Surveillance of Lower Extremity Bypass Grafts



Surveillance of Lower Extremity Bypass Grafts



Kelley Hodgkiss-Harlow and Dennis F. Bandyk


Vascular laboratory surveillance of infrainguinal bypass graft function has evolved to a recommended standard of patient care. The rationale for testing is based on the progressive nature of atherosclerosis and the propensity of both autologous vein and prosthetic conduits to develop stenotic lesions that produce a low-flow state and result in graft thrombosis.


Infrainguinal vein bypasses, constructed by reversed, nonreversed, or in-situ grafting techniques, tend to form stenotic lesions within the conduit (70%) or at anastomotic sites (30%) during the first several months to years following implantation. These stenotic lesions have the histologic appearance of myointimal hyperplasia and are known to develop at sites of vein injury, form at valve sites, result from preexisting vein disease, or arise de novo in response to arterialization in the atherosclerotic environment (Box 1).



BOX 1   Lesions That Can Precipitate Graft Failure




Similarly, lower limb expanded polytetrafluoroethylene (ePTFE) and polyester grafts demonstrate a steady attrition rate (∼10%/year) as a result of progressive inflow and outflow occlusive lesions caused by myointimal hyperplasia or atherosclerotic disease progression. The location and appearance time of these lesions differ from those of vein grafts. Intragraft lesions are uncommon (5%–7%), with most stenoses developing at the anastomotic sites to the outflow (58%) or inflow (30%) arteries.


Diagnostic testing of a failing graft must be capable of identifying stenosis and providing an assessment of graft flow rate using appropriate methodology and interpretation criteria. Less than half of the patients with a documented graft stenosis admit to symptoms of limb ischemia (claudication, rest pain). Thus, detection of graft stenoses before thrombosis requires objective use of a direct testing method such as duplex ultrasound.


Ultrasound graft imaging should be combined with measurement of Doppler-derived ankle systolic blood pressures to improve diagnostic accuracy of both sensitivity and positive predictive value. Surveillance studies based on duplex scanning have confirmed that stenoses develop in 20% to 30% of infrainguinal vein bypasses during the first postoperative year. The development of more than 70% stenosis is associated with a threefold increase in graft occlusion and accounts for 80% of graft failures within 5 years of the procedure.


Duplex surveillance also aids in the timing of graft revision and selection of the repair technique. Data that link severe graft stricture detected by either angiography or duplex scanning to an increased risk of graft occlusion are persuasive. Grigg and Moody observed a 21% to 23% incidence of thrombosis in stenotic vein bypasses when a conservative no-revision policy was followed. Idu and coworkers reported all infrainguinal vein grafts that had a stenosis greater than 70% diameter reduction eventually occluded, compared to 10% of grafts with similar but repaired lesions (p < .01). Mattos and associates also reported infrainguinal grafts that had stenosis by color duplex scanning (velocity ratio >2) had a significantly lower 4-year patency of 57% compared to 83% observed in normal grafts. Intervention, based on a duplex surveillance protocol, has resulted in 5-year assisted primary patency rates of 82% to 93%, significantly higher than the 30% to 50% secondary patency rates of thrombosed vein grafts. Clinical studies indicate that routine infrainguinal bypass surveillance can enhance long-term patency by at least 15% to 20%.


In regard to repair techniques, a duplex finding of a focal (<4 cm length) stenosis supports endovascular repair by percutaneous transluminal angioplasty (PTA), with an open surgical repair reserved for diffuse vein conduit stenosis or treatment of an outflow occlusion by jump grafting. Finally, from an economic cost analysis perspective, Wixon’s group demonstrated that particularly within the first year, revision of a duplex-identified stenosis proved to be significantly less costly than revision after graft thrombosis.



Mechanisms and Hemodynamics of Graft Failure


Graft failure can occur by one of three mechanisms: occlusion by thrombosis or embolization, hemodynamic failure, or structural failure associated with aneurysmal degeneration or infection. The incidence of vein graft failure is highest during the first several postoperative days (4%–10%), decreases to approximately 1% per month during the first year, and then is approximately 2% to 4% per year thereafter.


Perioperative graft failure (within 30 days) accounts for one quarter of all failures and may be a result of technical errors in bypass construction (e.g., suture stenosis, intimal flaps, retained thrombus, graft entrapment, torsion), inadequate outflow, infection, or unrecognized hypercoagulable states.


Failure between 30 days and 2 years is usually the result of focal myointimal hyperplasia within the vein conduit or at anastomotic sites; rarely, diffuse stricture of the venous conduit occurs. Late graft failure is most often the result of atherosclerotic disease progression. Graft failure as a result of aneurysmal degeneration, anastomotic false aneurysm, or thromboembolism can occur at any time after implantation but is uncommon and accounts for less than 10% of all failures.


The incidence of early graft failure can be minimized by careful operative assessment, but conditions such as hypercoagulable states, use of marginal sclerotic venous conduits, low cardiac output, or poor outflow can produce graft thrombosis despite a technically perfect reconstruction. Infrainguinal bypasses, especially prosthetic grafts, with poor runoff can demonstrate a blood flow velocity near the thrombotic threshold velocity of the conduit and be prone to thrombosis with slight decreases in blood flow. Assessment of graft hemodynamics is an underemphasized principle of surveillance, despite studies that document a 5% to 10% incidence of vascular defects when quantitative Doppler spectral analysis was performed. Reluctance to use duplex scanning at operation has been attributed to its complexity, instrument availability, and the erroneous assumption that arteriography is superior.


Bypass graft abnormalities can persist unsuspected, especially when in-situ or nonreversed saphenous vein grafting techniques are used. Retained valve cusps, errors in tunneling, vein conduit injury, or partial anastomotic occlusion can reduce graft flow so that thrombus formation can occur and precipitate an occlusion. Residual lesions can also be the origin of myointimal hyperplasia, a lesion known to cause graft failure during the first months after operation. The application of early (1 to 3 weeks) duplex surveillance can detect these abnormalities and identify those that should be repaired based on severity of stenosis.


Atherosclerosis can also develop in grafts or adjacent native arteries to produce graft failure. This mechanism of graft failure tends to occur after postoperative year 2 in autologous vein bypasses but has been observed earlier in ePTFE bypasses. Structural failure is an uncommon cause of vein graft failure and is manifest late as aneurysmal degeneration. The mechanism of graft thrombosis involves accumulation of mural thrombus within the aneurysmal segment, leading to occlusion or distal embolization. This mode of failure should be suspected when thrombosis occurs in the setting of normal graft surveillance studies.


Stenotic lesions produce graft occlusion by decreasing blood flow velocity below a minimum velocity at which thrombus formation can ensue. Duplex scanning can identify focal stenoses based on velocity spectral criteria: peak systolic velocity (PSV) greater than 180 cm/sec and velocity ratio across the stenosis (Vr) greater than 2. Grafts demonstrating both a high-grade focal stenosis and low-flow state (mean graft velocity [MGV] < 45 cm/sec) in a normal-diameter graft segment are at increased risk for thrombosis. Early duplex testing can dictate management of both moderate graft stenosis (PSV 180–300 cm/sec), of which about 30% improve when detected early, as well as criteria for graft revision, such as duplex-detected stenosis with a PSV greater than 300 and a Vr greater than 3.5.


Tests are interpreted based on pulsed Doppler velocity spectra changes and real-time B-mode imaging at graft lesion sites. Information necessary to implement graft revision can be provided by finding a high-grade (>70% diameter reduction) stenosis: PSV > 300 cm/sec and Vr > 3.5. These lesions have a damped velocity waveform downstream of the stenosis and reduction in MGV; the MGV is calculated as the average of graft PSV measured at two or three nonstenotic graft segments of less than 30 cm/sec compared to levels when no graft stenosis was present.


A decrease in the ankle-to-brachial index (ABI) also predicts an acquired graft lesion, but it is associated with a low positive predictive value for graft thrombosis. In selected patients, such as those with a high-grade stenosis identified in the body of the graft or at an anastomosis and a low graft flow velocity or ABI, duplex scanning can supplant arteriography for clinical decision making and the need for graft revision. Serial duplex testing beginning in the early postoperative period, repeated within 1 to 2 months, and then at 6-month intervals if no graft abnormality is detected offers several advantages. It predicts initial technical success, identifies the graft with residual stenosis, and detects deterioration in graft functional patency, so developing occlusive lesions can be easily managed by elective surgical revision or percutaneous transluminal angioplasty.


A wide range of duplex-derived blood flow velocities can be measured in infrainguinal grafts after successful bypass grafting. In general, PSV in mid and distal graft segments exceeds 40 to 45 cm/sec unless the conduit diameter is greater than 6 mm or the graft runoff is limited to an isolated tibial artery segment or dorsalis pedis artery. The graft PSV varies with luminal diameter, and it is recommended that duplex surveillance be performed using diameter-specific criteria. Belkin and colleagues found graft flow velocity was lower (p < .04) in inframalleolar grafts (59 cm/sec) compared to tibial (77 cm/sec) and popliteal (71 cm/sec) grafts. Only four of 72 grafts, all to inframalleolar arteries, had a measured PSV below 45 cm/sec. Arm vein or varicose saphenous segment grafts were also associated with low graft conduit flow velocity. Lower limb prosthetic bypasses have an MGV of 50 to 70 cm/sec, axillofemoral bypass has an MGV greater than 150 cm/sec, and femorofemoral bypass has an MGV greater than 100 cm/sec. Thus, the hemodynamic parameter by itself does not predict impending thrombosis but can guide decision making regarding the potential benefit of instituting postoperative oral anticoagulation. A low graft flow velocity because of poor runoff is an infrequent finding.


Management of low-flow grafts caused by poor runoff is controversial, but options include anticoagulation, sequential bypass grafting, or adjunctive distal arteriovenous fistulas, the last two modalities being constructed to augment graft flow.


Interpretation of vascular laboratory testing allows the bypass graft to be classified as normal or abnormal (Figure 1, Table 1). Normal graft hemodynamics in limbs revascularized for critical ischemia have a low-resistance graft blood-flow pattern, with antegrade flow throughout the pulse cycle reflecting hyperemic flow. Within days to several weeks, the hyperemic graft flow dissipates, and the velocity waveform gradually changes to a triphasic configuration typical of normal peripheral artery blood flow and ABI. If the normal triphasic graft velocity waveform changes to a monophasic configuration, coupled with an MGV decrease, a graft stenosis should be suspected. The reduction in waveform pulsatility and the presence of a diastolic blood flow component indicates a pressure-reducing stenosis and compensatory arteriolar dilatation. The site of graft stenosis may be proximal or distal to the recording site.


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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Surveillance of Lower Extremity Bypass Grafts

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