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Surgical Management of Cardiovascular Thrombotic Conditions Chapter | 25 375
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Subxiphoid approach with right anterior thoracotomy:Iftheoutflow graft cannot be accessed through a s ubxiphoid
incision alone, or the outflow graft or aortic anastomosis requires revision, we perform a right anterior thoracotomy
in the third inte rcostal space. New-generation pumps are using evolving technology to cool the pumps (ReliantHeart) or try to use a pulsatile flow pattern. Future clinical studies will show which modification will be more
effective.
REFERENCES
[1] Horlander KT, Mannino DM, Leeper KV. Pulmonary embolism mortality in the United States, 1979-1998: an analysis using multiple-cause
mortality data. Arch Intern Med 2003;163:1711e7.
[2] United States Department of Health, Human Services. The Surgeon General’s call to action to prevent deep vein thrombosis and pulmonary
embolism. 2008.
[3] Girard P, Decousus M, Laporte S, et al. Diagnosis of pulmonary embolism in patients with proximal deep vein thrombosis: specificity of symptoms
and perfusion defects at baseline and during anticoagulant therapy. Am J Respir Crit Care Med 2001;164:1033e7.
[4] Kistner RL, Ball JJ, Nordyke RA, et al. Incidence of pulmonary embolism in the course of thrombophlebitis of the lower extremities. Am J Surg
1972;124:169e76.
[5] Moser KM, LeMoine JR. Is embolic risk conditioned by location of deep venous thrombosis? Ann Intern Med 1982;94:439e44.
[6] Weinmann EE, Salzman EW. Deep-vein thrombosis. N Engl J Med 1994;331:1630e41.
[7] van Langevelde K, Srámek A, Vincken PW, et al. Finding the origin of pulmonary emboli with a total-body magnetic resonance direct thrombus
imaging technique. Haematologica 2013;98:309e15.
[8] Nakos G, Kitsiouli EI, Lekka ME. Bronchoalveolar lavage alterations in pulmonary embolism. Am J Respir Crit Care Med 1998;158:1504e10.
[9] Kucher N, Rossi E, Rosa M. Massive pulmonary embolism. Circulation 2006;113:577e82.
[10] Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and
chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation 2011;123:1788e830.
[11] Konstantinides SV, Torbicki A, Agnelli G, et al. 2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J
2014;35:3033e69.
[12] Leacche M, Unic D, Goldhaber SZ, et al. Modern surgical treatment of massive pulmonary embolism: results in 47 consecutive patients after rapid
diagnosis and aggressive surgical approach. J Thorac Cardiovasc Surg 2005;12:1018e23.
[13] He C, Von Segesser LK, Kappetein PA, et al. Acute pulmonary embolectomy. Eur J Cardio Thorac Surg 2013;43:1087e95.
[14] Amirghofran AA, Nia AE, Javan R, et al. Surgical embolectomy in acute massive pulmonary embolism. Asian Cardiovasc Thorac Ann
2007;15:149e53.
[15] Zarrabi K, Zolghadrasli A, Ostovan MA, et al. Short term results of retrograde pulmonary embolectomy in massive and submassive pulmonary
embolism: a single-center study of 30 patients. Eur J Cardio Thorac Surg 2011;40:890e3.
[16] Sukhija R, Aronow WS, Lee J, et al. Association of right ventricular dysfunction with in-hospital mortality in patients with acute pulmonary
embolism and reduction in mortality in patients with right ventricular dysfunction by pulmonary embolectomy. Am J Cardiol 2005;95:695e6.
[17] Greelish JP, Leacche M, Solenkova NS, et al. Improved midterm outcomes for type A (central) pulmonary emboli treated surgically. J Thorac
Cardiovasc Surg 2011;142:1423e9.
[18] Worku B, Gulkarov I, Girardi LN, et al. Pulmonary embolectomy in the treatment of submassive and massive pulmonary embolism. Cardiology
2014;129:106e10.
[19] Aymard T, Kadner A, Widmer A, et al. Massive pulmonary embolism: surgical embolectomy versus thrombolytic therapydshould surgical in-
dications be revisited? Eur J Cardio Thorac Surg 2013;43:90e4.
[20] Weinberg I, Jaff MR. Treating large pulmonary emboli: do the guidelines guide us? Curr Opin Pulm Med 2013;19:413e21.
[21] Yusuff HO, Zochios V, Vuylsteke A. Extracorporeal membrane oxygenation in acute massive pulmonary embolism: a systematic review. Perfusion
2015;30(8):611e6.
[22] Malekan R, Saunders PC, Yu CJ, et al. Peripheral extracorporeal membrane oxygenation: comprehensive therapy for high-risk massive pulmonary
embolism. Ann Thorac Surg 2012;94(1):104e8.
[23] Berman M, Tsui S, Vuylsteke A, et al. Successful extracorporeal membrane oxygenation support after pulmonary thromboendarterectomy. Ann
Thorac Surg 2008;86(4):1261e7.
[24] Maggio P, Hemmila M, Haft J, Bartlett R. Extracorporeal life support for massive pulmonary embolism. J Trauma Inj Infect Crit Care
2007;62(3):570e6.
[25] Misawa Y. Extracorporeal membrane oxygenation support for acute pulmonary embolism. Circulation 2004;109(20):229.
[26] Deehring R, Kiss AB, Garrett A, Hillier AG. Extracorporeal membrane oxygenation as a bridge to surgical embolectomy in acute fulminant
pulmonary embolism. Am J Emerg Med 2006;24(7):879e80.
[27] Neely R, Byrne JG, Gosev I, et al. Surgical embolectomy for acute massive and submassive pulmonary embolism in a series of 115 patients. Ann
Thorac Surg 2015;100:1245e52.
[28] Kalra R, Bajaj NS, Arora P, et al. Surgical embolectomy for acute pulmonary embolism: systematic review and comprehensive meta-analyses. Ann
Thorac Surg 2017;103:982e90.
376 Cardiovascular Thrombus
https://t.me/med1917
[29] Edmunds Jr LH, Clark RE, Cohn LH, et al. Guidelines for reporting morbidity and mortality after cardiac valvular operations. Ad Hoc Liaison
Committee for standardizing definitions of prosthetic heart valve morbidity of the American Association for Thoracic Surgery and The Society of
Thoracic Surgeons. J Thorac Cardiovasc Surg 1996;112:708e11.
[30] Dürrleman N, Pellerin M, Bouchard D, et al. Prosthetic valve thrombosis: twenty-year experience at the Montreal Heart Institute. J Thorac
Cardiovasc Surg 2004;127:1388e92.
[31] Thorburn CW, Morgan JJ, Shanahan M, et al. Long-term results of tricuspid valve replacement and the problem of prosthetic valve thrombosis. Am
J Cardiol 1983;51(7):1128e32.
[32] Roudaut R, Lafitte S, Roudaut M, et al. Fibrinolysis of mechanical prosthetic valve thrombosis a single-center study of 127 cases. J Am Coll Cardiol
2003;4(4):653e8.
[33] Roudaut R, Lafitte S, Roudaut M, et al. Management of prosthetic heart valve obstruction: fibrinolysis versus surgery. Early results and long-term
follow-up in a single-centre study of 263 cases. Arch Cardiovasc Dis 2009;102:269e77.
[34] Nishimura R, Otto C, Bonow R, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease. A report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines 2014. 2014.
[35] Chakravarty T, Søndergaard L, Friedman J, et al. Subclinical leaflet thrombosis in surgical and transcatheter bioprosthetic aortic valves: an
observational study. Lancet 2017;389:2383e92.
[36] Holmes DR, Mack MJ. Aortic valve bioprostheses leaflet immobility and valve thrombosis. Circulation 2017;135:1749e56.
[37] Hansson N, Grove E, Andersen H, et al. Transcatheter aortic valve thrombosis incidence, predisposing factors, and clinical implications. J Am Coll
Cardiol 2016;68(19):2059e69.
[38] Ghodsizad A, Kar BJ, Layolka P, et al. Less invasive off-pump implantation of axial flow pumps in chronic ischemic heart failure: survival effects.
J Heart Lung Transplant 2011;30(7):834e7.
[39] Laschinger JC, Wu C, Ibrahim NG, Shuren JE. Reduced leaflet motion in bioprosthetic aortic valves: the FDA perspective. N Engl J Med
2015;373:1996e8.
[40] Slaughter MS, Naka Y, John R, et al. Post-operative heparin may not be required for transitioning patients with a HeartMate II left ventricular assist
system to long-term warfarin therapy. J Heart Lung Transplant 2010;29:616e24.
[41] Netuka I, Litzler PY, Berchtold-Herz M, et al. Minimal adverse events in HeartMate II patients with no antiplatelet therapy: preliminary results from
the European TRACE study. J Heart Lung Transplant 2014;33(4):S11.
[42] Fine NM, Topilsky Y, Oh JK, et al. Role of echocardiography in patients with intravascular hemolysis due to suspected continuous-flow LVAD
thrombosis. J Am Coll Cardiol: Cardiovasc Imag 2013;6:1129e40.
[43] Jahanyar J, Noon GP, Koerner MM, Youker KA, et al. Recurrent device thrombi during mechanical circulatory support with an axial-flow pump is a
treatable condition and does not preclude successful long-term support. J Heart Lung Transplant 2007;26(2):200e3.
[44] Acharya D, Hashim T, Kirklin JK, et al. Use of retrospectively gated CT angiography to diagnose systolic LVAD inflow obstruction. Am Soc Artif
Intern Org J 2013;59(5):542e6.
Chapter 26
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The Spectrum of Clinical Presentations
and Management Options for the
Treatment of Degenerative
Atherothrombotic Disease of Saphenous
Vein Grafts
Ran Eliaz1, On Topaz
1
Hadassah Hebrew University Medical Center, Jerusalem, Israel;2Charles George Veterans Affairs Medical Center, Asheville, NC, United States;
3
Duke University School of Medicine, Durham, NC, United States
2,3
and Haim D. Danenberg
1
INTRODUCTION
Cardiovascular disease accounted for 17.3 million deaths worldwide in 2012, and yet, despite steady improvement in
the survival rate, this disease is expected to cause more than 23.6 million deaths by 2030 [1]. Coronary artery
bypass gra ft (CABG) surgery is the mainstay operation for treatment of corona ry artery disease, as it offers angina
relief, improved quality of life, and improved survival r ate [1,2].Specifically, CABG surgery is conside red the standard
of care for patients with three-vessel or left main coronary artery disease with reduced left-ventricle ejection fraction. In
these patients the operation decreases morbidity and mortality compared with PCI (percutaneous coronary intervention)
[3]. Saphenous vein grafts (SVGs) are the most commonly utilized bypass conduits in CABG [4]; howe ver , strong
evidence exists as to their poor mid- and long-term patency rates. Grafted internal mammary arteries provide a
significantly better long-term patency than SVGs, yet, unfortunately, only 5%e10% of surgical patients receive optimal
revascularization with bilateral mammary grafts, mainly due to increased perioperative morbidity, mortality, duration of
operation, a nd risk of sternal wound [5]. Consequently, surgical reliance on SVGs continues, yet the long-term efficacy
of CABG remains considerably compromised by the development of vein graft failure (VGF), mainly due to atherosclerotic disease; thrombus superimposition, which is found in as many as 80% of the old vein grafts [6]; and native
coronary disease distal to the SVG anastomosis. The purp ose of thi s chapter is to describe the SVG atherosclerotic
thrombotic disease and the mechanisms accounting for VGF and to delineate the contemporary revascularization
treatment options.
PATHOPHYSIOLOGY OF VENOUS GRAFT FAILURE
The great saphenous vein grafts are prone to a high failure rate [7]. SVG failure at 1 year postsurgery reaches 10%e25%;
from year 1e5 an additional 5%e10% of grafts occlude and then from 6 to 10 years an additional 20%e25% of grafts
fail. Altogether, at 10 years postsurgery, the SVG patency rate is around 40%e50%, with only half of these grafts actually
free of atheroscle rotic disease [8]. Fig. 26.1 presents VGF 10 years after CABG surgery from two perspectives: the failure
per vein graft and the graft failure per patient.
Cardiovascular Thrombus. https://doi.org/10.1016/B978-0-12-812615-8.00026-0
Copyright © 2018 Elsevier Inc. All rights reserved.
377
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Failure per vein graft
1 mo
70
60
50
40
30
20
10
0
3
4
5
6
7
1 yr
9
8
3
5
4
10
6
11
17
9
8
7
10
5 yr
6
5
4
7
9
8
13
12
10 yr
5
4
12
14
Hadinata et al
FitzGibbon et al
FitzGibbon et al
Khot et al
Shah et al
Kim et al
Zacharias et al
Cho et al
FitzGibbon et al
FitzGibbon et al
Desai et al
Hadinata et al
Alexander et al
Khot et al
Shah et al
Zacharias et al
Kim et al
Cho et al
FitzGibbon et al3FitzGibbon et al
Hadinata et al
Khot et al
Shah et al
Zacharias et al
Lytle et al
Kim et al
Collins et al
FitzGibbon et al
Lytle et al
Hadinata et al
Schwann et al
Vein graft failure per patient
1 mo
1 yr
5 yr
10 yr
70
60
50
40
30
20
10
0
15
Grondin et al16Grondin et al
Goldman et al
Goldman et al
17
15
Alexander et al
Widimsky et al
Widimsky et al
16
(on pump)
(on pump)
18
18
Shroyer et al
Shroyer et al
(on pump)
19
19
(off pump)
Goldman et al
15
Goldman et al
16
15
Grondin et al
FIGURE 26.1 Data on vein graft failure rates in 10 years of follow-up. From Harskamp RE, Lopes R, Clinton B, et al. Saphenous vein graft failure after
coronary artery bypass surgery: pathophysiology, management, and future directions. Ann Surg 2013;257:824e33 with permission.
Several pathologic processes account for VGF after CABG surgery, each causing unique deleterious effects over a
specific time period [4]. Among these processes, thrombus formation and deposition are considered major determinants [9].
Over time, endothelial damage to the vein graft occurs, followed by the creation of abnormal flow patter ns and blood
stasis, all of which initiate thrombus formation. Then a constant process of thrombus deposition in layers ensues. In the
early period postsurgery (defined as up to 2 years duration) thrombosis is the leading cause of VGF. Thereafter,
atherosclerotic degeneration and neointimal hyperplasia are the main processes accountable for vein graft occlusion
[10e12]. Nevertheless, thrombus does not cease to form and accumulate, as evident by the composition of late SVG
occlusions. This is especially apparent in cases of plaque rupture within the graft, as depicted in Fig. 26.2. Table 26.1
presents the et iol ogie s accountable for SVG f ailur e. Notably, vein grafts lack the distinct muscular arterial layer; thus,
the exposure of these bypass conduits to systemic arterial pressures causes furt he r lu mina l dilatation and development of
neointimal hyperplasia [13]. Moreove r, surgic al harves tin g and handling of SVGs are important iatrogenic causes of vein
graft damage and resultant intragraft thrombus formation [14].
Multiple patient-related risk factors for VGF have been identified, including the following: female gender (early VGF),
smoking (early and late graft thrombosis) [15], fibrinogen (early VGF), hyperlipidemia (late VGF), triglyceridemia (late
VGF), and lipoprotein(a) (late VGF). Hypertension d oes not directly correlate with either early or late VGF but is a risk
factor for development of intimal hyperplasia in the graft [16]. The role of diabetes in VGF remains unclear [15,16], while
genetic determinants such as thrombomodulin gene variants have been identified and are under investigation as of this
writing [17].
The Spectrum of Clinical Presentations and Management Options Chapter | 26 379
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FIGURE 26.2 Angiographic demonstration of degenerative atherothrombotic disease of an old saphenous vein graft in a patient presenting with acute
coronary syndrome (ACS) 10 years post-CABG surgery. The graft’s original diameter of 3.5 mm decreased over time to just 1 mm, corresponding to
chronic deposition of thrombotic layers along the graft’s entire body. Acute plaque rupture (rupture site encircled by red circle) in the middle portion of the
graft resulted in additional thrombus accumulation, which compromised the antegrade flow. These pathologic processes accounted for the patient’s
presentation with ACS and ischemia. Courtesy of the book editor.
TABLE 26.1 Overview of Causes of Vein Graft Failure (VGF) at Different Time Intervals
Acute VGF (<30 days) Early VGF (1e24 months) Late VGF (>2 years)
Technical failure
Thrombosis
Conduit related
Small diameter
Preexisting vein pathology
Extrinsic
Thrombosis
Limited outflow
Hypercoagulability
From Harskamp RE, Lopes R, Clinton B, et al. Saphenous vein graft failure after coronary artery bypass surgery: pathophysiology, management, and
future directions. Ann Surg 2013;257:824e33.With permission.
Neointimal hyperplasia at anastomosis sites Atherosclerotic degeneration
Thrombosis Generalized neointimal hyperplasia
PERIOPERATIVE MEASURES TO DECREASE GRAFT FAILURE
Recognizing the proven superiority of internal mammary arterial grafts [18], certain strat egies attempt to improve
the short- and long-term patency of vein grafts. These include avoiding unwarranted intraoperative manipulations that
can cause vein distension , development of “no-tou ch” techniques, and minimizing trauma during graft harvesting,
handling, and implantation. These measures are mainly effective in prevention of early graft failure [10]. When bypass
grafts are anastomosed to the distal coronary arteries (to noneleft anterior descending arteries) their longevity is
compromised [19] and they are associated as well with worse long-term clinical outcomes [14]. Alternative surgical
techniques such as off-pump CABG surgery and utilization of endoscopic vein harvesting have not resulted in decreased
rates of VGF [14]. In animal models, external stent placement around the saphenous vein markedly inhibits medialintimal thickening, thus preserving the integrit y of elastic fibers, smooth muscle, and endothelial cells [20e22].
380 Cardiovascular Thrombus
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Another option for external graft support is the a pplication o f fibrin glue spray imme diat ely upon completion of the graft
anastomosis, just prior to exposure to the high systemic arterial pressure [23].InexvivomodelsusinghumanSVGsthe
fibrin glue prevented graft overdistension and reduced the w al l-stre ss -i nduc ed injury [14,24].
DIAGNOSIS AND TREATMENT OPTIONS
In the clinical setting, a categorical definition of SVG failure is mainly based on an angiographic diagnosis, while cardiac
symptoms may or may not directly relate to the extent of the vein graft degenerative disease. The distribution of SVG
lesions is within the graft’s body in 57%, in the ostium in 35%, and at the distal anastomosis in 9% [25]. During SVG
angiography, the diagnosis of SVG disease can be further substantiated by utilization of intravascular ultrasonography
combined with near-infrared spectroscopy, an approach that provides excellent virtual histology [25] as shown in Fig. 26.3.
(A)
(B)
(D)
(E)
FIGURE 26.3 Virtual histology of a saphenous vein graft (SVG) as obtained by application of near-infrared spectroscopy and intravascular ultraso-
nography to analyze the ostium (AeC) and the body (DeF) segments of an SVG lesion. LCBI, Lipid Core Burden Index. From Wood FO, Badhey N,
Garcia B, et al. Analysis of saphenous vein graft lesion composition using near-infrared spectroscopy and intravascular ultrasonography with virtual
histology. Atherosclerosis 2010;212:528e33 with permission.
(C)
(F)
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Optical coherence tomography is another precision imaging tool for accurate depiction of underlying SVG disease;
however, because of concerns with potential catheter-induced thromboembolism, it is not used as commonly as in native
coronary vessels.
Incorporation of a quantifying method for assessment of the extent of the SVG failure is warranted. Accordingly,
Fig. 26.4 presents a useful grading system for the angiographic assessment of SVG patency as introduced by FitzGibbon
and colleagues [26].
The FAME study, which compared fractional flow reserve with angiography, demonstrated that, in fact, in 20% of
angiographically significant (>70% stenosis) native coronary lesions there is no evidence of active ischemia [27]. Indeed,
the deterioration of certain SVG lesions may not carry significant clinical importance due to the effective residual
competitive flow in the recipient coronary artery or because the corresponding graft supplies only a small myocardial
territory. In other cases, the actual need for a patent SVG is restricted because the recipient native coronary artery is capable
of developing an effective collateral blood vessels network. In instances of acute SVG failure adverse coronary events can
ensue, whereas in slow-onset SVG failure complications may not occur, owing to the creation of protecting collateral
vessels. Thus, conceivably, in selected cases the development of early postoperative SVG failure may carry a higher
clinical relevance than in cases with late graft failure [28].
As of this writing, bare metal stents (BMSs) and drug-eluting stents (DESs) are among the most common devices
utilized in revascularization of SVGs [29,30]. However, PCI of SVG carries a significant risk of major adverse cardiac
events (MACEs), mainly reduced antegrade flow (i.e., the “no-reflow” phenomenon), distal embolization, and myocardial
infarction (MI). Delayed arterial healing with poor strut coverage is recognized as the primary substrate for stent
thrombosis among the first-generation DESs [31]. Development of in-stent neoatherosclerosis is another complication of
first- and second-generation DESs, causing late stent failure from restenosis or stent thrombosis induced by slow flow or by
rupture of an underlying plaque [32,33].
Repeat cardiac surgery is a management option that is associated with a higher mortality rate and a poor clinical
outcome compared with the first cardiac operation [34]. Consequently, PCI has become the dominant management strategy
[35]. Nevertheless, Andreas Gruentzig, who performed the first coronary balloon angioplasty and keenly observed the poor
outcome of PCI in SVG lesions at that time (which was associated with a very high restenosis rate of 60%), postulated: “A
different kind of disease may explain the high incidence of recurrence in graft stenoses” [36]. Interestingly, nowadays,
despite the large experience gained over a course of 5 decades, the performance of PCI for SVG disease is still associated
with less favorable short- and long-term outcomes compared with PCI of native coronary vessels [37].
Definitions of Graft Grades, Assessed by FOUR-Plane Angiography
Grade
Patency
A
B
O
Disease
I
II
III
HP
LP
Grades A, B and O assess graft flow. Grades I, II, III, HP and LP reflect
disease severity.
FIGURE 26.4 A grading system for assessment of saphenous vein graft patency. From 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;28:616e26 with permission.
Excellent graft with unimpaired runoff
Stenosis reducing caliber of proximal or distal anastomoses
or trunk to <50% of the grafted coronary artery. Overall
graft B grade was determined by the lowest of the three
specific site grades
Occlusion
No intimal irregularity
Irregularity of <50% of estimated intimal surface
Irregularity of >50% of estimated intimal surface
High profile lesion produces >50% stenosis of graft
Low profile lesion produces <50% stenosis of graft
Definition
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CONSIDERATIONS OF SAPHENOUS VEIN GRAFTS AND PERCUTANEOUS
CORONARY INTERVENTION
Compared with atherosclerotic plaques in native coronary arteries, SVG plaques are softer, longer, more friable [38].
Patients with acute coronary syndrome (ACS) who undergo SVG PCI carry the highest risks of atheromatous, thrombotic
distal embolization; no-reflow phenomenon; and periprocedural MI. This frequently occurs during or following stent
implantation as a result of thrombus fragmentation and protrusion of the metal stent struts [39]. Since the late 1990s, the
introduction of technologic improvements such as distal protection filters, thrombectomy devices, and dedicated stents has
contributed to ameliorating SVG PCIerelated adverse angiographic and clinical outcomes. Nevertheless, SVG PCI should
still be considered a high-risk procedure [37,40].
EMBOLIC PROTECTION DEVICES
This useful technology includes flow occlusion, aspiration, and filter devices, which were developed to reduce the risk of
distal embolization. Due to the marked vari ability in the anatomic morphology of diseased vein grafts, the operator
should tailor the selection of an embolic protection device (EPD) to the anatomic features of the treated vessel [41].
Fig. 26.5 display s several available EPDs.
The proximal and distal occlusione aspiration devices stop the antegrade flow during intervention. Then the blood,
which contains debris and humoral mediators, is aspirat ed before the di stal occlusion is relieved, thus allowing the
retrieval of any size particles. Disadvantages include poor vessel imaging during the procedure, di stal embolization
while crossing the lesion, distal ischemia, and possible balloon-induced injury to the SVG wall [41].Thedistalfilter
devices enable distal perfusion and allow contrast injections during PCI while trapping most pa rti cula te deb ri s. Thei r
main limitations include a needforpositioninginanangiographic nondiseased “landing zone,” aneedforlesion
preparation by predilatation, a high risk of embolization while crossing the tar ge t thrombotic lesion, and a failur e to
capture debris smaller than 100 mm.
The benefit of EPDs in SVG PCI procedures has been established in several trials: the SAFER study (Saphenous
Vein Graft Angioplasty Free of Emboli Randomized trial) [42,43] compared the distal occlusion device Per cuS ur ge
GuardWire (Medtronic) with a conv entio nal g uide wire i n SVG PCI with stent implantation in 801 patients. The trial was
stopped early bec au se of a sign ificant benefit associated with the use of the GuardWire in terms of MACE (death, MI,
FIGURE 26.5 Display of various distal embolic protection devices. From Sbarzaglia P, Notaristefano S, Cavallini C. Best treatment of saphenous vein
graft lesions. Intervent Cardiol Rev 2010;5:46e50 with permission.
The Spectrum of Clinical Presentations and Management Options Chapter | 26 383
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need for emergency bypass surgery, and target-v ess el re vasc ul ariz ati on [TV R]) at 30 days. The use of the Gu ardW ir e led
to a 6.9% absolute (42% relative) re duc tio n in the 3 0 -day primary end point (9.6% vs. 16.5% ; P ¼ .004), with a
significant reduction in the incidence of MI (8.6% vs. 14.7%; P ¼ .008) and no-reflow phenomenon (3% vs. 9%;
P ¼ .001), mirrored by an increase in postprocedural TIMI (thrombolysis in myocardial infarction) 3 flow (98% vs. 95%;
P ¼ .04 [43]. Five noninferiority trials compared different typesofEPDsasfollows:FIRE(FilterWireEXRandomised
Evaluation) [39], PRIDE (Protection During Saphenous Vein Graft Intervention to Prevent Distal Embolization) [44],
SPIDER (Saphenous Vein Graft in a Distal Embolic Randomized) [45], PROXIMAL (Proximal Protection During
Saphenous Vein Graft Intervention) [46], and AMEthyst (Assessment of the Medtronic AVE Interceptor Saphenous
Vein Graft Filter System) [47] . Tables 26.2, 26.3, and 26.4 present the outcomes of several studies involving the uti-
lization of EPDs and the resultant MACEs [48].
TABLE 26.2 Randomized Trials of Embolic Protection Devices in Saphenous Vein Graft Intervention
Trial/Reference n Device
SAFER (2002) 801 GuardWire
FIRE (2003) 651 FilterWire vs.
PRIDE (2005) 631 Triactive sys-
AMEthyst (2008) 797 Interceptor
PROXIMAL
(2007)
vs. PCI
GuardWire
tem vs. FilterWire EX/
GuardWire
Plus vs.
GuardWire/
FilterWire EZ
594 Proxis system
vs. GuardWire/
FilterWire
GP IIb/IIIa
Use
57.1% vs.
58.7%
51.5 vs.
53.3%
54.0% vs.
54.7%
40% vs.
39.4%
42.5% vs.
44.3%
Primary
End Point Results Findings
MACE
(30 days)
MACE
(30 days)
MACE
(30 days)
MACE
(30 days)
MACE
(30 days)
9.6% vs.
16.5%,
P ¼ .004
9.9% vs.
11.6%,
P ¼ .0008 (NI)
11.2% vs.
10.1%,
P ¼ .02 (NI)
8% vs. 7.3%,
P ¼ .023 (NI)
9.2% vs.
10.1%,
P ¼ .0061 (NI)
Embolic protection showed a
6.9% absolute risk reduction
and a 42% relative risk reduction in the primary end point at
30 days. Not powered to show
a significant reduction in mortality, but had a trend toward
less mortality with embolic
protection (1.0% vs. 2.3%,
P ¼ .17).
No difference between the
groups in the primary end point.
FilterWire EX system shown to
be noninferior to GuardWire in
percutaneous intervention of
SVG.
No difference between the
groups in the primary end point.
Triactive system shown to be
noninferior to approved GuardWire and FilterWire devices in
percutaneous intervention of
SVG.
No difference between the
groups in the primary end point.
Interceptor Plus embolic protection device shown to be noninferior to approved GuardWire
and FilterWire in percutaneous
intervention of SVG.
No difference between the
groups in the primary end point.
Proxis embolic protection system shown to be noninferior to
distal embolic protection devices (GuardWire, FilterWire
EX, and FilterWire EZ) in percutaneous intervention of SVG.
AMEthyst, Assessment of the Medtronic AVE Interceptor Saphenous Vein Graft Filter System; FIRE, FilterWire EX Randomised Evaluation; GP, glycoprotein; MACE, major adverse cardiac event; NI, noninferior; PCI, percutaneous coronary intervention; PRIDE, Protection During Saphenous Vein Graft
Intervention to Prevent Distal Embolization; PROXIMAL, Proximal Protection During Saphenous Vein Graft Intervention; SAFER, Saphenous Vein Graft
Angioplasty Free of Emboli Randomized; SVG, saphenous vein graft.
From reference Topaz O. Thrombectomy during primary PCI for STEMIdcall of the thrombus. Cath Cardiovasc Interv 2012;80:1181e2 with permission.
384 Cardiovascular Thrombus
https://t.me/med1917
TABLE 26.3 The Incidence of Distal Embolization Per Graft Degeneration in Utilization of Protection Device
35
30
25
20
15
% MACE
10
5
0
MACE, major adverse cardiac event; SVG, saphenous vein graft.
From Baim DS, Wahr D, George B, et al. Saphenous vein graft Angioplasty Free of Emboli Randomized (SAFER) trial investigators. Randomized trial of a
distal embolic protection device during percutaneous intervention of saphenous vein aorto-coronary bypass grafts. Circulation 2002;105:1285e90 with
permission.
GuardWireTM
Control
51%
0–25%
46%
26–50% 51–75% 76–100%
SVG % Degeneration
35%
4%
The EPD received a class IB recommendation in the European Society of Cardiology (ESC) 2006 guidelines [49],
whereas the American College of Cardiology/American Heart Association recommend class IA [50]. The revised ESC
guidelines for PCI procedures of degenerated SVG recommended class IB for distal protection devices and class IIB for
proximal protection devices (based on the aforementioned studies SAFER, PROXIMAL, and FIRE). Despite these
recommendations, the utilization of these devices is ma rke dly uncommon in everyday practice . Registry data show that
EPDs are utilized in only 22% of SVG PCI [51]. The reasons behind this low rate may relate to anatomic challenges such
TABLE 26.4 Distal Embolic Protection with Filter Catheter and Balloon Occlusion
20%
16%
12%
30-Day MACE (%)
EP, embolic protection; MACE, major adverse cardiac event.
From 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;108:548e53 with permission.
8%
4%
0%
16.5%
SAFER
(n = 801)
9.6%
4
P=0.004
11.6%
FIRE
(n = 651)
9.9%
5
P=NS
Non-EP group
GuardWire™ Plus System
FilterWire EX™
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