option to treat postoperative myocardial infarction.
Highlights
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Percutaneous coronary intervention (PCI) after CABG surgery may be necessary in acute or chronic graft failure.
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PCI after early graft failure is a valuable option to treat postoperative myocardial infarction.
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PCI on degenerated saphenous vein graft is often associated with poor angiographic and clinical outcome and requires focused approach.
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Hybrid coronary revascularization combines the advantages of the two techniques and is a valuable option in selected patients.
1
Introduction
The number of coronary procedures on patients who underwent prior myocardial revascularization increases over time as a consequence of the larger cumulative number of patients treated with CABG surgery or PCI and the longer life expectancy . Repeat myocardial revascularization procedures, whether surgical or interventional, are markedly different from de novo interventions, with increased procedural risk and technical-demanding complexity. Indeed, patients who need repeat revascularization present typically a high-risk profile. They are older, with many comorbidities, extensive vascular disease, complex coronary anatomy and degenerate grafts. They are more likely to present concurrent cardiovascular risk factors and diffusely atherosclerotic and calcified vessels, features that lead to suboptimal stent expansion, defective graft anastomosis and fewer amenable options for re-intervention .
It has been calculated that 14% to 17% of patients who underwent coronary revascularization in the past 10 years had a history of CABG surgery . The likelihood of undergoing more than one coronary intervention has been increased dramatically in the last 30 years due to the ageing of the population and the possibility of disease progression or surgical graft failure . Moreover the age at the moment of the first intervention is predictive of the need of repeat revascularizations, with the younger patients being more likely to undergo repeat procedures .
Therefore it will be more and more common to deal with this kind of high risk and complex patients in the catheterization laboratory in the next years.
2
PCI in graft failure
Graft failure may occur either early after CABG or after several months or years after surgical revascularization (late graft failure). The type of lesion responsible for graft failure depends on the time of onset of ischemic symptoms.
Ischemia in early postoperative setting (acute graft failure) is mostly due to surgical problems as incomplete revascularization or vascular injury . Late graft failure is usually caused by disease progression, graft degeneration and atherosclerosis. The longer the time from CABG surgery is, the higher is the possibility to deal with complex atherosclerotic plaques with high risk of embolization, especially for saphenous vein grafts (SVGs) .
2.1
Acute graft failure
Perioperative myocardial infarction (PMI) is one of the most serious complications after CABG since it is associated with increased perioperative morbidity and mortality as well as poor long-term outcome . The reported incidence of PMI varied considerably, from 3% to 30%, because of different diagnostic criteria and variable patient populations . In the contemporary large cohort of the PREVENT IV trial, PMI was relatively common in patients undergoing CABG surgery, occurring in approximately 10% of cases. In this trial, PMI was associated with a higher complication rate, longer duration of mechanical ventilation, longer intensive care unit and hospital length of stay. Moreover, patients with PMI had worse outcomes at 2 years compared with those without PMI .
Early graft failure after CABG may occur in 8–30% of cases , depending on the accuracy of the diagnostic method applied to investigate this complication. Systematic perioperative angiography showed defects in 8% of saphenous vein grafts (SVGs) and 7% of left internal mammary artery (IMA) grafts , but only a minority of these patients become clinically symptomatic. The rate of early graft occlusion varies from 3% to 12% for vein grafts, 3% to 4% for radial arteries and 1% to 2.5% for internal mammary arteries .
In most of symptomatic patients after CABG (up to 75%), the main cause of chest pain is ischemia due to early graft failure, while other causes including pericarditis and coronary spasm can be diagnosed in a smaller percentage of patients. (Figs. 1 and 2 ).
The early identification of patients with graft failure allows adequate early re-intervention strategy such as percutaneous coronary intervention or reoperation with surgical graft revision.
However, early diagnosis of perioperative myocardial ischemia is challenging, since from 5% to 30% of patients present elevation of biomarkers of myonecrosis and/or ischemic electrocardiographic changes after CABG surgery .
ECG signs of ischemia, biomarkers modifications, wall motion abnormalities at echocardiography and arrhythmias may raise the suspicion of acute graft failure.
When the diagnosis of graft failure is suspected it should be rapidly assessed by coronary angiography, in particular if this causes hemodynamic impairment .
Causes leading to myocardial damage after CABG surgery are classified as graft-related or non-graft-related injuries. Perioperative myocardial ischemia is caused most of the time by the newly implanted graft (graft related injuries), although in a relatively high percentage of case (13–42%) coronary angiography does not reveal any graft failure or new native artery occlusion . In these cases ischemia is ascribed to air-embolism or microcirculatory damage or inappropriate myocardial protection (non graft-related injuries) .
Graft-related ischemia is caused by problems related to the anatomy and the function of the graft such as stenosis in the sites of anastomosis, kinking, overstretching or tension of the grafts, significant spasm, early graft thrombosis, or competitive flow with native coronary vessels .
Cardiac troponin (cTn) levels have been proposed as a valuable tool in identifying patients who developed graft-related ischemia and consequently most likely to benefit from early invasive strategy. Particularly cTn levels were significantly increased in patients with graft-related PMI compared with patients with non-graft-related PMI. However, cardiac biomarkers for myocardial damage did not separate between graft-related and non-graft related PMI until 12 h after CABG, reaching accurate discrimination capability only 24 h after CABG .
Early graft failure, occurring within 30 days from surgery, is primarily triggered by graft thrombosis derived from technical failure in graft manipulation and implantation and consequent endothelial damage and dysfunction. After the implantation of a graft a local inflammatory response can be activated by cytokines and other inflammatory agents, resulting in an endothelial dysfunction, platelets adhesion can lead to thrombosis and early graft occlusion.
Other acute graft failure mechanisms included conduit related problems such as small diameter and pre-existing vein pathology.
It is recommended, when feasible, to confirm acute graft failure by coronary angiography before returning to operating room in order to avoid unnecessary reoperation since a limited but significant percentage of CABG patients presenting with myocardial ischemia signs and symptoms showed no evidence of graft failure at coronary angiography .
In early postoperative graft failure, emergency PCI aims to limit the extent of myocardial infarction . Comparison data between redo-CABG and PCI in the contest of PMI are limited but reported PCI angiographical and clinical outcomes resulted equivalent or better compared with redo-CABG .
Nevertheless, rescue PCI for acute graft failure is associated with significant higher morbidity and mortality compared with PCI in other contests. In acute postoperative setting, the risk of perforation is high especially at the new anastomosis site. In one series rescue PCI was associated with an overall mortality rate of 21% (15% in-hospital and 6% during the follow-up period) .
2.2
Late graft failure
Late graft failure (> 6 months after CABG surgery) is usually caused by saphenous vein graft attrition or by the progression of the atherosclerotic process in the native arteries .
Saphenous vein grafts (SVGs) are routinely used in CABG surgery as additional conduits to arterial grafts. However SVGs typically present accelerated atherosclerosis resulting in high rate of stenosis or occlusion of the graft.
About 10% of SVGs are occluded early postoperatively, 20% at 1 year and 50% at 10 years of follow-up. Moreover 70% of SVGs are diffusely diseased at 10 years .
The prognostic implications of chronic vein graft occlusion have not been completely defined. Vein graft occlusion contributes to higher morbidity and mortality when is the culprit lesion of new MI or is responsible for reoccurrence of angina . In a substudy of the PREVENT-IV trial, the composite end point of repeat revascularization, death and MI occurred more frequently in patients with vein graft failure but the difference was driven by higher rates of revascularization but not by death or MI .
The remodeling process is typical of vein grafts. In fact, vein grafts need to compensate the shear stress developed by pulsatile flow which comes from the arterial system and it consists in neointimal formation from vascular smooth muscle cells. The cytokines and local mediators involved in this process help to develop a highly atherogenic substrate on which atherosclerosis develops .
It has been shown that the remodeling process of neointimal formation and reendothelialization in the early postoperative period is a critical determinant of vessel patency .
Remodeling of the newly implanted graft, with neointimal formation, is followed by a process of increased wall stiffness during the first 6 months .
Hyperplasia of neo smooth muscle cells involves mostly the anastomosis site, leading to a progressive stenosis of the graft lumen and anastomosis. Commonly after the first year from surgery, atherosclerosis rather than remodeling is the cause of late graft failure .
SVGs attrition is characterized by accelerated forms of atherosclerosis, with friable plaques at high risk for embolization and thrombosis as previously described in detail by our group . A process of “arterialization” with intimal fibrous thickening, medial hypertrophy and lipid deposition has been described by IVUS studies , where SVGs usually show an echolucent zone around the vessel that mimics the arterial external elastic membrane. Intracoronary OCT is able to demonstrate SVGs attrition at very early stage with the evidence of wall thickening .
Arterial graft patency at long term after CABG surgery is significantly higher compared with SVG ( Table 1 ).
Graft | Patency at 1 year | Patency at 4–5 years | Patency at 10–15 years | References |
---|---|---|---|---|
SVG | > 90% | 65–80% | 25–50% | |
RA | 86–96% | 89% | not reported | |
Left IMA | > 91% | 88% | 88% | |
Right IMA | Not reported | 96% | 65% |
Arterial grafts, contrary to SVGs, rarely undergo attrition from accelerated form of atherosclerosis and they usually require intervention as a consequence of the narrowing of coronary anastomosis in response to a surgical injury .
Procedures on radial grafts are more challenging than interventions on IMA grafts or even SVGs because they often develop coronary spasm during intervention .
2.3
PCI, redo-CABG or medical therapy
Repeat revascularization in patients with graft failure is indicated both in presence of severe symptoms despite anti-angina medication, and in less or asymptomatic patients with suspected coronary disease at non-invasive testing .
According to the latest European guidelines for myocardial revascularization routine stress testing may be considered in asymptomatic patients more than 5 years after CABG surgery . However, in specific patients subsets, particularly in cases of suboptimal or incomplete revascularization, patients with complicated course during revascularization (e.g. PMI), diabetic patients, or patients with multivessel disease and residual intermediate lesions, or with silent ischemia, early imaging testing should be considered even in asymptomatic patients.
In symptomatic patients the risk should be stratified according to stress testing and stress imaging with stress echocardiography, magnetic resonance imaging or myocardial perfusion scintigraphy should be considered rather than stress ECG (Class IC) .
Patients with demonstration of ischemia at low-workload at stress testing, with multiple zones of high-grade wall motion abnormality or reverse perfusion defect are considered at intermediate to high risk. In these patients coronary angiography is recommended. Otherwise, in patients with low-risk findings at stress testing, medical therapy optimization and lifestyle changes are recommended .
PCI in patients previously treated with CABG is associated with worse acute and long-term outcomes compared to de novo procedures. Similarly, patients undergoing redo-CABG have a 2- to 4-fold higher mortality than the first operation . A large series of the Cleveland Clinic Foundation showed that the risk of reoperation was mainly driven by comorbidity and less by the reoperation itself .
There are limited data comparing the efficacy of PCI versus redo-CABG in patients with previous CABG. In a propensity analysis of long-term survival after redo-CABG or PCI in patients with multiple vessel disease and high-risk features, short-term outcome after either technique was very favorable, with nearly identical survival at one and five years . In the AWESOME RCT and registry, overall in-hospital mortality was higher with CABG (9.1%) than with PCI (0.5%) .
The local heart team should discuss the best strategy individually after the confirmation of graft failure at coronary angiography.
Many aspects should be discussed in the decision making principally regarding the angiographic findings, the graft characteristics, the amount of myocardium at risk, the patient general conditions, comorbidities and preferences.
PCI is generally the favorite strategy for early graft failure and clinical presentation as acute coronary syndromes . PCI should be preferred for more fragile patients, with relevant comorbidities, especially those with renal and/or respiratory insufficiency. PCI is generally preferred over CABG when patent graft on LAD is present, especially if patent IMA graft was implanted, and when a single graft lesion is present .
On the contrary redo-CABG is usually the favorite in those situations where surgical risk is acceptable, adequate venous or arterial conduits are available, and multiple graft lesions and total occlusions of native arteries and larger amount of ischemic myocardium are present. Furthermore redo-CABG is preferred in graft lesions supplying the LAD artery, when no patent IMA grafts are present. The IMA is in fact the conduit of choice for revascularization during redo-CABG .
Reoperation is furthermore preferred when relevant valvular disease likely requiring future surgery coexists.
2.4
PCI in graft lesions: Practical and technical aspects
Whenever possible, PCI on the native vessel that was supplied by the occluded graft is recommended . In a large series graft PCI was associated with higher in-hospital mortality and higher rates of post-procedural complications compared with native arteries PCI. Particularly patients undergoing bypass graft PCI more frequently required intra-aortic balloon pump counterpulzation, required longer fluoroscopy time and larger amount of contrast, less frequently achieved TIMI flow grade 3 post-stenting and were more likely to receive blood transfusions .
In chronic total occlusion (CTO) of native coronary vessel, PCI should be performed by specialized operators with > 80% of success rate. PCI of CTO is indicated upon relevant cardiac ischemic symptoms, in the presence of a moderate to large area of viable myocardium or non-transmural extent of MI according to MRI . Surgical conduits can be used to perform retrograde recanalization of CTOs by experienced operators .
If PCI of the native vessel appears impossible, angioplasty of the occluded SVG is an option. PCI of surgical conduits is considered a high-risk procedure because patients present in many cases with hemodynamic instability and acute myocardial infarction and the procedure is burden with high rate of poor procedural outcome (TIMI flow < 3).
PCI in SVGs is associated with higher risk of atheroma embolization resulting in no-reflow phenomenon, graft perforation and restenosis than in native coronary vessels .
In chronically occluded SVG, the success rates are considerably lower with even higher complication and restenosis rates than in non-occluded SVG . Nevertheless PCI on graft conduits, mainly on SVG, is performed in up to 37% of patients with previous CABG surgery . Generally, chronically occluded SVGs should not be considered a target for PCI contrary to occluded SVGs that are culprit lesion of acute coronary syndromes .
The use of intracoronary embolic protection devices (EPD) in SVG intervention should always be considered because of the reduced risk of embolization and post-procedural myocardial enzyme elevation . The choice of the best device should be made according to the anatomical feature of the lesion. For proximal stenosis distal EPD are recommended. Vice versa proximal EPD are needed for distal lesions. EPD are useful especially in severely diseased SVGs where, however its application can arise some difficulties and requires experience.
PCI with stenting has proven to be superior to balloon angioplasty in SVGs. Although the problem of restenosis after SVGs stenting has decreased after the introduction of drug-eluting stents (DES) , the efficacy of DES is lower than in native vessel PCI and the choice of the type of stent is still undefined.
A cautious strategy with direct stenting, minimal catheter maneuvers and the avoidance of pre-stent and post-stent dilation is recommended in order to minimize the risk of distal embolization. In the event of significant under-deployment of the stent, high-pressure post-dilation must be done using EPD in place .
Additional devices might play a role in this particular subset of PCI patients, especially since protection devices require landing zone and do not fit all procedures.
When EPD cannot be used, the M-Guard stent, a stainless steel platform wrapped by a micron-level polymer net, is an alternative to reduce distal embolization. The potential benefit of this device is clear since it reduces the protruding debris. The improved of the arterial wall theoretically isolates thrombogenic surfaces and reduces plaque protrusion, thereby limiting inflation embolization . However some concerns have been raised regarding a not negligible restenosis rate in the contest of SVGs-PCI .
Although covered stents are not recommended for the treatment of SVGs attrition, they could be extremely valuable in the not infrequent event of perforation of the venous vessel wall.
Intracoronary imaging studies with IVUS and/or OCT are useful to identify the presence of distal embolization, to assess strut apposition and vessel injury after PCI, and to ensure adequate stent expansion and guide intervention .
PCI should target only functional relevant stenosis, especially in the setting of diffusely diseased vessels. Before considering PCI, patients should be screened with integrated functional imaging techniques in order to identify the real need for repeat revascularization, according to myocardial ischemia and vitality .
Functional stenosis assessment with fractional-flow reserve (FFR) can be considered but it has not been validated in the context of CABG patients, and should probably not be used for functional assessment of SVGs because of their typical atherosclerotic accelerated process.
Transmyocardial laser revascularization is an option in patients with end-stage coronary disease with unsuitable anatomy for surgical or percutaneous revascularization. This surgical procedure aims to relief symptoms by creating multiple transmyocardial channels through the endocardium in order to supply blood flow in the ischemic area , but it is rarely used in clinical practice.
2
PCI in graft failure
Graft failure may occur either early after CABG or after several months or years after surgical revascularization (late graft failure). The type of lesion responsible for graft failure depends on the time of onset of ischemic symptoms.
Ischemia in early postoperative setting (acute graft failure) is mostly due to surgical problems as incomplete revascularization or vascular injury . Late graft failure is usually caused by disease progression, graft degeneration and atherosclerosis. The longer the time from CABG surgery is, the higher is the possibility to deal with complex atherosclerotic plaques with high risk of embolization, especially for saphenous vein grafts (SVGs) .
2.1
Acute graft failure
Perioperative myocardial infarction (PMI) is one of the most serious complications after CABG since it is associated with increased perioperative morbidity and mortality as well as poor long-term outcome . The reported incidence of PMI varied considerably, from 3% to 30%, because of different diagnostic criteria and variable patient populations . In the contemporary large cohort of the PREVENT IV trial, PMI was relatively common in patients undergoing CABG surgery, occurring in approximately 10% of cases. In this trial, PMI was associated with a higher complication rate, longer duration of mechanical ventilation, longer intensive care unit and hospital length of stay. Moreover, patients with PMI had worse outcomes at 2 years compared with those without PMI .
Early graft failure after CABG may occur in 8–30% of cases , depending on the accuracy of the diagnostic method applied to investigate this complication. Systematic perioperative angiography showed defects in 8% of saphenous vein grafts (SVGs) and 7% of left internal mammary artery (IMA) grafts , but only a minority of these patients become clinically symptomatic. The rate of early graft occlusion varies from 3% to 12% for vein grafts, 3% to 4% for radial arteries and 1% to 2.5% for internal mammary arteries .
In most of symptomatic patients after CABG (up to 75%), the main cause of chest pain is ischemia due to early graft failure, while other causes including pericarditis and coronary spasm can be diagnosed in a smaller percentage of patients. (Figs. 1 and 2 ).