Review Article

Current State of the Art in Approaches to Saphenous Vein Graft Interventions

Register or Login to View PDF Permissions
Permissions× For commercial reprint enquiries please contact Springer Healthcare: ReprintsWarehouse@springernature.com.

For permissions and non-commercial reprint enquiries, please visit Copyright.com to start a request.

For author reprints, please email rob.barclay@radcliffe-group.com.

  • Views: 5410

  • Likes: 2

  • Downloads: 36

  • Citations: 14

  • Read time: 15m
Average (ratings)
No ratings
Your rating

Abstract

Saphenous vein grafts (SVGs), used during coronary artery bypass graft surgery for severe coronary artery disease, are prone to degeneration and occlusion, leading to poor long-term patency compared with arterial grafts. Interventions used to treat SVG disease are susceptible to high rates of periprocedural MI and no-reflow. To minimise complications seen with these interventions, proper stents, embolic protection devices (EPDs) and pharmacological selection are crucial. Regarding stent selection, evidence has demonstrated superiority of drug-eluting stents over bare-metal stents in SVG intervention. The ACCF/AHA/SCA American College of Cardiology/ American Heart Association Task Force on Clinical Practice Guidelines and the Society for Cardiovascular Angiography and Interventions guidelines recommend the use of EPDs during SVG intervention to decrease the risk of periprocedural MI, distal embolisation and no-reflow. The optimal pharmacological treatment for slow or no-reflow remains unclear, but various vasodilators show promise.

Keywords

Saphenous vein graft, percutaneous coronary intervention, drug-eluting stent, distal embolisation, no-reflow phenomenon,

Disclosure:The authors have no conflicts of interest to declare.

Received:

Accepted:

DOI:https://doi.org/10.15420/icr.2017:4:2

Correspondence Details:Michael S Lee, Division of Cardiology, UCLA Medical Center, 100 UCLA Medical Plaza, Suite 630, Los Angeles, CA 90095, USA. E: MSLee@mednet.ucla.edu

Copyright Statement:

The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content.

Saphenous vein grafts (SVGs) are commonly used during coronary artery bypass graft surgery (CABG) for severe coronary artery disease. However, SVGs are prone to both degeneration and occlusion, leading to poor long-term patency compared with arterial grafts. Previous reports suggest rates of SVG failure in the first 12–18 months may be as high as 25 %.1–4 SVG neointimal hyperplasia and accelerated atherosclerosis diminish the long-term benefits of CABG, while subsequent SVG interventions are plagued by plaque embolisation and no-reflow phenomenon. Percutaneous coronary intervention (PCI) of SVGs is associated with worse clinical outcomes compared with native coronary artery PCI,5,6 but certain strategies may help mitigate complications. In this review, we discuss risk factors for SVG intervention and the optimal approaches for treating this challenging subset of patients.

Pathophysiology of Saphenous Vein Graft Complications

Various factors contribute to SVG deterioration and occlusion, which may ultimately require revascularisation. Approximately 10–15 % of SVGs occlude within 1 year and 50 % fail by 10 years.7 Platelet aggregation, growth factor secretion, endothelial dysfunction, inflammation, luminal foam cell accumulation, decreased local fibrinolytic potential from plasminogen activator inhibitor-1 upregulation and marked intimal hyperplasia contribute to SVG occlusion within the first 12–18 months post-CABG.8–14 Occlusions after 12–18 months occur following lipid deposition within intimal hyperplasia, eventually forming atherosclerotic plaque.14 Increased pressure load from vein graft arterialisation induces this development of neointimal growth and atherosclerosis.7 Deteriorating SVG lesions also possess thinner, more friable fibrous caps compared with native coronary artery lesions.15,16 this increases the incidence of plaque embolisation and platelet aggregation,17,18 especially during SVG interventions.

Atheroembolic debris liberated during SVG intervention becomes lodged in distal capillaries, while the release of neurohormonal factors such as serotonin can induce vasospasm. Slow or no-reflow phenomena may subsequently follow, which are associated with both periprocedural angina and ischaemic ST-segment changes.19 The exact mechanism of no-reflow remains unclear, but it has been hypothesised that endothelial swelling, neutrophil infiltration and platelet aggregation induce microvasculature spasm and obstruction.20,21 SVG intervention is thus associated with higher rates of in-stent restenosis, target vessel revascularisation (TVR), periprocedural MI and in-hospital mortality compared with PCI for native coronary circulation. The severity of these potential consequences makes proper patient selection and optimal technique essential during invasive SVG revascularisation.

Predictors of Adverse Outcomes

The strongest predictors of SVG intervention 30-day major adverse cardiac events (MACE) are angiographic estimations of SVG degeneration and plaque volume.22,23 Another study analysing patients undergoing SVG intervention with distal embolic protection reported that lesion length has the strongest correlation with short-term adverse events.24 A graded increase in MACE was observed with increasing lesion lengths, perhaps correlating to the increase in SVG plaque burden.

The data on the impact of gender have provided mixed results. One study suggested that male patients were more inclined to have worse outcomes,25 but another study reported that female patients had a higher 30-day cumulative mortality rate (4.4 % versus 1.9 %, P=0.02).26 Female patients also had significantly higher rates of vascular complications (12 % versus 7.3 %; P=0.006) and post-procedural acute renal failure (8.1 % versus 4 %; P=0.02) compared with male patients.

Chronic renal insufficiency (serum creatinine ≥1.5 mg/dl) was a significant predictor of 1-year MACE in patients who underwent SVG intervention with drug-eluting stents (DES) (hazard ratio [HR] 2.2; 95 % CI [1.1–4.3]; P=0.03).27 There was also a trend toward higher rates of TVR in the renal insufficiency group (21.8 % versus 10.3 %; HR 2.42; 95 % CI [0.94–6.24]; P=0.059). Another study reported that patients with renal insufficiency had higher mortality rates following SVG PCI.28

Patients commonly experienced elevations in levels of creatine kinasemyocardial band (CK-MB) following SVG intervention.17 Approximately 15 % of patients who underwent SVG intervention were found to have CK-MB levels >5x the upper limit of normal (ULN), which increased the 1-year mortality rate in patients with normal CK-MB from 4.8 % to 11.7 % (P<0.05 analysis of variance [ANOVA]). Even minor elevations in CK-MB levels (>1x to <5x ULN) were associated with an increased 1-year mortality rate (6.5 %; P<0.05 ANOVA).17

Lesion Evaluation and Patient Selection

Lesion Evaluation

The decision to perform SVG revascularisation should predominantly be based on patient symptoms and evidence of myocardial ischaemia in regions supplied by the SVG.

Fractional flow reserve (FFR) is used to determine the significance of native coronary vessel stenosis, but has not been well studied in SVG lesions. Limited studies show that FFR has low sensitivity, but an acceptable specificity and negative predictive value compared with stress myocardial perfusion imaging in assessing the significance of SVG lesions.29 Myocardial perfusion imaging has good specificity for detecting ischaemia after CABG, but variable sensitivity in detecting angiographically significant graft stenosis.30

Intravascular ultrasound (IVUS) may play a role in SVG disease evaluation, as positive remodelling on IVUS is a strong predictor of post-intervention no-reflow.31 However, IVUS has not been adequately evaluated in prospective SVG intervention trials to support intervention based on IVUS findings alone.

Multidetector computed tomography (MDCT) provides adequate visualisation of SVGs given their reduced motion and large lumens.32 Although it provides a sensitivity of 96 % and a specificity of 95 % in evaluating graft patency,33 it is limited in its ability to visualise distal anastomosis sites. Further advancements in this technique are needed to match the gold standard of coronary angiography.

Patient Selection

Prophylactic stenting of intermediate SVG lesions has been advocated given that the progression of SVG disease can be rapid. In the Moderate Vein Graft Lesion Stenting With the Taxus Stent and Intravascular Ultrasound (VELETI) trial, 57 patients with moderate (30–60 %) SVG stenosis were randomised to medical therapy alone or revascularisation with DES.34 Both minimal luminal diameter and percent stenosis were decreased in the DES group. The MACE rates at 1 and 3 years were lower in the DES group compared with the medical therapy group (At 1 year: 3 % versus 19 %, P=0.09; at 3 years: 3 % versus 26 %, P=0.02).35,36 The VELETI trial was underpowered for clinical endpoints. The larger 450-patient VELETI II trial randomised patients with intermediate SVG lesions to either SVG intervention with paclitaxeleluting stents or medical therapy alone.37 This study was terminated prematurely due to slow patient enrolment.

Percutaneous revascularisation is not recommended in patients with chronic total SVG occlusion. A study of 34 patients with chronic total SVG occlusions reported that successful recanalisation with stent implantation was low (68 %).36 Rates of TVR and in-stent restenosis at 18-month follow-up were very high (61 % and 68 %, respectively) in patients who underwent successful stenting.

Intervention Technique

Preparation

Given inferior long-term outcomes of SVG intervention compared with native vessel PCI,38,39 revascularisation of the bypassed native vessel should be considered only if the indication is clear. Knowledge of the CABG operative report details, including graft locations, number of grafts and complications encountered during the surgery, is helpful. Previous angiography can provide additional benefit in guiding angiography and revascularisation.

Optimal guiding-catheter support is imperative to the procedural success of SVG intervention. The size of the aorta combined with the position and angle of the SVG determines the type and size of catheter best suited for engagement. The multipurpose catheter is often used for right coronary graft interventions, especially if the graft take-off is steep and inferior. The Judkins right (JR) catheter or Amplatz left (AL) catheter may be used if the angle of the origin of the SVG to the right coronary artery is more horizontal. The JR catheter can engage left coronary artery grafts as well, especially those with a horizontal takeoff from the aorta. Other available catheters include the AL, left bypass and hockey stick catheters.

Pre-dilation Versus Direct Stenting

Although pre-dilation with balloon angioplasty is often employed in native vessel PCI to optimise lesions, this strategy may not be suitable for SVG interventions. Direct stenting provides the potential benefit of trapping debris and decreasing distal embolisation that can occur with pre-dilatation. Patients who underwent direct stenting were associated with nearly a 50 % reduction in CK-MB level elevations >4x normal (13.6 % versus 23 %; P<0.12), overall lower maximum CK-MB release (9.5 versus 19.6 IU/L; P<0.001) and reduction in non-Q-wave MI (10.7 % versus 18.4 %; P<0.02) compared with angioplasty first without distal protection.40 However, one retrospective study of patients undergoing direct stenting without distal protection versus angioplasty followed by stenting with distal protection reported that the rate of increase in CK-MB levels >2x ULN and rates of MACE were no different in-hospital or at 30 days.41 Prospective randomised trials are needed to confirm whether direct stenting versus pre-dilation is most effective in reducing distal embolisation.

Stent Selection

Stent Sizing

Proper stent sizing is crucial to ensuring long-term stent longevity and vessel patency. One study explored the concept of undersized stenting to reduce distal embolisation. Hong et al. analysed outcomes of SVG intervention with DES in three groups according to the ratio of stent diameter to average IVUS reference lumen diameter (group I: <0.89 mm, group II: 0.9 to 1.0 mm, group III: >1.0 mm).42 Incidence of CK-MB level elevation >3x normal was 6 %, 9 % and 19 %, respectively (P=0.03) without an increase in clinical events at 1 year. The hypothesised reduction in distal embolisation and periprocedural MI with undersized stenting must be weighed against the conceivable risk of increased stent restenosis and thrombosis.

Table 1: DES Versus BMS in Randomised Saphenous Vein Graft Trials

Article image
Download

Bare-metal Stents

The Saphenous Vein De Novo (SAVED) trial reported that bare-metal stents (BMS) were associated with higher procedural success rates compared with balloon angioplasty (47 % versus 36 %; P=0.11) with a lower MACE rate throughout 240 days (26 % versus 38 %; P=0.04).43

Covered Stents

Covered stents comprised of polytetrafluoroethylene (PTFE) membranes were developed to act as local filters that would trap plaque debris extruding between stent struts. A multicentre registry suggested favourable results with their use in SVG intervention.44 However, randomised trials failed to show superiority over BMS.45–48 The Stents in Grafts (STING) trial reported no differences in MI, target lesion revascularization (TLR) or death with PTFE-covered stents compared with conventional stents.45 The Randomized Evaluation of Polytetrafluoroethylene Covered Stent in Saphenous Vein Grafts (RECOVERS) trial also reported similar clinical outcomes between PTFE-covered stents and BMS with higher rates of non-fatal MI with PTFE-covered stents.46 These findings were confirmed in the Symbiot III trial, which found PTFE-covered stents to have similar clinical outcomes and rates of restenosis as BMS.47 Finally, the Barrier Approach to Restenosis: Restrict Intima to Curtail Adverse Events (BARRICADE) trial reported more long-term target vessel failure in patients with covered stents compared with BMS.48

There remain two covered stents that show potential benefit in treating degenerated SVGs, although they lack long-term head-to-head comparison data with BMS. The SESAME first-in-human trial reported that patients treated with a nanosynthesised, membrane-covered self-expanding, super-elastic, all-metal endoprosthesis stent (SESAME stent, Advanced Bioprosthetic Surfaces Ltd) had 0 % 30-day and 14 % 9-month MACE rates.49 The other stent under study is the MGuard stent (InspireMD), with preliminary evaluation in one study demonstrating an excellent performance with no angiographic/procedural complications or adverse events in 30-day follow-up.50

Drug-eluting Stents

The Is Drug-eluting Stenting Associated With Improved Results in CABG (ISAR-CABG) trial, which randomised 610 patients with diseased SVG to DES or BMS, reported that DES were associated with lower rates of TVR (7.2 % versus 13.1 %; P=0.02) and met the primary endpoint of 1-year MACE (15.4 % versus 22.1 %; P=0.03) (see Table 1).51 The Stenting of Saphenous Vein Grafts (SOS) trial also demonstrated a significant reduction in MACE rates with paclitaxel-eluting stents (Taxus, Boston Scientific Corp.) compared with BMS,52 which was driven by lower TLR rates without increased MI or death through nearly 3-year follow-up.53 Sirolimus-eluting stents (SES; Cordis) were studied in the Reduction of Restenosis In Saphenous Vein Grafts With Cypher Sirolimus-eluting Stent (RRISC) trial, which demonstrated a reduction in TLR, TVR, binary restenosis rate and late stent loss in the DES group compared with the BMS group at 6 months.54 Conversely, the DELAYED RRISC study found the TVR benefit was lost at 3-year follow-up,55 and that the DES group had increased mortality rates. However, the study was not statistically powered for clinical outcomes such as mortality.

Multiple meta-analyses (including non-randomised studies) comparing DES with BMS in SVG intervention support the superiority of DES demonstrated in the randomised trials discussed above.15,56–63 One meta-analysis reported that 39,213 DES patients had lower rates of MACE (odds ratio [OR] 0.63; 95 % CI [0.54–0.74]; P<0.001), TVR (OR 0.70; 95 % CI [0.57–0.86]; P<0.001) and TLR (OR 0.64; 95 % CI [0.50–0.84]; P<0.01), with no difference in stent thrombosis (OR 0.90; 95 % CI [0.61–1.32]; P=0.58) compared with 26,461 BMS patients.15 These benefits persisted at 36-month follow-up.

Lee et al. compared SES and paclitaxel-eluting stents head to head in a multicentre analysis of 172 real-world patients undergoing SVG intervention and found nonsignificant differences in survival (HR 1.28; 95 % CI [0.39–4.25; P=0.69) and TVR (HR 2.54; 95 % CI [0.84–7.72; P=0.09).64 A 2014 study compared first-generation DES with secondgeneration everolimus-eluting stents (EES) in SVG PCI, reporting that EES showed no significant differences in MI, TVR or cardiac death following risk adjustment during 4-year follow-up.65 In summary, although there is no specified class recommendation for DES in SVG PCI, the 2011 American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Society for Cardiovascular Angiography and Interventions (ACCF/AHA/SCAI) guidelines do note a ‘preference’ for their use over BMS.66

Figure 1: Saphenous Vein Graft (SVG) Intervention of a&lt;br /&gt;&#10;20-year-old SVG to the Left Anterior Descending Artery

Article image
Download

Table 2: Strengths and Weaknesses of Embolic Protection&lt;br /&gt;&#10;Devices

Article image
Download

Bioresorbable vascular scaffolds have not been adequately studied in SVG intervention and therefore cannot be recommended at this time. However, given the large diameter of the SVG, it can be considered in select situations (see Figure 1).

Embolic Protection Devices

Embolic protection devices (EPD) were designed to capture and retrieve plaque particles that embolise during SVG intervention (see Table 2). In fact, MACE rates have been shown to double in SVG intervention compared with that of native coronary vessels.67 Despite the ACCF/AHA/SCAI class I indication for the use of EPDs during SVG intervention to decrease the risk of periprocedural MI, distal embolisation and no-reflow,66 they remain underutilized.68 EPDs can be categorised into distal occlusion aspiration devices, distal embolic filters and proximal occlusion aspiration devices.

Distal Occlusion Aspiration Devices

Distal occlusion aspiration devices use an interventional guidewire with an occlusion balloon that is inflated distal to the SVG lesion. Inflation obstructs antegrade flow, trapping plaque debris that is subsequently removed via an aspiration catheter. Such devices include the PercuSurge GuardWire (6F; Medtronic) and TriActiv® system (7F or 8F; Kensey Nash). The TriActiv includes a flush catheter for infusing heparinised saline during the procedure, which is absent in the GuardWire. Advantages of these EPDs include a low crossing profile and unlimited debris capture of particles <100 μm and soluble vasoactive mediators. Disadvantages include risk of embolisation during the wiring and device-crossing phase, ischaemia during balloon occlusion, limited contrast opacification and the risk of shunting debris into proximal side branches. Furthermore, guidewire selection cannot be tailored to procedural requirements and relatively disease-free distal landing zones are required.

The PercuSurge GuardWire became the first FDA-approved EPD following the results of the Saphenous vein graft Angioplasty Free of Emboli Randomized (SAFER) trial, which randomised 801 patients with SVG stenosis to stent placement over the GuardWire device shaft or a conventional angioplasty guidewire.69 EPDs significantly reduced the frequency of no-reflow (3 % versus 9 %; P=0.02), MI (8.6 % versus 14.7 %; P=0.008) and 30-day MACE (9.6 % versus 16.5 %; P=0.004). The TriActiv system was later FDA approved in the Protection During Saphenous Vein Graft Intervention to Prevent Distal Embolization (PRIDE) trial, which compared the TriActiv with both the GuardWire and the FilterWire EX™ (Boston Scientific) systems.70 TriActiv was non-inferior to the other devices in terms of 30-day MACE (11.2 % versus 10.1 %; P=0.65 [P=0.02 for non-inferiority]), but was associated with more vascular complications (10.9 % versus 5.4 %; P=0.01) and required more blood transfusions (7.7 % versus 3.5 %; P=0.02). These complications could be due to the larger calibre (8F) guiding catheters that were used in the TriActiv study arm.

Distal Embolic Filters

Distal embolic filters use filter bags with 100–110 μm-sized pores attached to the distal portion of a 0.014-inch guidewire with a delivery sheath. The filter bag is deployed distal to the target lesion to trap debris that embolises during the intervention and is later retrieved with its retained contents via a retrieval catheter. Advantages include the ability to maintain contrast opacification and perfusion during the procedure, along with ease of use. Disadvantages include the potential risk of distal embolisation during the wiring and device-crossing phases, debris embolisation during filter retrieval, inability to completely contain microparticles and soluble vasoreactive substances, large-diameter delivery sheath requirement and inability to deploy filters without a distal landing zone. Such devices include the FilterWire, Spider FXTM (Medtronic), Interceptor® PLUS Coronary Filter System (Medtronic Vascular) and CardioShield (MedNova).

The FilterWire EX became the first FDA-approved filter after completion of the FilterWire EX Randomized Evaluation (FIRE) trial, which compared the FilterWire EX with the GuardWire in 651 patients who received SVG PCI.71 The 30-day composite endpoint of MI, TVR or death was equivalent in both the FilterWire EX and GuardWire groups (9.9 % versus 11.6 %; superiority P=0.53, non-inferiority P<0.001), as were the 6-month MACE rates (19.3 % versus 21.9 %; P=0.44).72 The second-generation FilterWire EZ was then introduced with a lower crossing profile (3.2F versus 3.9F), smaller pore size (100 μm versus 110 μm) and overall improved delivery system compared with its predecessor. The Embolic Protection Transluminally with the FilterWire EZ Device in Saphenous Vein Grafts (BLAZE) registry reported that the success rate of this device was 97.8 %, and 30-day MACE rate was 6.7 % due entirely to non-Q-wave MI.73

The Spider Rx filtration device is also FDA approved for SVG intervention and was non-inferior to the FilterWire and GuardWire (MACE: 9.1 % versus 8.4 %; P=0.001 for non-inferiority) in the Saphenous Vein Graft protection In a Distal Embolic Protection Randomized Trial (SPIDER) trial.74 The Interceptor PLUS device was also non-inferior to the Filterwire and GuardWire in the (Assessment of the Medtronic AVE Interceptor Saphenous Vein Graft Filter System) AMEthyst trial.75 A multicentre, randomised clinical trial evaluating the CardioShield, a third-generation EPD, found the 30-day MACE primary endpoint occurred in 11.4 % with CardioShield versus 9.1 % with GuardWire (P=0.37), whereas intentionto- treat analysis demonstrated a strong trend for CardioShield noninferiority (P=0.57).76 A secondary modified intention-to-treat analysis including only patients receiving treatment device without protocol deviation also supported non-inferiority of CardioShield (P=0.022).76

Proximal Occlusion Aspiration Devices

The Proxis™ (7F; St. Jude Medical), which is no longer commercially available, is a proximal occlusion aspiration device that uses a guiding catheter with an inflatable balloon tip deployed proximal to the SVG lesion. This temporary suspension of antegrade flow generates a column of stagnant blood containing debris that is later aspirated via the guiding catheter. The balloon is deflated to restore antegrade perfusion following the intervention. Its advantages include use in lesions without a distal landing zone, retrieval of both atheromatous debris and vasoactive substances, protection from emboli prior to lesion crossing, protection of proximal side branches and the ability to tailor guidewire selection to procedural requirements. Notable disadvantages include limited contrast opacification and ischaemia during balloon occlusion. The Proximal Protection During Saphenous Vein Graft Intervention (PROXIMAL) trial evaluated the Proxis system in 594 patients undergoing stenting in 639 SVG lesions.77 The Proxis study arm was non-inferior to the control arm with distal EPDs (FilterWire or GuardWire) in the primary composite endpoint of MI, TVR or death at 30 days (10.0 % versus 9.2 %; P=0.0061).77

Recommendations

The trial data demonstrate the efficacy of all three EPD classes in minimising ischaemic complications. Its use must account for the degree of distal embolisation risk and the complexity of the coronary anatomy itself, especially when certain EPDs require distal landing zones. As indicated in the ACCF/AHA/SCAI guidelines, EPDs should ultimately be used during SVG intervention whenever feasible.66

Although these devices have proven effective during SVG intervention, they remain remarkably underutilised. An evaluation of 19,546 SVG PCI procedures in the American College of Cardiology-National Cardiovascular Data Registry found that EPDs were used in only 22 % of cases, despite being independently associated with a lower incidence of no-reflow (OR 0.68; P=0.032).78 One potential reason for this underutilisation could be that the delivery sheath heft makes distal filter deployment challenging. A recent study by Kaliyadan et al. highlighted the use of adjunct delivery techniques to optimize filter delivery in SVG procedures.79 Deployment failure in this study was reduced from 21.9 % initially to 7.6 % after using adjunct delivery techniques (P<0.01).79 Such techniques that facilitate device delivery success could potentially improve clinical outcomes and promote more frequent use of distal protection.

Adjunctive Pharmacology

Various pharmacological strategies can be used to decrease ischaemic complications during SVG intervention.

Glycoprotein IIb/IIIa Inhibitors

Adjunctive use of glycoprotein (GP) IIb/IIIa antagonists does not provide significant benefit in SVG intervention.80–82 The ACCF/AHA/SCAI guidelines recommend a class III (no benefit) indication for use of these agents in SVG lesions.66 The Evaluation of IIb/IIIa platelet receptor antagonist 7E3 in Preventing Ischemic Complications (EPIC) trial reported a reduction in the rate of distal embolisation in patients treated with GP IIb/IIIa inhibitors, but 30-day and 6-month clinical endpoints were comparable to those of the control group.80 Post hoc analysis of the FIRE trial showed a trend toward improved procedural success when GP IIb/IIIa inhibitors were used with filter-based embolic protection (P=0.058), but 30-day MACE rates were unchanged.83 Its potential benefit must be balanced by the potential risk of bleeding during SVG intervention.

Anticoagulants

Dual antiplatelet therapy recommendations for optimal treatment of SVG disease prior to hospitalisation are similar to that in native coronary vessel PCI.66,84 However, the ideal anticoagulants for SVG intervention have not been specifically established. A single-centre, retrospective, observational study reported that bivalirudin was associated with a significant reduction in major CK-MB level elevation compared with unfractionated heparin.85 Net clinical endpoints and rates of ischaemic bleeding were similar with bivalirudin monotherapy, bivalirudin plus a GP IIb/IIIa inhibitor and heparin plus a GP IIb/IIIa inhibitor in a subset of patients undergoing SVG intervention in the Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial.86 Bivalirudin alone had fewer minor bleeding complications compared with heparin plus a GP IIb/IIIa inhibitor (26 % versus 38 %; P=0.05). Heparin remains a popular choice for all forms of PCI, as the current ACCF/AHA/SCAI guidelines recommend a class I indication for its use in this setting.66

Vasodilators

Intragraft administration of vasodilators targets microvasculature to combat slow and no-reflow phenomena. Microcatheters can maximise pharmacotherapy delivery to these vessels. Pretreatment with intracoronary adenosine, a potent dilator of arteries and arterioles, decreases MI incidence after elective PCI,87,88 while it improves myocardial flow89,90 and lowers the incidence of no-reflow in the setting of acute MI.89,91 Adenosine may help reverse slow and no-reflow phenomena in patients undergoing SVG intervention.92,93 High doses of intragraft adenosine (at least five boluses of 24 μg each) significantly improved final Thrombolysis In Myocardial Infarction (TIMI) flow grade compared with low doses (less than five boluses) of adenosine (2.7 ± 0.6 versus 2.0 ± 0.8; P=0.04) and led to more slow and no-reflow reversal (91 % versus 33 %; P=0.02).93

Intragraft verapamil was effective in reducing no-reflow in SVG PCI.94–96 Intragraft verapamil (100–500 μg) improved flow in all 32 episodes of no-flow (TIMI flow grade 1.4 ± 0.8 pre- to 2.8 ± 0.5 post-intragraft verapamil; P<0.001) and re-established TIMI flow grade 3 in 88 % of cases.94 Prophylactic intragraft verapamil prior to SVG intervention mitigated occurrence of no-reflow compared with placebo (0 % versus 33.3 %; P=0.10) and increased TIMI frame count (53.3 ± 22.4 % faster versus 11.5 ± 38.9 %; P=0.016).96

Prophylactic intragraft nicardipine without the use of a distal protection device followed by direct stenting for degenerated SVG was shown to be safe and effective with low rates of slow-/no-reflow (2.4 %) and in-hospital MACE (4.4 %).97 Despite the lack of a control group for direct comparison, nicardipine appeared clinically beneficial compared with historical control data of SVG PCI procedures performed without nicardipine or distal protection devices.98,99 Nicardipine is not only used prophylactically during PCI, but is also safe and highly efficacious in reversing no-reflow, as demonstrated by Huang et al.100

Nitroprusside promotes nitric oxide production to induce vasodilation. One case-control study of patients who underwent SVG intervention pretreatment with nitroprusside (50–300 μg) reported significant reduction in periprocedural elevation of CK-MB levels >3x and >5x ULN, but no reduction in slow or no-reflow.101 However, another study found that nitroprusside (median dose 200 μg) injected into a diseased SVG led to highly significant and rapid improvement in both angiographic flow (P<0.01 compared with pretreatment angiogram) and blood flow velocity (P<0.01 compared with pretreatment angiogram) in SVG interventions complicated by either impaired flow or no-reflow.102

Conclusion

SVG conduit degeneration, restenosis and friable lesions with high embolic potential attenuate long-term CABG survival, while SVG intervention remains susceptible to high rates of periprocedural MI and no-reflow. When SVG disease requires intervention, proper stents, EPDs and pharmacological selection are essential for minimising complications. Both first- and second-generation DES demonstrate superiority over BMS in SVG intervention. The ACCF/AHA/SCAI guidelines recommend EPD use whenever feasible during SVG intervention to decrease the risk of embolisation complications. The optimal pharmacological treatment for slow or no-reflow is unclear, but various vasodilators show promise. When achievable, pan-arterial revascularisation or hybrid native coronary stenting with arterial revascularisation should be considered to minimise vein graft conduits in CABG.

References

  1. Fitzgibbon GM, Kafka HP, Leach AJ, et al. Coronary bypass graft fate and patient outcome: angiographic follow-up of 5,065 grafts related to survival and reoperation in 1,388 patients during 25 years. J Am Coll Cardiol 1996;28:616–26.
    Crossref | PubMed
  2. Björk VO, Ekeström S, Henze A, et al. Early and late patency of aortocoronary vein grafts. Scand J Thorac Cardiovasc Surg 1981;15:11–21.
    Crossref | PubMed
  3. Cataldo G, Braga M, Pirotta N, et al. Factors influencing 1-year patency of coronary artery saphenous vein grafts. Studio Indobufene nel Bypass Aortocoronarico (SINBA). Circulation 1993;88:II93–8.
    PubMed
  4. Roth JA, Cukingnan RA, Brown BG, et al. Factors influencing patency of saphenous vein grafts. Ann Thorac Surg 1979;28:176.
    Crossref | PubMed
  5. Blachutzik F, Achenbach S, Troebs M, et al. angiographic findings and revascularization success in patients with acute myocardial infarction and previous coronary bypass grafting. Am J Cardiol 2016;118:473–6.
    Crossref | PubMed
  6. Bundhoo SS, Kalla M, Anantharaman R, et al. Outcomes following PCI in patients with previous CABG: a multi centre experience. Catheter Cardiovasc Interv 2011;78:169–76.
    Crossref | PubMed
  7. Harskamp RE, Lopes RD, Baisden CE, et al. Saphenous vein graft failure after coronary artery bypass surgery: pathophysiology, management, and future directions. Ann Surg 2013;257:824–33.
    Crossref | PubMed
  8. Shi Y, O’Brien JE Jr, Mannion JD, et al. Remodeling of autologous saphenous vein grafts. The role of perivascular myofibroblasts. Circulation 1997;95:2684–93.
    Crossref | PubMed
  9. Yang Z, Oemar BS, Carrel T, et al. Different proliferative properties of smooth muscle cells of human arterial and venous bypass vessels: role of PDGF receptors, mitogenactivated protein kinase, and cyclin-dependent kinase inhibitors. Circulation 1998;97:181–7.
    Crossref | PubMed
  10. Chello M, Mastroroberto P, Perticone F, et al. Nitric oxide modulation of neutrophil-endothelium interaction: difference between arterial and venous coronary bypass grafts. J Am Coll Cardiol 1998;31:823–6.
    Crossref | PubMed
  11. Lüscher TF, Diederich D, Siebenmann R, et al. Difference between endothelium-dependent relaxation in arterial and in venous coronary bypass grafts. N Engl J Med 1988;319: 462–7.
    Crossref | PubMed
  12. Kauhanen P, Sirén V, Carpén O, et al. Plasminogen activator inhibitor-1 in neointima of vein grafts: its role in reduced fibrinolytic potential and graft failure. Circulation 1997;96: 1783–9.
    Crossref | PubMed
  13. Kockx MM, De Meyer GR, Bortier H, et al. Luminal foam cell accumulation is associated with smooth muscle cell death in the intimal thickening of human saphenous vein grafts. Circulation 1996;94:1255–62.
    Crossref | PubMed
  14. Motwani JG, Topol EJ. Aortocoronary saphenous vein graft disease: pathogenesis, predisposition, and prevention. Circulation 1998;97:916–31.
    Crossref | PubMed
  15. Mosleh W, Gandhi S, Elsiddig M, et al. Comparison of drugeluting stents with bare-metal stents for PCI of saphenous vein graft lesions: systematic review and meta-analysis. J Invasive Cardiol 2016;28:E139–69.
    PubMed
  16. Cox JL, Chiasson DA, Gotlieb AI. 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.
    Crossref | PubMed
  17. Hong MK, Mehran R, Dangas G, et al. Creatine kinase-MB enzyme elevation following successful saphenous vein graft intervention is associated with late mortality. Circulation 1999;100:2400–5.
    Crossref | PubMed
  18. Califf RM, Abdelmedgud AE, Kuntz RE, et al. Myonecrosis after revascularization procedures. J Am Coll Cardiol 1998;31:241–51.
    Crossref | PubMed
  19. Sdringola S, Assali AR, Ghani M, et al. Risk assessment of slow or no-reflow phenomenon in aortocoronary vein graft percutaneous intervention. Catheter Cardiovasc Interv 2001;54:318–24.
    Crossref | PubMed
  20. Kloner RA, Rude RE, Carlson N, et al. Ultrastructural evidence of microvascular damage and myocardial cell injury after coronary artery occlusion: which comes first? Circulation 1980;62:945–52.
    Crossref | PubMed
  21. van Gaal WJ, Banning AP. Percutaneous coronary intervention and the no-reflow phenomenon. Expert Rev Cardiovasc Ther 2007;5:715–31.
    Crossref | PubMed
  22. Coolong A, Baim DS, Kuntz RE, et al. Saphenous vein graft stenting and major adverse cardiac events: a predictive model derived from a pooled analysis of 3958 patients. Circulation 2008;117:790–7.
    Crossref | PubMed
  23. Naidu SS, Turco MA, Mauri L. Contemporary incidence and predictors of major adverse cardiac events after saphenous vein graft intervention with embolic protection (an AMEthyst trial substudy). Am J Cardiol 2010;105:1060–4.
    Crossref | PubMed
  24. Kirtane AJ, Heyman ER, Metzger C, et al. Correlates of adverse events during saphenous vein graft intervention with distal embolic protection: a PRIDE substudy. J Am Coll Cardiol Interv 2008;1:186–91.
    Crossref | PubMed
  25. Domanski MJ, Borkowf CB, Campeau L, et al. Prognostic factors for atherosclerosis progression in saphenous vein grafts: the postcoronary artery bypass graft (Post-CABG) trial. Post-CABG Trial Investigators. J Am Coll Cardiol 2000;36:1877–83.
    Crossref | PubMed
  26. Ahmed JM, Dangas G, Lansky AJ, et al. Influence of gender on early and one-year clinical outcomes after saphenous vein graft stenting. Am J Cardiol 2001;87:401–5.
    Crossref | PubMed
  27. Lee MS, Hu PP, Aragon J, et al. Impact of chronic renal insufficiency on clinical outcomes in patients undergoing saphenous vein graft intervention with drug-eluting stents: a multicenter Southern Californian Registry. Catheter Cardiovasc Interv 2010;76:272–8.
    Crossref | PubMed
  28. Gruberg L, Weissman NJ, Pichard AD, et al. Impact of renal function on morbidity and mortality after percutaneous aortocoronary saphenous vein graft intervention. Am Heart J 2003;145:529–34.
    Crossref | PubMed
  29. Aqel R, Zoghbi GJ, Hage F, et al. Hemodynamic evaluation of coronary artery bypass graft lesions using fractional flow reserve. Catheter Cardiovasc Interv 2008;72:479–85.
    Crossref | PubMed
  30. Lakkis NM, Mahmarian JJ, Verani MS. Exercise thallium-201 single photon emission computed tomography for evaluation of coronary artery bypass graft patency. Am J Cardiol 1995;76:107–11.
    Crossref | PubMed
  31. Hong YJ, Jeong MH, Ahn Y, Mintz GS, et al. Intravascular ultrasound analysis of plaque characteristics and postpercutaneous coronary intervention catheterization outcomes according to the remodeling pattern in narrowed saphenous vein grafts. Am J Cardiol 2012;110:1290–5.
    Crossref | PubMed
  32. Kohsaka S, Makaryus AN. Coronary angiography using noninvasive imaging techniques of cardiac CT and MRI. Curr Cardiol Rev 2008;4:323–30.
    Crossref | PubMed
  33. Schlosser T, Konorza T, Hunold P, et al. Noninvasive visualization of coronary artery bypass grafts using 16-detector row computed tomography. J Am Coll Cardiol 2004;44:1224–9.
    Crossref | PubMed
  34. Rodés-Cabau J, Bertrand OF, Larose E, et al. Comparison of plaque sealing with paclitaxel-eluting stents versus medical therapy for the treatment of moderate nonsignificant saphenous vein graft lesions: the moderate vein graft lesion stenting with the taxus stent and intravascular ultrasound (VELETI) pilot trial. Circulation 2009;120:1978–86.
    Crossref | PubMed
  35. Rodés-Cabau J. Plaque sealing with paclitaxel-eluting stents for the treatment of moderate non-significant saphenous vein graft lesions. Three-year follow-up of the VELETI (Moderate Vein Graft Lesion Stenting With the Taxus Stent and Intravascular Ultrasound) trial. Presented at: ACC i2 Summit Meeting 2010, Atlanta, GA, 14 March 2010.
  36. AI-Lamee R, Ielasi A, Latib A, et al. Clinical and angiographic outcomes after percutaneous recanalization of chronic total saphenous vein graft occlusion using modern techniques. Am J Cardiol 2010;106:1721–7.
    Crossref | PubMed
  37. ClinicalTrial.gov. Sealing Moderate Coronary Saphenous VEin Graft Lesions With Paclitaxel-Eluting Stents (VELETI II). Available at: https://clinicaltrials.gov/ct2/show/NCT01223443 (accessed 29 June 2017)
  38. Hindnavis V, Cho SH, Goldberg S. Saphenous vein graft intervention: a review. J Invasive Cardiol 2012;24:64–71.
    PubMed
  39. Brilakis ES, Rao SV, Banerji S, et al. Percutaneous coronary intervention in native arteries versus bypass grafts in prior coronary artery bypass grafting patients: a report from the National Cardiovascular Data Registry. JACC Cardiovasc Interv 2011;4:844–50.
    Crossref | PubMed
  40. Leborgne L, Cheneau E, Pichard A, et al. Effect of direct stenting on clinical outcome in patients treated with percutaneous coronary intervention on saphenous vein graft. Am Heart J 2003;146:501–6.
    Crossref | PubMed
  41. Okabe T, Lindsay J, Torguson R, et al. Can direct stenting in selected saphenous vein graft lesions be considered an alternative to percutaneous intervention with a distal protection device? Catheter Cardiovasc Interv 2008;72:799–803.
    Crossref | PubMed
  42. Hong YJ, Pichard AD, Mintz GS, et al. Outcome of undersized drug-eluting stents for percutaneous coronary intervention of saphenous vein graft lesions. Am J Cardiol 2010;105:179–85.
    Crossref | PubMed
  43. Savage MP, Douglas JS, Fischman DL, et al. Stent placement compared with balloon angioplasty for obstructed coronary bypass grafts. Saphenous Vein De Novo Trial Investigators. N Engl J Med 1997;337:740–7.
    Crossref | PubMed
  44. Baldus S, Koster R, Elsner M, et al. Treatment of aortocoronary vein graft lesions with membrane-covered stents: a multicenter surveillance trial. Circulation 2000;102:2024–7.
    Crossref | PubMed
  45. Schachinger V, Hamm CW, Munzel T, et al; STING (STents IN Grafts) Investigators. A randomized trial of polytetrafluoroethylene-membrane-covered stents compared with conventional stents in aortocoronary saphenous vein grafts. J Am Coll Cardiol 2003;42:1360–9.
    Crossref | PubMed
  46. Stankovic G, Colombo A, Presbitero P, et al. Randomized Evaluation of polytetrafluoroethylene COVERed stent in Saphenous vein grafts (RECOVERS) Trial. Circulation 2003;108:37–42.
    Crossref | PubMed
  47. Turco MA, Buchbinder M, Popma JJ, et al. Pivotal, randomized U.S. study of the SymbiotTM covered stent system in patients with saphenous vein graft disease: eight-month angiographic and clinical results from the Symbiot III trial. Catheter Cardiovasc Interv 2006;68:379–88.
    Crossref | PubMed
  48. Stone GW, Goldberg S, O’Shaughnessy C, et al. 5-year followup of polytetrafluoroethylene-covered stents compared with bare-metal stents in aortocoronary saphenous vein grafts. The randomized BARRICADE (barrier approach to restenosis: restrict intima to curtail adverse events) trial. JACC Cardiovasc Interv 2011;4:300–9.
    Crossref | PubMed
  49. Abizaid A, Weiner B, Bailey SR, Londero H. Use of a selfexpanding super-elastic all-metal endoprosthesis; to treat degenerated SVG lesions: the SESAME first in man trial. Catheter Cardiovasc Interv 2010;76:781–6.
    Crossref | PubMed
  50. Maia F, Costa JR Jr, Abizaid A, et al. Preliminary results of the INSPIRE trial with the novel MGuard stent system containing a protection net to prevent distal embolization. Catheter Cardiovasc Interv 2010;76:86–92.
    Crossref | PubMed
  51. Mehilli J. ISAR-CABG: randomized, superiority trial of drugeluting- stent and bare metal stent in saphenous vein graft lesions. Presented at: American College of Cardiology 2011 Scientific Session, New Orleans, LA, USA, 4 April 2011.
  52. Brilakis ES, Lichtenwalter C, de Lemos JA, et al. A randomized controlled trial of a paclitaxel-eluting stent versus a similar bare-metal stent in saphenous vein graft lesions: the SOS (Stenting of Saphenous Vein Grafts) trial. J Am Coll Cardiol 2009;53:919–28.
    Crossref | PubMed
  53. Brilakis ES, Lichtenwalter C, Abdel-Karim AR, et al. Continued benefit from paclitaxel-eluting compared to bare-metal stent implantation in saphenous vein graft lesions during long-term follow-up of the SOS (Stenting of Saphenous Vein Grafts) trial. J Am Coll Cardiol Interv 2011;4:176–82.
    Crossref | PubMed
  54. Vermeersch P, Agostoni P, Verheye S, et al. Randomized double-blind comparison of sirolimus-eluting stent versus bare-metal stent implantation in diseased saphenous vein grafts: six-month angiographic, intravascular ultrasound, and clinical follow-up of the RRISC Trial. J Am Coll Cardiol 2006;48:2423–31.
    Crossref | PubMed
  55. Vermeersch P, Agostoni P, Verheye S; DELAYED RRISC Investigators, et al. Increased late mortality after sirolimuseluting stents versus bare-metal stents in diseased saphenous vein grafts: results from the randomized DELAYED RRISC Trial. J Am Coll Cardiol 2007;50:261–7.
    Crossref | PubMed
  56. Wiisanen ME, Abdel-Latif A, Mukherjee D, Ziada KM. Drugeluting stents versus bare-metal stents in saphenous vein graft interventions: a systematic review and meta-analysis. J Am Coll Cardiol Interv 2010;3:1262–73.
    Crossref | PubMed
  57. Lee MS, Yang T, Kandzari DE, et al. Comparison by metaanalysis of drug-eluting stents and bare metal stents for saphenous vein graft intervention. Am J Cardiol 2010;105:1076– 82.
    Crossref | PubMed
  58. Meier P, Brilakis ES, Corti R, et al. Drug-eluting versus bare-metal stent for treatment of saphenous vein grafts: a meta-analysis. PLoS One 2010;5:e11040.
    Crossref | PubMed
  59. Joyal D, Filion KB, Eisenberg MJ. Effectiveness and safety of drug-eluting stents in vein grafts: a meta-analysis. Am Heart J 2010;159:159–69.e4.
    Crossref | PubMed
  60. Sanchez-Recalde A, Jimenez Valero SJ, Moreno R, et al. Safety and efficacy of drug-eluting stents in saphenous vein grafts lesions: a meta-analysis. EuroIntervention 2010;6:149–60.
    Crossref | PubMed
  61. Testa L, Agostoni P, Vermeersch P, et al. Drug eluting stent versus bare metal stent in the treatment of saphenous vein graft disease: a systematic review and meta-analysis. EuroIntervention 2010;6:527–36.
    Crossref | PubMed
  62. J.-M. Paradis, P. Bélisle, L. Joseph, et al. Drug-eluting or bare metal stents for the treatment of saphenous vein graft disease: a Bayesian meta-analysis. Circ Cardiovasc Interv 2010;3:565–76.
    Crossref | PubMed
  63. Hakeem A, Helmy T, Munsif S, et al. Safety and efficacy of drug eluting stents compared with bare metal stents for saphenous vein graft interventions: a comprehensive meta-analysis of randomized trials and observational studies comprising 7,994 patients. Catheter Cardiovasc Interv 2011;77:343–55.
    Crossref | PubMed
  64. Lee MS, Hu PP, Aragon J, et al. Comparison of sirolimuseluting stents with paclitaxel-eluting stents in saphenous vein graft intervention (from a multicenter Southern California Registry). Am J Cardiol 2010;106:337–41.
    Crossref | PubMed
  65. Taniwaki M, Räber L, Magro M, et al. Long-term comparison of everolimus-eluting stents with sirolimus- and paclitaxeleluting stents for percutaneous coronary intervention of saphenous vein grafts. EuroIntervention 2014;9:1432–40.
    Crossref | PubMed
  66. Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/ SCAI Guideline for Percutaneous Coronary Intervention: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. Catheter Cardiovasc Interv 2012;79:453–95.
    Crossref | PubMed
  67. Stone GW, Rogers C, Hermiller J, et al. Randomized comparison of distal protection with a filter-based catheter and a balloon occlusion and aspiration system during percutaneous intervention of diseased saphenous vein aorto-coronary bypass grafts. Circulation 2003;108:548–53.
    Crossref | PubMed
  68. Mauri L, Rogers C, Baim DS. Devices for distal protection during percutaneous coronary revascularization. Circulation 2006;113:2651–6.
    Crossref | PubMed
  69. Baim DS, Wahr D, George B, et al. Randomized trial of a distal embolic protection device during percutaneous intervention of saphenous vein aorto-coronary bypass grafts. Circulation 2002;105:1285–90.
    PubMed
  70. Carrozza JP Jr, Mumma M, Breall JA, et al. Randomized evaluation of the TriActiv balloon-protection flush and extraction system for the treatment of saphenous vein graft disease. J Am Coll Cardiol 2005;46:1677–83.
    Crossref | PubMed
  71. Stone GW, Rogers C, Hermiller J, et al. Randomized comparison of distal protection with a filter-based catheter and a balloon occlusion and aspiration system during percutaneous intervention of diseased saphenous vein aorto-coronary bypass grafts. Circulation 2003;108:548–53.
    Crossref | PubMed
  72. Halkin A, Masud Z, Rogers C, et al. Six-month outcomes after percutaneous intervention for lesions in aortocoronary saphenous vein grafts using distal protection devices: results from the FIRE trial. Am Heart J 2006;151:915.e1–7.
    Crossref | PubMed
  73. Vermeersch P, Agostoni P, Verheye S, et al. Increased late mortality after sirolimus-eluting stents versus bare-metal stents in diseased saphenous vein grafts: results from the randomized DELAYED RRISC Trial. J Am Coll Cardiol. 2007; 50(3):261–7.
    Crossref | PubMed
  74. Dixon SR. Saphenous vein graft protection in a distal embolic protection randomized trial. Presented at: Transcatheter Cardiovascular Therapeutics 2005,; Washington, DC, USA, 18 October 2005.
  75. Kereiakes DJ, Turco MA, Breall J, et al. A novel filterbased distal embolic protection device for percutaneous intervention of saphenous vein graft lesions: results of the AMEthyst randomized controlled trial. JACC Cardiovasc Interv 2008;1:248–57.
    Crossref | PubMed
  76. Holmes DR, Coolong A, O’Shaughnessy C, et al. Comparison of the CardioShield filter with the GuardWire balloon in the prevention of embolisation during vein graft intervention: results from the CAPTIVE randomised trial. EuroIntervention 2006;2:161–8.
    PubMed
  77. Mauri L, Cox D, Hermiller J, et al. The PROXIMAL trial: proximal protection during saphenous vein graft intervention using the Proxis Embolic Protection System: a randomized, prospective, multicenter clinical trial. J Am Coll Cardiol 2007;50:1442–9.
    Crossref | PubMed
  78. Mehta SK, Frutkin AD, Milford-Beland S, et al. Utilization of distal embolic protection in saphenous vein graft interventions (an analysis of 19,546 patients in the American College of Cardiology-National Cardiovascular Data Registry). Am J Cardiol 2007;100:1114–8.
    Crossref | PubMed
  79. Kaliyadan AG, Chawla H, Fischman DL, et al. Importance of adjunct delivery techniques to optimize deployment success of distal protection filters during vein graft intervention. J Invasive Cardiol 2017;29:54–58.
    PubMed
  80. Mak KH, Challapalli R, Eisenberg MJ, et al. Effect of platelet glycoprotein IIb/IIIa receptor inhibition on distal embolization during percutaneous revascularization of aortocoronary saphenous vein grafts: EPIC Investigators. Evaluation of IIb/ IIIa platelet receptor antagonist 7E3 in Preventing Ischemic Complications. Am J Cardiol 1997;80:985–8.
    Crossref | PubMed
  81. Roffi M, Mukherjee D, Chew DP, et al. Lack of benefit from intravenous platelet glycoprotein IIb/IIIa receptor inhibition as adjunctive treatment for percutaneous interventions of aortocoronary bypass grafts: a pooled analysis of five randomized clinical trials. Circulation 2002;106:3063–7.
    Crossref | PubMed
  82. Ellis SG, Lincoff AM, Miller D. Reduction in complications of angioplasty with abciximab occurs largely independently of baseline lesion morphology: EPIC and EPILOG investigators. Evaluation of 7E3 for the Prevention of Ischemic Complications. Evaluation of PTCA to Improve Long-Term Outcome With Abciximab GPIIb/IIIa Receptor Blockade. J Am Coll Cardiol 1998;32:1619–23.
    Crossref | PubMed
  83. Jonas M, Stone GW, Mehran R, et al. Platelet glycoprotein IIb/IIIa receptor inhibition as adjunctive treatment during saphenous vein graft stenting: differential effects after randomization to occlusion or filter-based embolic protection. Eur Heart J 2006;27:920–8.
    Crossref | PubMed
  84. Harskamp RE, Beijk MA, Damman P, et al. Prehospitalization antiplatelet therapy and outcomes after saphenous vein graft intervention. Am J Cardiol 2013;111:153–8.
    Crossref | PubMed
  85. Rha SW, Kuchulakanti PK, Pakala R, et al. Bivalirudin versus heparin as an antithrombotic agent in patients who undergo percutaneous saphenous vein graft intervention with a distal protection device. Am J Cardiol 2005;96:67–70.
    Crossref | PubMed
  86. Kumar D, Dangas G, Mehran R. Comparison of bivalirudin versus bivalirudin plus glycoprotein IIb/IIIa inhibitor versus heparin plus glycoprotein IIb/IIIa inhibitor in patients with acute coronary syndromes having percutaneous intervention for narrowed saphenous vein aorto-coronary grafts (the ACUITY Trial Investigators). Am J Cardiol 2010;106:941–5.
    Crossref | PubMed
  87. Lee CH, Low A, Tai BC, et al. Pretreatment with intracoronary adenosine reduces the incidence of myonecrosis after nonurgent percutaneous coronary intervention: a prospective randomized study. Eur Heart J 2007;28:19–25.
    Crossref | PubMed
  88. Desmet WJ, Dens J, Coussement P, Van de Werf F. Does adenosine prevent myocardial micronecrosis following percutaneous coronary intervention? The ADELINE pilot trial. ADEnosine LImit myocardial Necrosis. Heart 2002;88:293–5.
    Crossref | PubMed
  89. Marzilli M, Orsini E, Marraccini P, Testa R. Beneficial effects of intracoronary adenosine as an adjunct to primary angioplasty in acute myocardial infarction. Circulation 2000;101:2154–9.
    Crossref | PubMed
  90. Stoel MG, Marques KM, de Cock CC, et al. High dose adenosine for suboptimal myocardial perfusion ater primary PCI: a randomized placebo-controlled pilot study. Catheter Cardiovasc Interv 2008;71:283–9.
    Crossref | PubMed
  91. Assali AR, Sdringola S, Ghani M, et al. Intracoronary adenosine administered during percutaneous intervention in acute myocardial infarction and reduction in the incidence of “no reflow” phenomenon. Catheter Cardiovasc Interv 2000;51:27–32.
    Crossref | PubMed
  92. Fischell TA, Carter AJ, Foster MT, et al. Reversal of “no reflow” during vein graft stenting using high velocity boluses of intracoronary adenosine. Cathet Cardiovasc Diagn 1998;45:360–5.
    Crossref | PubMed
  93. Sdringola S, Assali A, Ghani M, et al. Adenosine use during aortocoronary vein graft interventions reverses but does not prevent the slow-no reflow phenomenon. Catheter Cardiovasc Interv 2000;51:394–9.
    Crossref | PubMed
  94. Kaplan BM, Benzuly KH, Kinn JW, et al. Treatment of no-reflow in degenerate saphenous vein graft interventions: comparison of intracoronary verapamil and nitroglycerin. Cathet Cardiovasc Diagn 1996;39:113–8.
    Crossref | PubMed
  95. Piana RN, Paik GY, Mosucci M, et al. Incidence and treatment of ‘no-reflow’ after percutaneous coronary intervention. Circulation 1994;89:2514–8.
    Crossref | PubMed
  96. Michaels AD, Appleby M, Otten MH, et al. Pretreatment with intragraft verapamil prior to percutaneous coronary intervention of saphenous vein graft lesions: results of the randomized, controlled vasodilator prevention on no-reflow (VAPOR) trial. J Invasive Cardiol 2002;14:299–302.
    PubMed
  97. Fischell TA, Subraya RG, Ashraf K, et al. “Pharmacologic” distal protection using prophylactic, intragraft nicardipine to prevent no-reflow and non-Q wave myocardial infarction during elective saphenous vein graft intervention. J Invasive Cardiol 2007;19:58–62.
    PubMed
  98. Resnic FS, Wainstein M, Lee MK, et al. No-reflow is an independent predictor of death and myocardial infarction after percutaneous coronary intervention. Am Heart J 2003;145:42–6.
    Crossref | PubMed
  99. Abbo KM, Dooris M, Glazier S, et al. Features and outcome of no-reflow after percutaneous coronary intervention. Am J Cardiol 1995;75:778–82.
    Crossref | PubMed
  100. Huang R, Patel P, Walinsky P, et al. Efficacy of intracoronary nicardipine in the treatment of no-reflow during percutaneous coronary intervention. Catheter Cardiovasc Interv 2006;68:671–6.
    Crossref | PubMed
  101. Zoghbi GJ, Goyal M, Hage F, et al. Pretreatment with nitroprusside for microcirculatory protection in saphenous vein graft interventions. J Invasive Cardiol 2009;21:34–9.
    PubMed
  102. Hillegass WB, Dean NA, Liao L, et al. Treatment of no-reflow and impaired flow with the nitric oxide donor nitroprusside following percutaneous coronary interventions: initial human clinical experience. J Am Coll Cardiol 2001;37:1335–43.
    Crossref | PubMed
Previous Volume Article Next Volume Article