eMedicine Specialties > Vascular Surgery > Medical Topics
Infrainguinal Occlusive Disease
Updated: Jun 24, 2008
Introduction
This article is a review of chronic infrainguinal atherosclerotic arterial occlusive disease caused by atherosclerosis involving the femoral, popliteal, and/or infrapopliteal arteries. Because chronic atherosclerotic disease may result in acute circulatory compromise, acute arterial occlusion is also covered. Less common etiologies of lower extremity arterial insufficiency, such as atheroembolism, Buerger disease, popliteal artery entrapment syndrome, and cystic adventitial disease, are briefly discussed.
Decision-making in the management of vascular disease changes frequently as new information becomes available and as new technologies emerge.1 Furthermore, therapeutic recommendations for a given population may not be applicable to individual patients with even slightly differing risk factors, co-morbidities, or vascular anatomy.2
Problem
Although most patients with infrainguinal disease are treated nonoperatively, over 100,000 vascular reconstructive procedures are performed yearly in the United States alone. Unfortunately, intervention fails in up to 50% of cases within 5 years.3
Of the symptomatic patients under medical care, within 5 years, approximately 25% develop progressive symptoms, 5-10% require surgical intervention, and 1-2% undergo major amputation.4 The vast majority of patients with intermittent claudication remain stable or improve with noninvasive management. According to Baumgartner, Schainfeld, and Graziani, 25% of patients with claudication will eventually require revascularization and only 5% will develop critical limb ischemia.5 Within the first year after the initial diagnosis, 6-9% of patients require intervention.5 Subsequently 2-3% of patients per year require intervention.5
Because lower extremity atherosclerosis is a marker for systemic atherosclerotic disease, these patients have significant systemic morbidities. Thirty percent of patients with peripheral artery disease die within 5 years and 40% die within 10 years.4,6 Feringa et al observed a cohort of 2,642 patients having ankle-brachial indices less than or equal to 0.9.6 They discovered that the major factors associated with mortality in this group of patients included renal dysfunction, heart failure, ST-segment changes, age greater than 65 years, hypercholesterolemia, ankle-brachial index lower than 0.60, Q-waves, diabetes, cerebrovascular disease, and pulmonary disease. They also found that the use of statins, aspirin, and beta-blockers correlated with reduced 10-year mortality.
Frequency
Chronic atherosclerotic lower extremity disease is present in 20% of the population older than 55 years.7 Most affected persons are asymptomatic. In fact, estimates indicate that only approximately 20% of people with atherosclerotic lower extremity disease present to a physician because of symptoms. Another 20% are symptomatic but do not seek medical attention.
Etiology
Commonly accepted risk factors for both the occurrence and progression of atherosclerotic vascular disease include abnormal glucose tolerance, cigarette smoking, advanced age, hyperlipidemia, and hypertension.8
Certain biochemical factors have also been shown to be independent risk factors for atherosclerotic peripheral vascular disease. Such factors include increased plasma fibrinogen levels,9 hyperhomocysteinemia,10,11 and high-sensitivity C-reactive protein.12 These factors may also increase the risk of bypass graft stenosis and reocclusion.
When more than one risk factor is present, the cumulative risk is often greater than individual risk factors combined. This is especially true of cigarette smoking, which, when accompanied by another risk factor (such as hypertension or hyperlipidemia) increases the disease risk to more than twice the sum of the individual risks.
Pathophysiology
Atherosclerotic occlusive disease
With atherosclerotic occlusion of a major lower extremity artery, the limb is perfused via collateral pathways. Although this alternate pathway may be adequate at rest, it becomes inadequate as the oxygen demands of the leg musculature increase with activity. This results in calf muscle pain or fatigue, a symptom known as intermittent claudication. As the degree of atherosclerotic occlusion worsens, blood flow, even at rest, may become impaired. This may cause ischemic pain at rest, ischemic ulceration, and gangrene.
Acute arterial occlusion
Acute occlusion of peripheral arteries commonly involves the infrainguinal segment. Underlying atherosclerotic disease may result in intraluminal strictures that impair blood flow and cause acute thrombosis. Emboli typically lodge at bifurcations and, hence, tend to occlude the distal common femoral artery (the most common site, comprising 34% of all arterial emboli) or distal popliteal artery (14%). Popliteal artery aneurysms may thrombose as a result of turbulent blood flow. The clinical indications of acute occlusion of lower extremity arteries are the following classic 6 "P"s:
- Paresthesias
- Pain
- Poikilothermia (coolness)
- Pallor
- Pulselessness
- Paralysis
The anatomic level at which pulse loss occurs helps identify the location of the occlusion.
Presentation
Most people harboring atherosclerotic disease of the lower extremities are asymptomatic; others develop ischemic symptoms. Some patients attribute ambulatory difficulties to "old age," unaware of the existence of a potentially correctible problem.
Symptomatic patients may present with intermittent claudication, ischemic pain at rest, nonhealing ulceration of the foot (see Image 1), or frank ischemia of the foot.
Cramping or fatigue of major muscle groups in one or both lower extremities that is reproducible upon walking a specific distance suggests intermittent claudication. This symptom increases during ambulation until walking is no longer possible, and it is relieved by several minutes of rest. The onset of claudication may occur sooner with more rapid walking or when walking uphill or up stairs. The claudication of infrainguinal occlusive disease typically involves the calf muscles, while symptoms that occur in the buttocks or thighs suggest aortoiliac occlusive disease.13
Physical
Physical examination discloses absent or diminished peripheral pulses below a certain level. Although diminished common femoral artery pulsation is characteristic of aortoiliac disease, infrainguinal disease alone is characterized by normal femoral pulses at the level of the inguinal ligament and diminished or absent pulses distally.
Specifically, loss of the femoral pulse just below the inguinal ligament occurs with a proximal superficial femoral artery occlusion. Loss of the popliteal artery pulse suggests superficial femoral artery occlusion, typically in the adductor canal. Loss of pedal pulses is characteristic of disease involving the distal popliteal artery or its trifurcation.
Importantly however, be aware that absence of the dorsalis pedis pulse may be a normal anatomic variant, noted in approximately 10% of the population. On the other hand, the posterior tibial pulse is present in 99.8% of persons aged 0-19 years. Hence, absence of both pedal pulses is a more specific indicator of peripheral arterial disease.
Other findings suggestive of atherosclerotic disease include a bruit heard overlying the iliac or femoral arteries, skin atrophy, loss of pedal hair growth, cyanosis of the toes, ulceration or ischemic necrosis, and, after 1-2 minutes of elevation above heart level, pallor of the involved foot followed by dependent rubor (see Image 2).
Differential diagnoses
Pseudoclaudication
Although ischemic findings in the face of absent pulses clearly pinpoint arterial insufficiency as the culprit, intermittent claudication, even when associated with absent pulses, is not always due to arterial insufficiency.
If symptoms are not always reproducible (ie, the patient sometimes has "good days" when ambulation is not limited by claudication) or if the symptoms are associated with low back pain or radiculopathy, the clinician should consider the possibility of pseudoclaudication, which occurs as a result of spinal stenosis or cauda equina syndrome.
In that case, the pulse deficit may be an incidental finding of asymptomatic atherosclerosis. Noninvasive vascular laboratory testing (see Lab Studies), lumbosacral imaging, and neurologic evaluation all may contribute to distinguishing between these possibilities.
Two rather unusual conditions, venous claudication due to extensive iliofemoral venous thrombosis and chronic compartment syndrome due to calf muscle hypertrophy in athletes, result in a bursting type of pain in the calf with ambulation, which subsides slowly with elevation. In each case, the etiology is impaired venous outflow.
Atheroembolism
Patchy areas of ischemia involving the feet, especially in the presence of palpable pedal pulses, suggest the possibility of atheroembolism of plaque fragments from ulcerated, although nonocclusive, proximal atherosclerotic plaques or from thrombus lining the wall of an infrarenal aortic aneurysm (see Abdominal Aortic Aneurysm).14
Buerger disease
Severe ischemia of the toes with absent pedal pulses but normal proximal pulses in a man aged 35-50 years who smokes cigarettes may be the result of Buerger disease (thromboangiitis obliterans).15 Ischemia of the fingers may also be present. The digits are cool, moist, mottled, and sometimes have tender shallow ulcers. Migratory superficial phlebitis may occur.
Collagen-vascular disease must be excluded.16 See the eMedicine article Buerger Disease (Thromboangiitis Obliterans). Angiography reveals pathognomonic findings of "corkscrew" arteries. Treatment is discontinuation of smoking and good local wound care. Vascular surgery is rarely possible because of the poor quality of the distal arteries.
Complex regional pain syndromes (eg, posttraumatic pain syndromes, causalgia, mimocausalgia, Sudeck atrophy, reflex sympathetic dystrophy)
Complex regional pain syndromes (CRPSs) have been classified by the World Health Organization as CRPS II (ie, causalgia), which is associated with a demonstrable nerve injury, and as CRPS I (ie, mimocausalgia, reflex sympathetic dystrophy, Sudeck atrophy), which includes the remainder. Causalgia (ie, causos, heat; algos, pain) was first described in patients with arterial and nerve injuries sustained during the American Civil War. Both variants remain poorly understood and often misdiagnosed.
Although the exact pathophysiology is elusive, the sympathetic nervous system clearly plays a focal role. Therefore, surgical sympathectomy—perfected decades ago by vascular surgeons to manage nonreconstructible arterial disease (a common situation at the time)—was once the mainstay for treatment of the CRPSs.
Although surgical sympathectomy is now mostly notable only for historic purposes, sympathetic blockade is quite effective and is commonly performed for the CRPSs. Hence, currently the treatment of CRPSs is performed mainly by pain management specialists. Nonetheless, because the vascular surgeon has always been primarily responsible for the diagnosis of extremity symptoms, it is not uncommon for patients with CRPS to report to a vascular surgeon because of extremity pain.
Such pain may occur after extremity trauma but may seem disproportionate to the degree of injury.17 Pain may also manifest after delayed revascularization of an acutely ischemic extremity. The diagnosis is often one of exclusion and thus requires a high index of clinical suspicion. The diagnosis should be considered more strongly if severe superficial burning pain and agonizing hypersensitivity are present and are associated with vasomotor abnormalities such as edema, erythema, and hyperhidrosis. Radiographic studies may demonstrate relative and patchy osteopenia in the involved extremity.
In addition to symptomatic relief, management of the CRPSs requires sympathetic blockade. This is best performed during the early, acute stage when the clinical course may be reversible. As the disease progresses, the erythema gives way to cyanotic mottling, the acute edema transforms to brawny edema, and the pain becomes unrelenting and disabling. These findings occur at approximately the third month and represent the second, or dystrophic, stage. At this point, both plain radiographs and bone scans tend to demonstrate indicative findings.
Over time, disuse leads to atrophy, soft tissue fibrosis, and joint contractures. Radiographs confirm ankylosis and severe osteoporosis. This signals the third, or atrophic, stage. Note that atrophy can also occur because of intentional disuse for anticipated secondary gain. Such patients reportedly do not respond to treatment until litigation has concluded.
Typically, the clinician does not even consider the diagnosis of a CRPS until the second stage. At that point, a dramatic clinical response to sympathetic blockade may confirm the diagnosis. Unfortunately, too much damage may have already occurred for sympathetic ablation to be effective and to break the vicious cycle of pain, sympathetic overactivity, and pain; the progression of the CRPS may be inexorable and irreversible.
One other caveat is that in the face of coexisting arterial disease, the vascular surgeon who may attribute the symptoms to ischemia and thereby may consider bypass should be aware that a surgical incision tends to exacerbate the pain in an extremity afflicted with a CRPS.
For more information, also see the eMedicine article Complex Regional Pain Syndrome.
Popliteal artery entrapment syndrome
Intermittent claudication occurring in younger persons (from the teens to approximately age 45 y), particularly males, raises the possibility of popliteal artery entrapment syndrome.18
In this unusual condition, the artery follows an aberrant course around the gastrocnemius muscle, usually medial to the medial head instead of between the 2 heads of this muscle. Ambulation causes the muscle to compress the artery and results in transient loss of distal blood flow. Over time, the artery may thrombose or become aneurysmal.
Prior to complete thrombosis, this condition can sometimes be confirmed clinically by noting loss of the pedal pulse upon active plantar flexion or passive dorsiflexion of the foot. CT scanning or MRI can reveal the muscular abnormality, and angiography with stress views can confirm the diagnosis.
Treatment entails sectioning the aberrant muscle fibers. Bypass grafting is needed if the occlusion is chronic in nature. Assessing the contralateral side is important because one third of cases are bilateral.
Cystic adventitial disease of the popliteal artery
Intermittent claudication of abrupt onset occurring in a relatively young male also may be the result of cystic adventitial disease of the popliteal artery.19
This rare congenital anomaly is the result of ganglionlike cysts, perhaps from an adjacent synovium, compressing the artery. This compression may eventually lead to thrombosis of the artery.
Prior to occlusion, pedal pulses may be found to disappear with flexion of the knee joint. Ultrasonography, CT scanning, or MRI may demonstrate the cyst, while angiography may demonstrate a characteristic hourglass deformity, which has been termed the scimitar sign.
Cystic adventitial disease of the popliteal artery is treated surgically by removing the cyst. Vascular bypass is required if occlusion has occurred.20
Indications
Indications for lower extremity revascularization include gangrene, pain at rest, nonhealing arterial ulcer, and disabling claudication.
Relevant Anatomy
The inguinal (Poupart) ligament is a tough, fibrous band stretching from the anterior superior iliac spine to the pubic tubercle. The common femoral artery is a continuation of the external iliac artery, beginning just under the middle of the inguinal ligament. It is palpable as the femoral pulse and is well suited to both percutaneous and surgical access because of its relatively superficial position. Approximately 1-2 inches distal to the inguinal ligament, the common femoral artery divides into the deep femoral (profunda femoris) artery, usually arising in the posterolateral position, and the superficial femoral artery.
The deep femoral artery gives rise to several very proximal branches that tend to maintain patency even in persons with extensive atherosclerotic disease, thus providing the major source of collateral circulation around an occluded superficial femoral artery.
The term superficial femoral artery is somewhat of a misnomer in that it is superficial for only a few inches until it courses under the sartorius muscle and into the aponeurotic covering of the adductor (Hunter) canal.
When it emerges anterior to the adductor magnus, the superficial femoral artery becomes the popliteal artery. Because the popliteal artery is bounded posteriorly by the popliteal vein, nerve, and fascia and the semimembranosus, gastrocnemius, plantaris, and soleus muscles, it is the most difficult of the lower extremity pulses to accurately assess.
The popliteal artery passes posterior to the knee joint and into the upper leg where, just distal to the popliteus muscle, it divides into the anterior tibial artery and the tibioperoneal trunk. The anterior tibial artery passes laterally through the interosseous membrane and lies on the interosseous membrane throughout much of the leg. As it reaches the lower leg, it lies on the tibia and then becomes superficial at the ankle joint, at which point it is called the dorsalis pedis artery and, hence, is palpable as the dorsalis pedis pulse.
The tibioperoneal trunk divides within approximately 1 inch of its origin into the peroneal artery and the posterior tibial artery. The peroneal artery lies on the medial surface of the fibula and ends in terminal branches near the os calcis. The peroneal artery, which is too deep to be palpable as a pulse, often remains patent despite atherosclerotic occlusion of the anterior and posterior tibial arteries and, thus, may be a usable site for the distal anastomosis of bypass grafts in patients with advanced infrapopliteal occlusive disease. The posterior tibial artery runs along the medial side of the leg and posterior to the medial malleolus, where it is superficial and palpable as the posterior tibial pulse.
The greater (long) saphenous vein originates on the medial side of the dorsum of the foot and runs anterior to the medial malleolus. It then runs posteromedially to the tibia, posteriorly to the medial condyle of the femur, and along the medial thigh, coursing anteriorly until it enters the femoral vein through the foramen ovale, just below the inguinal ligament. The length and relatively superficial course of the greater saphenous vein make it ideally suited for use in infrainguinal bypass surgery.
Contraindications
In nonambulatory patients with ischemic pain at rest, gangrene, or extensive nonhealing wounds, primary lower extremity amputation may be a better choice than vascular bypass surgery.
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References
Rectenwald JE, Upchurch GR Jr. Impact of outcomes research on the management of vascular surgery patients. J Vasc Surg. Jun 2007;45 Suppl A:A131-40. [Medline].
Brothers TE, Robison JG, Elliott BM. Prospective decision analysis for peripheral vascular disease predicts future quality of life. J Vasc Surg. Oct 2007;46(4):701-708; discussion 708. [Medline].
Conte MS, Lorenz TJ, Bandyk DF, Clowes AW, Moneta GL, Seely BL. Design and rationale of the PREVENT III clinical trial: edifoligide for the prevention of infrainguinal vein graft failure. Vasc Endovascular Surg. Jan-Feb 2005;39(1):15-23. [Medline].
Nolan B, Finlayson S, Tosteson A, Powell R, Cronenwett J. The treatment of disabling intermittent claudication in patients with superficial femoral artery occlusive disease--decision analysis. J Vasc Surg. Jun 2007;45(6):1179-84. [Medline].
Baumgartner I, Schainfeld R, Graziani L. Management of peripheral vascular disease. Annu Rev Med. 2005;56:249-72. [Medline].
[Best Evidence] Feringa HH, Bax JJ, Hoeks S, van Waning VH, Elhendy A, Karagiannis S. A prognostic risk index for long-term mortality in patients with peripheral arterial disease. Arch Intern Med. Dec 10 2007;167(22):2482-9. [Medline].
[Best Evidence] Hankey GJ, Norman PE, Eikelboom JW. Medical treatment of peripheral arterial disease. JAMA. Feb 1 2006;295(5):547-53. [Medline].
Chi YW, Jaff MR. Optimal risk factor modification and medical management of the patient with peripheral arterial disease. Catheter Cardiovasc Interv. Feb 28 2008;71(4):475-489. [Medline].
Daskalopoulou SS, Pathmarajah M, Kakkos SK, Daskalopoulos ME, Holloway P, Mikhailidis DP. Association between ankle - brachial index and risk factor profile in patients newly diagnosed with intermittent claudication. Circ J. Mar 2008;72(3):441-8. [Medline].
Garofolo L, Barros N Jr, Miranda F Jr, D'Almeida V, Cardien LC, Ferreira SR. Association of increased levels of homocysteine and peripheral arterial disease in a Japanese-Brazilian population. Eur J Vasc Endovasc Surg. Jul 2007;34(1):23-8. [Medline].
Taute BM, Taute R, Heins S, Behrmann C, Podhaisky H. Hyperhomocysteinemia: marker of systemic atherosclerosis in peripheral arterial disease. Int Angiol. Mar 2004;23(1):35-40. [Medline].
Pradhan AD, Shrivastava S, Cook NR, Rifai N, Creager MA, Ridker PM. Symptomatic peripheral arterial disease in women: nontraditional biomarkers of elevated risk. Circulation. Feb 12 2008;117(6):823-31. [Medline].
[Best Evidence] Cournot M, Boccalon H, Cambou JP, Guilloux J, Taraszkiewicz D, Hanaire-Broutin H. Accuracy of the screening physical examination to identify subclinical atherosclerosis and peripheral arterial disease in asymptomatic subjects. J Vasc Surg. Dec 2007;46(6):1215-21. [Medline].
Reber PU, Patel AG, Stauffer E, et al. Mural aortic thrombi: An important cause of peripheral embolization. J Vasc Surg. Dec 1999;30(6):1084-9. [Medline].
Puéchal X, Fiessinger JN. Thromboangiitis obliterans or Buerger's disease: challenges for the rheumatologist. Rheumatology (Oxford). Feb 2007;46(2):192-9. [Medline].
Stone JH. Vasculitis: a collection of pearls and myths. Rheum Dis Clin North Am. Nov 2007;33(4):691-739, v. [Medline].
Kurvers HA. Reflex sympathetic dystrophy: facts and hypotheses. Vasc Med. 1998;3(3):207-14. [Medline].
Stager A, Clement D. Popliteal artery entrapment syndrome. Sports Med. Jul 1999;28(1):61-70. [Medline].
Pham TT, Kapur R, Harwood MI. Exertional leg pain: teasing out arterial entrapments. Curr Sports Med Rep. Dec 2007;6(6):371-5. [Medline].
Rispoli P, Moniaci D, Zan S, Cassatella R, Varetto G, Maselli M. Cystic adventitial disease of the popliteal artery. Report of 1 case and review of the literature. J Cardiovasc Surg (Torino). Apr 2003;44(2):255-8. [Medline].
[Best Evidence] Thatipelli MR, Pellikka PA, McBane RD, Rooke TW, Rosales GA, Hodge D. Prognostic value of ankle-brachial index and dobutamine stress echocardiography for cardiovascular morbidity and all-cause mortality in patients with peripheral arterial disease. J Vasc Surg. Jul 2007;46(1):62-70; discussion 70. [Medline].
Yamada T, Ohta T, Ishibashi H, Sugimoto I, Iwata H, Takahashi M. Clinical reliability and utility of skin perfusion pressure measurement in ischemic limbs--comparison with other noninvasive diagnostic methods. J Vasc Surg. Feb 2008;47(2):318-23. [Medline].
Safirstein R, Andrade L, Vieira JM. Acetylcysteine and nephrotoxic effects of radiographic contrast agents--a new use for an old drug. N Engl J Med. Jul 20 2000;343(3):210-2. [Medline].
Penfield JG, Reilly RF Jr. What nephrologists need to know about gadolinium. Nat Clin Pract Nephrol. Dec 2007;3(12):654-68. [Medline]. [Full Text].
Meaney JF, Goyen M. Recent advances in contrast-enhanced magnetic resonance angiography. Eur Radiol. Mar 2007;17 Suppl 2:B2-6. [Medline].
Burrill J, Dabbagh Z, Gollub F, Hamady M. Multidetector computed tomographic angiography of the cardiovascular system. Postgrad Med J. Nov 2007;83(985):698-704. [Medline].
Aronow WS. Management of peripheral arterial disease. Cardiol Rev. Mar-Apr 2005;13(2):61-8. [Medline].
Lumsden AB, Rice TW. Medical management of peripheral arterial disease: a therapeutic algorithm. J Endovasc Ther. Feb 2006;13 Suppl 2:II19-29. [Medline].
McDermott MM, Guralnik JM, Ferrucci L, Tian L, Pearce WH, Hoff F. Physical activity, walking exercise, and calf skeletal muscle characteristics in patients with peripheral arterial disease. J Vasc Surg. Jul 2007;46(1):87-93. [Medline].
Rice TW, Lumsden AB. Optimal medical management of peripheral arterial disease. Vasc Endovascular Surg. Aug-Sep 2006;40(4):312-27. [Medline].
Tulsyan N, Ouriel K, Kashyap VS. Emerging drugs in peripheral arterial disease. Expert Opin Emerg Drugs. Mar 2006;11(1):75-90. [Medline].
Jacoby D, Mohler ER 3rd. Drug treatment of intermittent claudication. Drugs. 2004;64(15):1657-70. [Medline].
Robless P, Mikhailidis D, Stansby G. Cilostazol for peripheral arterial disease. Cochrane Database Syst Rev. 2008;(1):CD003748. [Medline].
[Best Evidence] Hiatt WR, Money SR, Brass EP. Long-term safety of cilostazol in patients with peripheral artery disease: the CASTLE study (Cilostazol: A Study in Long-term Effects). J Vasc Surg. Feb 2008;47(2):330-336. [Medline].
Stewart AH, Eyers PS, Earnshaw JJ. Prevention of infection in peripheral arterial reconstruction: a systematic review and meta-analysis. J Vasc Surg. Jul 2007;46(1):148-55. [Medline].
Perera GB, Lyden SP. Current trends in lower extremity revascularization. Surg Clin North Am. Oct 2007;87(5):1135-47, x. [Medline].
Neufang A, Espinola-Klein C, Dorweiler B, Messow CM, Schmiedt W, Vahl CF. Femoropopliteal prosthetic bypass with glutaraldehyde stabilized human umbilical vein (HUV). J Vasc Surg. Aug 2007;46(2):280-8. [Medline].
DeRubertis BG, Pierce M, Chaer RA, Rhee SJ, Benjeloun R, Ryer EJ. Lesion severity and treatment complexity are associated with outcome after percutaneous infra-inguinal intervention. J Vasc Surg. Oct 2007;46(4):709-16. [Medline].
Conrad MF, Cambria RP, Stone DH, Brewster DC, Kwolek CJ, Watkins MT. Intermediate results of percutaneous endovascular therapy of femoropopliteal occlusive disease: a contemporary series. J Vasc Surg. Oct 2006;44(4):762-9. [Medline].
Vogel TR, Su LT, Symons RG, Flum DR. Lower extremity angioplasty for claudication: a population-level analysis of 30-day outcomes. J Vasc Surg. Apr 2007;45(4):762-7. [Medline].
Scott EC, Biuckians A, Light RE, Scibelli CD, Milner TP, Meier GH 3rd. Subintimal angioplasty for the treatment of claudication and critical limb ischemia: 3-year results. J Vasc Surg. Nov 2007;46(5):959-64. [Medline].
Marks NA, Ascher E, Hingorani AP, Shiferson A, Puggioni A. Gray-scale median of the atherosclerotic plaque can predict success of lumen re-entry during subintimal femoral-popliteal angioplasty. J Vasc Surg. Jan 2008;47(1):109-15; discussion 115-6. [Medline].
Morgan JH 3rd, Wall CE Jr, Christie DB, Harvey RL, Solis MM. The results of superficial femoral, popliteal, and tibial artery stenting for peripheral vascular occlusive disease. Am Surg. Nov 2005;71(11):905-9; discussion 909-10. [Medline].
Yoffe B, Yavnel L, Altshuler A, et al. Preliminary experience with the Xtrak debulking device in the treatment of peripheral occlusions. J Endovasc Ther. Apr 2002;9(2):234-40. [Medline].
Garvin R, Reifsnyder T. Cutting balloon angioplasty of autogenous infrainguinal bypasses: short-term safety and efficacy. J Vasc Surg. Oct 2007;46(4):724-30. [Medline].
Zeller T, Rastan A, Schwarzwalder U, et al. Midterm results after atherectomy-assisted angioplasty of below-knee arteries with use of the Silverhawk device. J Vasc Interv Radiol. Dec 2004;15(12):1391-7. [Medline].
Zeller T, Rastan A, Schwarzwalder U, et al. Percutaneous peripheral atherectomy of femoropopliteal stenoses using a new-generation device: six-month results from a single-center experience. J Endovasc Ther. Dec 2004;11(6):676-85. [Medline].
Berceli SA, Hevelone ND, Lipsitz SR, Bandyk DF, Clowes AW, Moneta GL. Surgical and endovascular revision of infrainguinal vein bypass grafts: analysis of midterm outcomes from the PREVENT III trial. J Vasc Surg. Dec 2007;46(6):1173-1179. [Medline].
Schanzer A, Hevelone N, Owens CD, Belkin M, Bandyk DF, Clowes AW. Technical factors affecting autogenous vein graft failure: observations from a large multicenter trial. J Vasc Surg. Dec 2007;46(6):1180-90; discussion 1190. [Medline].
Kumins NH, Landau DS, Montalvo J, Zasadzinski J, Wojciechowski J, Jovanovich BD. Expanded indications for the treatment of postcatheterization femoral pseudoaneurysms with ultrasound-guided compression. Am J Surg. Aug 1998;176(2):131-6. [Medline].
Schneider C, Malisius R, Küchler R, Lampe F, Krause K, Bahlmann E. A prospective study on ultrasound-guided percutaneous thrombin injection for treatment of iatrogenic post-catheterisation femoral pseudoaneurysms. Int J Cardiol. Jan 11 2008;[Medline].
Dalager S, Falk E, Kristensen IB, Paaske WP. Plaque in superficial femoral arteries indicates generalized atherosclerosis and vulnerability to coronary death: an autopsy study. J Vasc Surg. Feb 2008;47(2):296-302. [Medline].
Kalbaugh CA, Taylor SM, Blackhurst DW, Dellinger MB, Trent EA, Youkey JR. One-year prospective quality-of-life outcomes in patients treated with angioplasty for symptomatic peripheral arterial disease. J Vasc Surg. Aug 2006;44(2):296-302; discussion 302-3. [Medline].
Gavrilenko AV, Skrylev SI. Long-term results of venous blood flow arterialization of the leg and foot in patients with critical lower limb ischemia. Angiol Sosud Khir. 2007;13(2):95-103. [Medline].
Ryer EJ, Trocciola SM, DeRubertis B, Lam R, Hynecek RL, Karwowski J. Analysis of outcomes following failed endovascular treatment of chronic limb ischemia. Ann Vasc Surg. Jul 2006;20(4):440-6. [Medline].
Brumberg RS, Back MR, Armstrong PA, Cuthbertson D, Shames ML, Johnson BL. The relative importance of graft surveillance and warfarin therapy in infrainguinal prosthetic bypass failure. J Vasc Surg. Dec 2007;46(6):1160-6. [Medline].
DeRubertis BG, Pierce M, Ryer EJ, Trocciola S, Kent KC, Faries PL. Reduced primary patency rate in diabetic patients after percutaneous intervention results from more frequent presentation with limb-threatening ischemia. J Vasc Surg. Jan 2008;47(1):101-8. [Medline].
Hertzer NR, Bena JF, Karafa MT. A personal experience with the influence of diabetes and other factors on the outcome of infrainguinal bypass grafts for occlusive disease. J Vasc Surg. Aug 2007;46(2):271-279. [Medline].
Das T. Optimal therapeutic approaches to femoropopliteal artery intervention. Catheter Cardiovasc Interv. Sep 2004;63(1):21-30. [Medline].
Rogers JH, Laird JR. Overview of new technologies for lower extremity revascularization. Circulation. Oct 30 2007;116(18):2072-85. [Medline].
Perry JT, Statler JD. Advances in vascular imaging. Surg Clin North Am. Oct 2007;87(5):975-93, vii. [Medline].
Bock M, Wacker FK. MR-guided intravascular interventions: techniques and applications. J Magn Reson Imaging. Feb 2008;27(2):326-38. [Medline].
Williams DM. Engineering improvements in endovascular devices: design and validation. Ann N Y Acad Sci. Nov 2006;1085:213-23. [Medline].
Jimenez JC, Lawrence PF. Minimally invasive distal limb bypasses. Techniques and results. J Cardiovasc Surg (Torino). Aug 2006;47(4):415-23. [Medline].
Lu XW, Idu MM, Ubbink DT, Legemate DA. Meta-analysis of the clinical effectiveness of venous arterialization for salvage of critically ischaemic limbs. Eur J Vasc Endovasc Surg. May 2006;31(5):493-9. [Medline].
Giangrande PH, Zhang J, Tanner A, Eckhart AD, Rempel RE, Andrechek ER. Distinct roles of E2F proteins in vascular smooth muscle cell proliferation and intimal hyperplasia. Proc Natl Acad Sci U S A. Aug 7 2007;104(32):12988-93. [Medline].
Conte MS, Bandyk DF, Clowes AW, Moneta GL, Seely L, Lorenz TJ. Results of PREVENT III: a multicenter, randomized trial of edifoligide for the prevention of vein graft failure in lower extremity bypass surgery. J Vasc Surg. Apr 2006;43(4):742-751; discussion 751. [Medline].
Hoel AW, Conte MS. Edifoligide: a transcription factor decoy to modulate smooth muscle cell proliferation in vein bypass. Cardiovasc Drug Rev. 2007;25(3):221-34. [Medline].
Soni AB, Illig KA, Sternbach Y, Anthony P, Jacob P, Reddy G. Benefits of external beam irradiation for peripheral arterial bypass: preliminary report on a phase I study. Int J Radiat Oncol Biol Phys. Nov 15 2002;54(4):1174-9. [Medline].
Further Reading
Keywords
infrainguinal occlusive disease, peripheral atherosclerotic disease, peripheral vascular disease, chronic arterial insufficiency, femoropopliteal occlusive disease, aortoiliac occlusive disease, stent, stenting, ischemic lower extremity disease, arteriosclerosis obliterans, complex regional pain syndromes, CRPS, posttraumatic pain syndromes, causalgia, mimocausalgia, Sudeck atrophy, reflex sympathetic dystrophy, intermittent claudication, gangrene, amputation
