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J. D. Newman et al.
extremity, renal, mesenteric, and abdominal aortic): a col­laborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/ AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation. 2006;113(11):e463–654.
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37. Sprouse LR 2nd, Meier GH 3rd, Lesar CJ, Demasi RJ, Sood J, Parent FN, et al. Comparison of abdominal aortic aneurysm diameter measurements obtained with ultrasound and computed tomography: is there a difference? J Vasc Surg. 2003;38(3):466– 71; discussion 471–2.
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46. Choke E, Cockerill G, Wilson WR, Sayed S, Dawson J, Loftus I, etal. A review of biological factors implicated in abdominal aortic aneurysm rupture. Eur J Vasc Endovasc Surg. 2005;30(3):227–44.
47. Kotze C, Menezes L, Endozo R, Groves A, Ell P, Yusuf S.Increased metabolic activity in abdominal aortic aneurysm detected by 18F-uorodeoxyglucose (18F-FDG) positron emission tomogra­phy/computed tomography (PET/CT). Eur J Vasc Endovasc Surg. 2009;38(1):93–9.
48. Reeps C, Essler M, Pelisek J, Seidl S, Eckstein HH, Krause BJ.Increased 18F-uorodeoxyglucose uptake in abdominal aortic aneurysms in positron emission/computed tomography is associ­ated with inammation, aortic wall instability, and acute symp­toms. J Vasc Surg. 2008;48(2):417–23; discussion 424.
49. Lindholt JS, Norman P.Screening for abdominal aortic aneurysm reduces overall mortality in men. A meta-analysis of the mid- and long-term effects of screening for abdominal aortic aneurysms. Eur J Vasc Endovasc Surg. 2008;36(2):167–71.
50. Final Recommendation Statement: Abdominal Aortic Aneurysm: Screening. U.S. Preventive Services Task Force. 2014; Available at: https://www.uspreventiveservicestaskforce.org/Page/Document/
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52. Lederle FA, Johnson GR, Wilson SE, Chute EP, Littooy FN, Bandyk D, etal. Prevalence and associations of abdominal aor­tic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group. Ann Intern Med. 1997;126(6):441–9.
53. Scott RA, Wilson NM, Ashton HA, Kay DN.Inuence of screen­ing on the incidence of ruptured abdominal aortic aneurysm: 5-year results of a randomized controlled study. Br J Surg. 1995;82(8):1066–70.
54. Lederle FA, Wilson SE, Johnson GR, Reinke DB, Littooy FN, Acher CW, et al. Immediate repair compared with surveil­lance of small abdominal aortic aneurysms. N Engl J Med. 2002;346(19):1437–44.
55. Lederle FA, Johnson GR, Wilson SE, Ballard DJ, Jordan WD Jr, Blebea J, etal. Rupture rate of large abdominal aortic aneu­rysms in patients refusing or unt for elective repair. JAMA. 2002;287(22):2968–72.
56. Powell JT, Brown LC, Forbes JF, Fowkes FG, Greenhalgh RM, Ruckley CV, etal. Final 12-year follow-up of surgery ver­sus surveillance in the UK Small Aneurysm Trial. Br J Surg. 2007;94(6):702–8.
57. Chaikof EL, Brewster DC, Dalman RL, Makaroun MS, Illig KA, Sicard GA, etal. SVS practice guidelines for the care of patients with an abdominal aortic aneurysm: executive summary. J Vasc Surg. 2009;50(4):880–96.
58. United Kingdom Small Aneurysm Trial Participants. Long­term outcomes of immediate repair compared with surveil-
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lance of small abdominal aortic aneurysms. N Engl J Med. 2002;346(19):1445–52.
59. Cao P, De Rango P, Verzini F, Parlani G, Romano L, Cieri E, etal. Comparison of surveillance versus aortic endografting for small aneurysm repair (CAESAR): results from a randomised trial. Eur J Vasc Endovasc Surg. 2011;41(1):13–25.
60. Ouriel K, Clair DG, Kent KC, Zarins CK. Positive Impact of Endovascular Options for treating Aneurysms Early (PIVOTAL) Investigators. Endovascular repair compared with surveillance for patients with small abdominal aortic aneurysms. J Vasc Surg. 2010;51(5):1081–7.
61. Hendy K, Gunnarson R, Golledge J. Growth rates of small abdominal aortic aneurysms assessed by computerised tomography--a systematic literature review. Atherosclerosis. 2014;235(1):182–8.
62. Titus J, Butler B. Endoleak management. In: Dieter R, Dieter RJ, Dieter RI, editors. Endovascular interventions: a case based approach. NewYork: Springer Science + Business Media; 2014. p.373–81.
63. Harris PL, Vallabhaneni SR, Desgranges P, Becquemin JP, van Marrewijk C, Laheij RJ.Incidence and risk factors of late rupture, conversion, and death after endovascular repair of infrarenal aortic aneurysms: the EUROSTAR experience. European Collaborators on Stent/graft techniques for aortic aneurysm repair. J Vasc Surg. 2000;32(4):739–49.
64. Manning BJ, O’Neill SM, Haider SN, Colgan MP, Madhavan P, Moore DJ. Duplex ultrasound in aneurysm surveillance follow­ing endovascular aneurysm repair: a comparison with computed tomography aortography. J Vasc Surg. 2009;49(1):60–5.
65. Bredahl KK, Taudorf M, Lonn L, Vogt KC, Sillesen H, Eiberg JP.Contrast enhanced ultrasound can replace computed tomog­raphy angiography for surveillance after endovascular aortic aneurysm repair. Eur J Vasc Endovasc Surg. 2016;52(6):729–34.
66. Ashoke R, Brown LC, Rodway A, Choke E, Thompson MM, Greenhalgh RM, etal. Color duplex ultrasonography is insensitive for the detection of endoleak after aortic endografting: a system­atic review. J Endovasc Ther. 2005;12(3):297–305.
67. Raman KG, Missig-Carroll N, Richardson T, Muluk SC, Makaroun MS. Color-ow duplex ultrasound scan versus com­puted tomographic scan in the surveillance of endovascular aneu­rysm repair. J Vasc Surg. 2003;38(4):645–51.
68. Habets J, Zandvoort HJ, Reitsma JB, Bartels LW, Moll FL, Leiner T, etal. Magnetic resonance imaging is more sensitive than com­puted tomography angiography for the detection of endoleaks after endovascular abdominal aortic aneurysm repair: a systematic review. Eur J Vasc Endovasc Surg. 2013;45(4):340–50.
69. Garg T, Baker LC, Mell MW. Postoperative surveillance and long-term outcomes after endovascular aneurysm repair among Medicare beneciaries. JAMA Surg. 2015;150(10):957–63.
70. Hoornweg LL, Storm-Versloot MN, Ubbink DT, Koelemay MJ, Legemate DA, Balm R.Meta analysis on mortality of rup­tured abdominal aortic aneurysms. Eur J Vasc Endovasc Surg. 2008;35(5):558–70.
71. Kent K.Clinical practice. Abdominal aortic aneurysms. NEJM. 2014;371:2101–8.
72. Kent KC, Zwolak RM, Egorova NN, Riles TS, Manganaro A, Moskowitz AJ, etal. Analysis of risk factors for abdominal aortic aneurysm in a cohort of more than 3 million individuals. J Vasc Surg. 2010;52(3):539–48.
73. Tenforde AS, Cheng CP, Suh GY, Herfkens RJ, Dalman RL, Taylor CA. Quantifying invivo hemodynamic response to exer­cise in patients with intermittent claudication and abdominal aortic aneurysms using cine phase-contrast MRI.J Magn Reson Imaging. 2010;31(2):425–9.
74. Nakahashi TK, Hoshina K, Tsao PS, Sho E, Sho M, Karwowski JK, et al. Flow loading induces macrophage antioxidative gene
expression in experimental aneurysms. Arterioscler Thromb Vasc Biol. 2002;22(12):2017–22.
75. Myers J, McElrath M, Jaffe A, Smith K, Fonda H, Vu A, etal. A randomized trial of exercise training in abdominal aortic aneu­rysm disease. Med Sci Sports Exerc. 2014;46(1):2–9.
76. Best PJ, Tajik AJ, Gibbons RJ, Pellikka PA.The safety of tread­mill exercise stress testing in patients with abdominal aortic aneu­rysms. Ann Intern Med. 1998;129(8):628–31.
77. Propanolol Aneurysm Trial Investigators. Propranolol for small abdominal aortic aneurysms: results of a randomized trial. J Vasc Surg. 2002;35(1):72–9.
78. Sweeting MJ, Thompson SG, Brown LC, Greenhalgh RM, Powell JT.Use of angiotensin converting enzyme inhibitors is associated with increased growth rate of abdominal aortic aneurysms. J Vasc Surg. 2010;52(1):1–4.
79. Takagi H, Matsui M, Umemoto T. A meta-analysis of clinical studies of statins for prevention of abdominal aortic aneurysm expansion. J Vasc Surg. 2010;52(6):1675–81.
80. Bailey MA, Dunne JA, Grifn KJ, Coughlin PA, Scott DJ.Systematic review and meta-analysis of the effects of statin therapy on abdominal aortic aneurysms (Br J Surg 2011; 98: 362-
353). Br J Surg. 2011;98(5):744–5; author reply 745.
81. Meijer CA, Stijnen T, Wasser MN, Hamming JF, van Bockel JH, Lindeman JH, et al. Doxycycline for stabilization of abdomi­nal aortic aneurysms: a randomized trial. Ann Intern Med. 2013;159(12):815–23.
82. Thompson A, Cooper JA, Fabricius M, Humphries SE, Ashton HA, Hafez H.An analysis of drug modulation of abdominal aortic aneurysm growth through 25 years of surveillance. J Vasc Surg. 2010;52(1):55–61.e2.
83. Sieunarine K, Lawrence-Brown MM, Goodman MA.Comparison of transperitoneal and retroperitoneal approaches for infra­renal aortic surgery: early and late results. Cardiovasc Surg. 1997;5(1):71–6.
84. Annambhotla S, Kibbe M. Infrarenal abdominal aortic aneu­rysm: EVAR.In: Dieter RS, Dieter Jr RA, Dieter III RA, editors. Endovascular interventions: a case-based approach. New York: Springer Science+Business Media; 2014. p.355–65.
85. Aziz F.Endovascular abdominal aortic aneurysm repair for rup­tured abdominal aortic aneurysm. In: Dean S, Satiani B, Abraham W, editors. Color atlas of vascular diseases. NewYork: McGraw­Hill; 2015.
86. Prinssen M, Verhoeven EL, Buth J, Cuypers PW, van Sambeek MR, Balm R, etal. A randomized trial comparing conventional and endovascular repair of abdominal aortic aneurysms. N Engl J Med. 2004;351(16):1607–18.
87. Blankensteijn JD, de Jong SE, Prinssen M, van der Ham AC, Buth J, van Sterkenburg SM, etal. Two-year outcomes after conven­tional or endovascular repair of abdominal aortic aneurysms. N Engl J Med. 2005;352(23):2398–405.
88. De Bruin JL, Baas AF, Buth J, Prinssen M, Verhoeven EL, Cuypers PW, etal. Long-term outcome of open or endovascular repair of abdominal aortic aneurysm. N Engl J Med. 2010;362(20):1881–9.
89. EVAR trial participants. Endovascular aneurysm repair versus open repair in patients with abdominal aortic aneurysm (EVAR trial 1): randomised controlled trial. Lancet. 2005;365(9478):2179–86.
90. Greenhalgh RM, Brown LC, Kwong GP, Powell JT, Thompson SG, EVAR trial participants. Comparison of endovascular aneu­rysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: ran­domised controlled trial. Lancet. 2004;364(9437):843–8.
91. Patel R, Sweeting MJ, Powell JT, Greenhalgh RM, EVAR trial investigators. Endovascular versus open repair of abdominal aor­tic aneurysm in 15-years’ follow-up of the UK endovascular aneu­rysm repair trial 1 (EVAR trial 1): a randomised controlled trial. Lancet. 2016;388(10058):2366–74.
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Abdominal Aortic Occlusive Disease
https://t.me/med1917
SunghoLim andPaulR.Crisostomo
15
Introduction
Atherosclerosis of the abdominal aorta or iliac arteries is one of the most common causes of lower extremity ischemia. The rst implication of the disease was uncovered in the late eighteenth century by British anatomist John Hunter. However, two more centuries passed before Rene Leriche described a patient with claudication and erectile dysfunc­tion in 1948, ultimately linking clinical symptoms with pathophysiology and anatomy [1].
Surgical revascularization of aortoiliac artery was rst described by Wylie etal. in San Francisco in 1952 [2]. Since then, tremendous advances have occurred in synthetic graft conduits, tissue engineering, and, most recently, percutane­ous endovascular devices which allow a wide range of treat­ment options based on patient morbidity and anatomic defect. This chapter will review clinical characteristics of abdominal aortic occlusive disease and contemporary management.
Epidemiology
The majority of patients with aortic occlusive disease present with diffuse disease involving multi-level peripheral vascula­ture including femoropopliteal or infrapopliteal vessels. This subset of patients with diffuse multi-level disease are typi­cally older, more likely male, with a higher prevalence of dia­betes and hypertension and with concomitant coronary artery disease, cerebrovascular disease, and visceral atherosclerosis [3, 4]. Such patients with multi-vessel disease often present with ischemic pain, tissue loss, or gangrene. Not surprisingly,
S. Lim Surgery, Loyola University Medical Center, Maywood, IL, USA
P. R. Crisostomo ( Department of Surgery, Division of Vascular and Endovascular Therapy, Loyola University Chicago, Stritch School of Medicine, Maywood, IL, USA
*)
their life expectancy is lower than their age- matched counter­part [5]. In contrast, patients with isolated aortoiliac disease are generally younger and more likely female with a high prevalence of smoking or dyslipidemia [6].
“Hypoplastic aortic syndrome” or “small aorta syndrome” is a particularly virulent form of aortic atherosclerosis often found in young, small stature women who smoke [6]. This disease particularly involves the infrarenal aorta proximal to the aortic bifurcation. Radiographic ndings are typically atretic or narrowed vasculature with diffuse calcic athero­sclerosis. Due to the diminutive size of the aorta and iliac vessels, durability of either endovascular intervention or local endarterectomy is generally inferior, particularly in the presence of continued cigarette use.
Pathophysiology
Aortoiliac atherosclerosis typically starts at the iliac bifurca­tion and extends proximally and distally. Degree of the pro­gression may vary but ultimately could occlude aortic blood ow over time. Starrett et al. demonstrated one-third of patients experienced proximal disease progression up to the level of renal artery in the period of 6–10years [7]. In the same study, they also demonstrated a 30–40% chance of pro­funda femoris or supercial femoral artery distal involve­ment [7].
Due to the relatively slow progression of atherosclerosis, collateral circulation often develops. The primary compensa­tory vessels to the lower extremity include the internal tho­racic artery (mammary) to the inferior epigastric artery and the intercostal and lumbar artery to the deep circumex artery. Additional colonic collaterals arise from the SMA to the IMA via the marginal artery of Drummond and the arc of Riolan. Pelvic collaterals from the IMA to the hypogastric include the superior rectal to the middle rectal, the iliolum­bar to the lumbar, and the lateral sacral to the median sacral artery. It is important to recognize these compensatory path­ways and to preserve them during reconstruction.
© Springer Nature Switzerland AG 2019 R. S. Dieter et al. (eds.), Diseases of the Aorta, https://doi.org/10.1007/978-3-030-11322-3_15
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Prevalence (%)
Age-group
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S. Lim and P. R. Crisostomo
Clinical Presentation
Chronic atherosclerosis of the aortoiliac segment often accompanies infrainguinal arterial disease. Thus, this disease most frequently manifests as lower extremity arterial insuf­ciency. Symptoms vary widely depending on location of concomitant disease and degree of collateralization.
Patients with multi-level disease can present with typi­cal lower extremity arterial insufciency symptoms such as leg claudication, tissue loss, or gangrene. In contrast, patients with isolated aortoiliac segment disease may pres­ent with pelvic or buttock claudication. In male aortoiliac disease patients, up to 30% experience difculty achieving and maintaining an erection owing to decreased perfusion of the internal pudendal artery. The constellation of symp­toms associated with distal aortic occlusion, including pel­vic claudication, atrophy of the leg muscles, impotence, and decreased femoral pulses, is known as Leriche’s syn­drome [1].
Diagnosis
Patient History
Conducting a complete history and identifying cardiovas­cular risk factors are important in the diagnosis. Atherosclerosis is a pathologic process related with aging (Fig.15.1). Hypertension, diabetes, dyslipidemia, chronic kidney disease, and cigarette smoking are classic risk fac­tors that must be identied and addressed. It is critical to control these modiable factors to slow the progression of the atherosclerosis.
Male gender and non-Hispanic black race are known unmodiable risk factors for atherosclerosis. In patients who
lack these classic risk factors, hyperhomocysteinemia, hypercoagulability, and hyperbrinogenemia should be investigated.
Risk Factors for Atherosclerosis [8]
• Advanced age.
• Race (non-Hispanic blacks).
• Male gender.
• Hyperbrinogenemia.
• Diabetes mellitus.
• Hyperhomocysteinemia.
• Smoking.
• Hypercoagulability.
• Hypertension.
• Elevated C-reactive protein.
• Dyslipidemia.
• Chronic renal insufciency.
Physical Examination
Physical examination begins with inspection. Aortoiliac dis­ease may cause ischemic changes of the pelvis/buttocks and/ or the lower extremities. Visual signs of ischemia include pallor, muscular atrophy, and cyanosis or skin mottling.
Palpation and comparison of femoral pulses is the quickest and the most important way to diagnose aortoiliac occlusive disease. Grading a pulse is subjective, simply described as (1) normal, diminished, or absent and (2) symmetric versus asymmetric. If a pulse is not palpable, further assessment using Doppler should be pursued. The Doppler signal can be described as triphasic, biphasic, or monophasic. Palpation of the lower extremity is also helpful to assess the level of skin temperature and neurologic (motor and sensory) status.
Fig. 15.1 Prevalence of
symptomatic peripheral arterial disease. (From Norgren etal. [8]. Reprinted with permission from Elsevier)
7
6
5
4
3
2
1
0
30–34
35–39
40–44
45–49
50–54
55–59
60–64
65–69
70–74
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Auscultation of the abdomen commonly reveals bruits when signicant stenosis of the aorta or its branch is present. Middle to lower abdominal bruits may present with aortoil­iac occlusive disease, whereas epigastric or paramedian bruits can indicate visceral vessel stenosis or renal artery ste­nosis, respectively.
Patients with aortoiliac occlusive disease and robust col­lateral formation may have a deceiving lack of distinct physi­cal examination ndings. In that case, an exercise trial may augment changes in pulses or bruit. Lumbar disc herniation, spinal stenosis, or arthritis of the hip or knee joint should be included in the differential diagnosis. Discomfort related with certain positions, or prolonged standing in elderly often arises from neurogenic or musculoskeletal origins.
Vascular Laboratory
Non-invasive hemodynamic vascular laboratory testing begins with ankle-brachial index (ABI). Segmental systolic blood pressure measurement and pulse volume recording (PVR) may aid inlocating the area of concern. A difference of systolic blood pressure between the upper arm and proxi­mal thigh more than 20mmHg reects signicant stenosis in the aortoiliac or proximal femoral arteries. Further reduction of blood pressure in the distal segments or decreased PVR or ABI indicates concomitant outow disease. The combina­tion of a thorough history and physical examination with vascular laboratory testing often provides sufcient clinical data to decide upon the necessity of revascularization.
Duplex ultrasound (DUS) is the most commonly used diagnostic imaging study for delineating extremity vascular abnormalities. However, evaluation of aortoiliac, renal, and visceral arteries is somewhat limited mainly due to overlying bowel gas. Patient factors such as obesity or tortuosity of the vessel also complicate visualization and make it difcult to determine the precise anatomic location of the disease and its severity.
Axial Imaging
with sensitivity and specicity near 95% [10]. MRA can even be obtained without contrast, utilizing time of ight. MRA can be a reliable guide for percutaneous or open inter­vention of the aortoiliac disease. However, MRA has a ten­dency to overestimate the degree of stenosis and has limited evaluation of the severity of calcic disease. In addition, MRI cannot be utilized for patients with certain metallic implants such as cardiac pacemaker or debrillator.
Arteriography
Despite recent technical advances in CT or MRI with increased speed and accuracy, diagnostic catheter-based arteriography remains a valuable tool in a physician’s arma­mentarium. Femoral approach is the preferred way in our institution; however, brachial approach may be necessary in long-segment, near-occlusive, or occlusive aortic or bi-iliac disease. Real-time angiographic imaging utilizing lateral or oblique views may delineate the contribution of accessory renal vessels (Can they be sacriced?), IMA vs SMA perfu­sion (IMA reimplantation?), and lumbar vessels for spinal perfusion (risk of paralysis?) and/or clarify whether radio­graphic stenosis are truly hemodynamically signicant. For example, the presence of superior mesenteric artery occlu­sion, hypogastric occlusion, or prominent inferior mesen­teric artery may require preservation of the inferior mesenteric artery during aortic reconstruction to avoid bowel ischemia.
Treatment Modalities
Conservative Management
Smoking
Smoking cessation is without question desirable in aortic occlusive disease to slow down the progression of athero­sclerosis. Smoking cessation is associated with reduced risks of amputation, myocardial infarction, and mortality in this patient population [11, 12].
Computed tomographic angiography (CTA) is the gold stan­dard imaging modality for aortoiliac disease in our institu­tion. CTA is a non-invasive alternative to standard angiography and can be obtained quickly [9]. With recent advances in multi-detector CT scan, high-quality images with sub-milli­meter spatial resolution are now available. Disadvantages of CT scan include radiation exposure, risk of contrast-induced nephropathy, and hypersensitivity to iodine contrast.
In some institutions, magnetic resonance angiography (MRA) has become the imaging study of choice. MRA is an excellent diagnostic study for aortoiliac occlusive disease
Dyslipidemia
Use of statin has demonstrated a signicant reduction of adverse cardiovascular event in patient with atherosclerosis [1315]. Low-density lipoprotein cholesterol should be controlled under 100mg/dL or to 70mg/dL in very high-risk patients [16].
Diabetes
It is unclear whether aggressive diabetic control decreases adverse cardiovascular events. However, atherosclerosis tends to be more complicated, and amputation rate is higher
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in diabetic patient. This may be related to susceptibility to infection in this population and higher prevalence of distal sensory neuropathy from poor diabetic control.
Hypertension
Hypertension is recognized as a risk factor of atherosclero­sis; however, relative risk for atherosclerosis is less for hypertension than dyslipidemia or smoking. Treatment for hypertension is associated with low cardiovascular compli­cations, stroke, or death [17].
Antiplatelet Therapy
The American Heart Association and the Society for Vascular Surgery recommend the use of an antiplatelet agent in peripheral arterial occlusive disease [16, 18]. The same can be applied to aortoiliac atherosclerotic disease. Dual anti­platelet therapy can be applied at the physician’s discretion, but there is a lack of evidence to date that combination ther­apy is more effective than a single-agent therapy [19].
Supervised Exercise Therapy
Exercise therapy may improve intermittent claudication. A meta-analysis of 1200 patients demonstrated overall improvement of walking distance without improvement of ankle-brachial index [20]. The precise mechanism of action is still unknown, but it is thought to be related with nitric oxide-related vasodilation and improved bioenergetics of skeletal muscle. However, severe cardiopulmonary disease or arthritis may preclude adequate exercise participation.
Medical Therapy
Medical therapy aims for symptomatic relief of claudication. There are two Food and Drug Administration (FDA)­approved medications – pentoxifylline and cilostazol – whereas the Royal College of Physicians in the UK identied naftidrofuryl as the drug of choice over those two drugs. Naftidrofuryl is widely available in the European countries but has not been FDA approved in the USA.
Pharmacodynamics of pentoxifylline includes reducing blood viscosity and enhancing peripheral perfusion and tis­sue oxygenation. Multicenter prospective randomized trial proved its efcacy over placebo [21]. Pentoxifylline can be begun at 400mg three times daily with maximum dose of 1800mg/day. Side effects of this medication include hyper­tension, nausea, vomiting, and headache.
Cilostazol is a phosphodiesterase inhibitor that induces vasodilation and suppresses platelet aggregation. In addition to routine antiplatelet therapy, cilostazol (100 mg twice daily) can contribute to increased overall pain-free ambula­tory distance in as short as 4weeks [22]. However, this agent can exacerbate congestive heart failure and is contraindi­cated in a patient with any level of heart failure.
A multicenter, randomized, double-blind, parallel-group study compared cilostazol and pentoxifylline and found that while cilostazol signicantly improved walking distance, pent­oxifylline was not signicantly different than placebo [23].
Decision-Making toIntervention
The natural history of atherosclerosis in aortoiliac disease is a slow arterial process that impairs walking ability. With maximum medical treatment and exercise therapy, the chance of developing severe ischemic symptoms such as rest pain or tissue loss is relatively low (<5%) [8, 24]. Thus, the majority of patients need just reassurance from their physi­cian. However, patients with advanced ischemic symptoms or claudication that signicantly impacts their daily living or occupation should be under consideration for intervention.
It is important to recognize that determining the degree of functional impairment is not straightforward. Patient percep­tion of functional impairment may vary according to their baseline activity. For example, mild to moderate claudication in an active man may have a greater impact, while severe claudication in a sedentary patient may be less signicant. Patient morbidity is another important aspect to be consid­ered. Patients with severe arthritis or spinal degenerative dis­ease might not benet from invasive vascular intervention, whereas patients with severe coronary artery disease or pul­monary compromise may suffer from postoperative signi­cant morbidity or mortality.
Open revascularization has traditionally demonstrated improved patency over endovascular intervention at the expense of higher morbidity and mortality although support­ing data comparing the two strategies are still poor. The TransAtlantic Inter Society Consensus (TASC) document rst in 2000, then in 2007, and most recently updated in 2015, classied anatomic patterns of disease severity from types A through D for aortoiliac, femoropopliteal, and infr­apopliteal segments [25] (Fig. 15.2). Initially, the TASC working group advocated endovascular intervention for TASC type A lesions and open surgical treatment for TASC type D lesions. However, the latest TASC II update in 2015 recognized that with modern advances in endovascular instruments and practitioner skill, an endovascular rst approach has become the predominant modality when revas­cularization is decided. Moreover, hybrid open and endovas­cular procedures may be suitable for complex anatomy.
Endovascular Intervention
Arterial Access
Lesions at the aortic bifurcation or common iliac arteries can be treated with the usual retrograde approach from the common femoral arteries. Occlusions that cannot be crossed
T
T
• Shor
• Unilateral CIA occlusion
• Single or multiple stenosis totaling 3-10 cm in
• Unilateral EIA occlusion not in
• Bilateral CIA occlusions
• Bilateral EIA stenoses 3–10 cm long not e
• Unilateral EIA stenosis e
• Unilateral EIA occlusion that in
• Hea
• Infra-renal aor
• Diffuse disease in
• Diffuse multiple stenoses in
• Unilateral occlusions of both CIA and EIA
• Bilateral occlusions of EIA
• Iliac stenoses in patients with AAA requir
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ype A lesions
• Unilateral or bilateral stenoses of CIA
• Unilateral or bilateral single short (3 cm) stenosis of EIA
Type B lesions:
t (3cm) stenosis of infrarenal aorta
221
EIA not extending into the CFA
internal iliac or CFA
ype C lesions
the CFA
xtending into the CFA
internal iliac and/or CFA
vily calcified unilateral EIA occlusion with or without
involvement of origins of internal iliac and/or CFA
Type D lesions
volving the
volving the origins of
xtending into
volves the origins of
requiring treatment
EIA, and CFA
and not amenable to endograft placement or other lesions requiring open aortic or iliac surgery
toiliac occlusion
volving the aorta and both iliac arteries
Fig. 15.2 TransAtlantic Inter-Societal Classication of aortoiliac lesions. (From Norgren etal. [8]. Reprinted with permission from Elsevier)
from the ipsilateral femoral retrograde approach may require contralateral femoral artery or brachial artery access and subsequent antegrade approach. A left brachial artery approach may also decrease the risk of an aortic dissection, but this patient population not infrequently exhibits con-
volving the unilateral CIA,
ing treatment
comitant left subclavian artery stenosis that may require pretreatment prior to aortoiliac intervention.
After access is obtained, a diagnostic angiographic eval­uation should be performed prior to intervention. Aortogram and pelvic images are essential to evaluate extent of the dis-
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ease. A contralateral oblique view opens the iliac bifurca­tion, whereas an ipsilateral oblique view helps to clarify the femoral bifurcation. Infrainguinal runoffs also should be evaluated prior to intervention in case of distal embolization during the course of intervention.
Crossing theLesion
An angled GLIDEWIRE (Terumo Medical Corp, Somerset, NJ) and angled support catheter are the prototypical methods for crossing an iliac stenosis. Chronic total occlusions (CTO) often require a variety of wires, catheters, and sheath sup­port. The most difcult part of the occlusion is the proximal cap. After the wire is fully crossed over, true lumen location should be conrmed with contrast injection. Blood draw as conrmation may be false. A variety of CTO devices exist, some of which allow re-entry from a subintimal plane to the true lumen (Fig.15.3).
Aortic Bifurcation Disease
Lesions at the aortic bifurcation traditionally are treated with kissing iliac balloon and stent placement. Even in sce­narios with unilateral disease, if the lesion is close to the aortic bifurcation, simultaneous bilateral intervention has been advocated to prevent contralateral iliac dissection or thrombus dislodgement and subsequent embolism. Contralateral prophylactic treatment has also been recom­mended in order to treat spill over plaque originating from the aorta [26, 27]. However, a retrospective of 175 patients with unilateral iliac artery lesions treated with unilateral method revealed about 1% risk of contralateral extremity complications [28].
Selection ofBalloon andStent
Plain old balloon angioplasty (POBA) is inferior in patency to balloon angioplasty and stent within the aortoiliac system [2931]. The optimal vessel diameter is often derived from the normal equivalent segment on the contralateral side. A calibration imaging system can also be useful to facilitate measuring size and length of the lesion. Balloons and stents should be large enough to cover the diseased segment com­pletely but small enough not to injure normal vessels and aortic branches. Five to ten percent oversize of the balloon and stent is recommended except for a heavily calcied lesion that may rupture with larger devices.
A variety of stents are commercially available which fall into two main deployment categories: balloon-expandable and self-expanding. Selection of a stent often depends on device availability and the operator’s familiarity. However, it is noteworthy that a balloon-expandable stent is advanta­geous when precise stent placement is necessary. Such is the case in bilateral common iliac lesions which need kissing stents to be deployed precisely at the same level to allow equal opposition. In contrast, when the stent must follow a tortuous path or is to be placed from the contralateral side, a self-expanding stent provides greater exibility. The exter­nal iliac artery often benets from self-expanding stent placement.
A covered stent graft is a metal stent covered with Dacron or polytetrauorethylene (PTFE) which initially was devel­oped for exclusion of an aneurysmal segment or treatment of an iatrogenic perforation or rupture. Covered stents exclude the diseased segments from the circulation and, theoretically, may reduce in-stent restenosis. Although limited studies
Fig. 15.3 Reentry catheters.
(a) Pioneer catheter with needle deployed. (b) Outback LTD catheter. (Right: with needle retracted. Left: with needle deployed). (From Jacobs etal. [42]. Reprinted with permission from Elsevier)
Patency (%)
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100
80
60
95%
40
89%
20
0
01020
Primary assisted patency Primary patency
Fig. 15.4 Comparison of primary patency between stents and stent
grafts. (From Chang et al. [32]. Reprinted with permission from Elsevier)
95%
80%
30
Time (months)
40 50 60
95%
80%
have been conducted in patients with aortoiliac atheroscle­rotic disease, primary and primary-assisted patency rate at 5years are 80% and 95% which are superior to bare-metal stents [32] (Fig.15.4).
Drug-eluting stents (DES) were initially developed for the treatment of coronary artery disease. A drug such as paclitaxel or sirolimus delivered via stent inhibits resteno­sis and improves long-term patency. DES and drug-coated balloons (DCB) have similarly been FDA approved for the treatment of femoropopliteal artery disease [3335]. These newer-generation balloons and stents have been recom­mended over their nondrug coated counterparts but may require extended dual antiplatelet therapy [36]. Although these newer drug-coated devices have been used off label in the external iliac artery, data for the aortoiliac segment is lacking.
Concomitant Femoral Artery Disease
With coexisting severe common femoral artery disease, the artery can be accessed utilizing a hybrid femoral open cut down allowing arterial puncture under direct visualization. At the end of the intervention, proximal and distal control is obtained and the femoral artery can be endarterectomized using a longitudinal arteriotomy and closed with a patch angioplasty. This will improve inow perfusion to the ipsi­lateral leg and better maintain graft patency [32].
Postoperative Care
Aspirin therapy should be initiated and continued inde­nitely. Dual antiplatelet is recommended for at least 30days. Clinical surveillance with physical exam, ABI, and duplex
ultrasonography should be performed immediate postop (30days) and every 6months at least 1year and annually thereafter.
Results ofEndovascular Revascularization
The technical success rate of endovascular interventions in the aortoiliac segment is very high in many reports. However, maintaining long-term patency requires dedicated surveil­lance and may need multiple secondary interventions. Although a variety of factors can affect the outcome, the TASC classication well represents outcomes referencing disease location and severity [37]. Endovascular long-term outcomes are better in TASC A and B lesions compared to TASC C or D lesions. Cumulative primary patency of all lesions was 83% at 5years (Fig.15.5). Although many TASC D lesions can be treated successfully with an endovascular approach, open surgical revascularization especially in patients suitable for the procedure should be discussed.
Open Surgical Revascularization
In general, open surgical repair carries a higher perioperative morbidity and mortality compared to minimally invasive endovascular revascularization. Thus, cardiopulmonary comorbidities and renal function have to be assessed and optimized prior to operation. Coagulation prole should be checked routinely. Preoperative coronary evaluation may be necessary and is an important modiable risk factor in patients undergoing open vascular procedures. Preoperative nuclear cardiac stress test has been used in our institution frequently given most of aortic occlusive patients cannot complete an exercise stress test and are at high risk for post­operative myocardial infarction. Full assessment of the peripheral vasculature is indicated because the condition of the distal runoffs inuence the outcome of the aortoiliac intervention. Sometimes, concurrent distal bypass may be indicated.
Intraoperatively, appropriate antibiotic prophylaxis should be administered before the incision and through the perioperative period. Invasive arterial blood pressure moni­toring is routine in many hospitals.
Direct Surgical Revascularization (Aorto­Bifemoral Bypass)
Initial Approach andGroin Dissection
The patient is placed in supine position. Bilateral groin inci­sions are made. The choices of groin incisions are predomi­nated by preoperative ndings and patient factors. Oblique