Dr. Jonathan D. Marmur

Interventional Cardiology

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Primary Contacts

SUNY Downstate Medical Center
450 Clarkson Avenue
Room A2-523 (cardiac cath lab)
Brooklyn, NY 11203-2098
Cell: 917-885-8854 more contact information

Intermittent Claudication
Management of Lower Extremity Peripheral Vascular Disease

Adapted from: Christopher White, MD, NEJM 2007;356:1241-1250.

Peripheral arterial disease is a common manifestation of atherosclerosis, and its prevalence increases with age and the presence of cardiovascular risk factors. 1 , 2 Cigarette smoking and diabetes mellitus are the strongest risk factors; more than 80% of patients with peripheral arterial disease are current or former smokers. Hypertension, dyslipidemia, and hyperhomocysteinemia also significantly increase the risk of peripheral arterial disease.

Most persons with this disease are asymptomatic, and the condition is detected during routine physical examination of abnormal pulses, vascular bruits, or an abnormal value for the ankle–brachial index. 3 , 4 Less than 20% of patients with peripheral arterial disease report the typical symptom of intermittent claudication — leg-muscle discomfort on exertion that is relieved with rest. 5 Many patients present with atypical symptoms, including leg fatigue, difficulty walking, and leg pain that is not typical of claudication.

Studies of the natural history of intermittent claudication indicate that the risk of limb loss for patients who do not have diabetes is low (2% or less). 6 However, the risk of progression to limb-threatening ischemia is increased by a factor of three among patients with diabetes who require oral or insulin therapy as compared with patients without diabetes, and the risk increases by 20 to 25% for each 0.1-unit decrease in the ankle–brachial index. 7 , 8

Cardiovascular disease is the major cause of death in patients with intermittent claudication; the annual rate of cardiovascular events (myocardial infarction, stroke, or death from cardiovascular causes) is 5 to 7%. 9 Thus, the treatment of claudication is directed not only at improving walking distance but also, and more important, at reducing cardiovascular risk.

Strategies and Evidence

A careful history taking and examination will generally distinguish intermittent claudication from nonvascular causes that may mimic claudication (pseudoclaudication) ( Table 1 ). 9 , 10 The patient's lower legs and feet should be examined with shoes and socks off, with attention to pulses, hair loss, skin color, and trophic skin changes.

Intermittent Claudication
Calculation of the ankle–brachial index ( Figure 1 ) is recommended as the initial screening test. An abnormal result (0.9 or less) is sufficient to make the diagnosis of peripheral arterial disease in a clinically appropriate setting. When the disease is suspected on the basis of clinical observations but the resting ankle–brachial index is normal, the index should also be calculated after exercise — after the patient has performed toe raises (standing flat-footed and raising the heels off the ground repeatedly) or has walked on a treadmill. Patients with large-vessel "inflow" disease of the distal aorta or iliac arteries may have normal resting blood flow, but in the setting of exercise and associated vasodilatation, pressure gradients develop across the proximal stenoses, leading to symptoms and an abnormally low value for the ankle–brachial index.
To calculate the ankle–brachial index, systolic pressures are determined in both arms and both ankles with the use of a hand-held Doppler instrument. The highest readings for the dorsalis pedis and posterior tibial arteries are used to calculate the index.
Intermittent Claudication

If the diagnosis of peripheral arterial disease is uncertain, or if revascularization is being planned, further imaging with duplex ultrasound, computed tomographic angiography (CTA), or magnetic resonance angiography (MRA) may be useful. Segmental pressure recording and pulse-volume recording are used in some cases to assess the location and severity of the lesion. In patients with noncompressible vessels (usually patients with diabetes or renal failure), the diagnosis can be confirmed by measuring the toe–brachial index (determined according to the return of pulsatile flow on deflation of a small blood-pressure cuff on the great or second toe with a plethysmographic device).

Both CTA and MRA produce images of vascular structures in cross-sectional slices that can be reformatted into three-dimensional angiographic images ( Figure 2 ). In a randomized trial comparing MRA with CTA for initial imaging in peripheral arterial disease, the two techniques were similar in ease of use and clinical outcome, but total diagnostic costs were lower for CTA. 11

The digital-subtraction angiogram in Panel A shows occlusion of the right external iliac artery (arrow), bilateral narrowing of the superficial femoral arteries , and single-vessel runoff below the knees. The CTA in Panel B is a three-dimensional reconstruction showing very mild narrowing of the bilateral superficial femoral arteries (double-headed arrow). The MRA in Panel C, with enhancement from contrast material, shows bilateral occlusions of the superficial femoral arteries with a patent femoral–popliteal graft (arrow) on the right.


Intermittent Claudication  
The gold standard for diagnosis and evaluation of peripheral arterial disease is invasive digital-subtraction angiography, which is used if endovascular intervention is planned ( Figure 3 ). Serious complications of this procedure, which are infrequent, include reactions to the contrast material (in 4% of patients or less), bleeding (2% or less), nephropathy due to contrast material (0.2 to 1.4%), and cholesterol embolization (0.1% or less). 12 , 13
The CTA in Panel A shows discrete stenosis of the right superficial femoral artery (arrow). The corresponding digital-subtraction angiogram in Panel B shows stenosis of 99% of the artery (arrow). Endovascular intervention to treat such a stenosis has a high likelihood of success with a low procedural risk. Panel C shows the result of treatment with percutaneous transluminal angioplasty (arrow).
Intermittent Claudication



The advantages and disadvantages of digital-subtraction angiography, CTA, MRA, and duplex ultrasound are listed in Table 2 .


Intermittent Claudication

The mainstays of treatment for peripheral arterial disease include risk-factor modification, an exercise program, antiplatelet therapy, and, if warranted for symptomatic relief, additional pharmacologic therapy, and revascularization. Revascularization (endovascular or surgical) therapy is reserved for patients whose job performance or lifestyle is compromised by claudication, patients who do not have a response to exercise and pharmacotherapy, and patients for whom the risk–benefit ratio with revascularization is favorable. 9


Risk-Factor Modification


Since cardiovascular events are the major cause of death in patients with peripheral arterial disease, modification of atherosclerotic risk factors is routinely warranted, with a particular emphasis on smoking cessation and regular exercise. Pharmacologic therapy and dietary modification should be tailored to meet current guidelines for risk factors: low-density lipoprotein cholesterol, less than 100 mg per deciliter (2.6 mmol per liter) or, for those at very high risk for ischemic events, less than 70 mg per deciliter (1.8 mmol per liter); blood pressure, less than 140 mm Hg systolic and 90 mm Hg diastolic or, for patients with diabetes or renal disease, less than 130 mm Hg systolic and 80 mm Hg diastolic; and glycated hemoglobin, less than 7% in patients with diabetes. 14 , 15

Beta-blockers are effective as antihypertensive therapy and are not contraindicated in patients with peripheral arterial disease. In the Heart Outcomes Prevention Evaluation study, the risk of heart attack, stroke, and death from vascular causes was reduced by 22% for patients given an angiotensin-converting–enzyme inhibitor (ramipril).16


Antiplatelet and Other Pharmacologic Therapy


Antiplatelet therapy with aspirin (75 mg to 325 mg daily) reduces the risk of death from vascular causes, myocardial infarction, and stroke in patients with vascular diseases by 25% and is recommended for patients with peripheral arterial disease. 17 A large, randomized, 3-year trial involving high-risk patients, including patients with peripheral vascular disease, showed that rates of death from vascular causes, myocardial infarction, and stroke were significantly, albeit modestly, lower with clopidogrel than with aspirin; the rates of bleeding complications were similar. 18 Thus, the more expensive thienopyridines (ticlopidine and clopidogrel) may be considered as alternatives to aspirin, particularly in patients who cannot tolerate aspirin. Current data do not show an advantage of dual antiplatelet therapy (aspirin and clopidogrel) over single-agent therapy in patients with peripheral arterial disease.9

Cilostazol is a phosphodiesterase type 3 inhibitor with vasodilator and mild antiplatelet properties. Several randomized trials have shown that walking distance is increased by about 50% with cilostazol (100 mg twice a day), as compared with placebo, after 3 to 6 months of therapy. 19 The most common side effects include headache, diarrhea, palpitations, and dizziness. Cilostazol is contraindicated in patients with heart failure, because similar drugs, such as milrinone, are associated with increased mortality in this group. In a trial comparing cilostazol, pentoxifylline (a derivative of methylxanthine), and placebo, pentoxifylline was inferior to cilostazol and no better than placebo for relief from claudication. 20 Oral vasodilator prostaglandins, vitamin E, and chelation therapy with EDTA have not proved to be effective in reducing symptoms or increasing walking distance. 9 Table 3 summarizes the pharmacologic treatments for peripheral arterial disease and indicates the nature of the evidence supporting their use.

Antiplatelet and Other Pharmacologic Therapy



A Cochrane review of three randomized trials showed that exercise increased maximal walking distance by 150% over a period of 3 to 12 months, as compared with usual care. 21 A meta-analysis of eight randomized trials showed a greater symptomatic benefit with a supervised (as opposed to unsupervised) exercise program. 22 Supervised exercise commonly involves walking on a treadmill, with the initial workload set to elicit symptoms within 3 to 5 minutes of walking. The patient is permitted to rest until the symptoms resolve and then resumes exercise. In a meta-analysis of 18 randomized and nonrandomized trials, the greatest benefit (assessed according to the distance walked before claudication developed) was associated with continued walking until pain was nearly maximal and with sessions that lasted longer than 30 minutes, took place three or more times per week, and continued for more than 6 months. 23 Typically, it takes 1 to 2 months for the patient to begin to notice benefits, which gradually increase over a period of several months.




Superficial femoral-artery stenosis or occlusion is the most common lesion associated with claudication. Revascularization (surgery or percutaneous transluminal angioplasty [PTA]) is indicated for relief in patients with claudication that limits their lifestyle or ability to perform their job and that has proved to be unresponsive to exercise and pharmacologic therapy. 9 , 24 , 25 PTA is preferred when possible in patients who are 50 years of age or younger, because they have a higher risk of graft failure after surgical therapy than do older patients. 9 Data from two randomized trials indicate that surgery and angioplasty result in similar mortality and amputation rates and in similar patency rates at 4 years among patients with ischemia of the legs or feet. 26 However, because PTA is associated with lower estimated rates of both short-term mortality and major complications (0 to 2.9% and 2 to 10%, respectively) than is surgery (1.3 to 6.3% and 10 to 15%, respectively), PTA is preferred for lesions with favorable anatomical features, such as discrete stenoses or occlusions (those less than 15 cm long) ( Table 4 ). Cost-effectiveness analyses suggest that PTA is preferable to surgery as long as the expected 5-year patency rate for the treated vessel is 30% or higher. 28 Outcomes after femoral popliteal PTA have improved over time; patency rates of 87%, 69%, and 55% have been reported at 1, 3, and 5 years, respectively. 26


A single randomized trial comparing the effectiveness of surgery and exercise therapy showed no significant difference in outcomes — specifically, maximal walking distance and the need for further revascularization — at 8 to 9 months. 28 A large prospective, matched cohort study of 526 patients with intermittent claudication showed that revascularization (surgery or PTA) was associated with improved walking distance and reduced pain as compared with medical therapy, but therapy was not optimized in the nonintervention group (e.g., only 40% of the patients in this group reported engaging in regular exercise, and cilostazol was not used).a href="http://content.nejm.org/cgi/content/full/356/12/1241#R29%23R29" class="link_2">29 < Outcomes of revascularization were better in patients with higher postprocedure ankle–brachial indexes, suggesting that the effectiveness of the limb revascularization procedure is directly related to the degree of symptomatic improvement.

Data from studies directly comparing exercise therapy and PTA are scarce. In one small trial, walking distance at 6 years was better for patients treated with exercise therapy than for those treated with PTA. 30 A randomized trial comparing the effects of exercise and PTA (with both groups receiving pharmacologic therapy) demonstrated similar quality-of-life outcomes, similar maximal walking distances, and similar ankle–brachial indexes, but fewer patients in the PTA group had

occluded arteries (P=0.004). 31 An analysis of combined data from seven studies that compared exercise with PTA in patients with claudication showed that PTA resulted in a greater increase in the ankle–brachial index but with no significant difference in quality of life. 32 However, none of the studies included in the analysis compared the two interventions directly. A decision-analysis model comparing the costs and quality of life associated with PTA, bypass surgery, and exercise therapy showed that PTA, when feasible, was more effective than exercise therapy alone and was more cost-effective than bypass surgery ($38,000 vs. $311,000 per quality-adjusted year of life gained), 33 but this conclusion, too, was not based on data from comparative clinical trials.


Areas of Uncertainty



The role of primary stent placement in revascularization of the superficial femoral artery remains controversial. In contrast to the coronary arteries, for which stent placement has largely replaced angioplasty for revascularization, the superficial femoral artery is subject to longitudinal stretching, external compression, torsion, and flexion; these stresses may lead to stent fractures, which have been linked to restenosis. 34 In early randomized trials comparing PTA with stent placement for the treatment of lesions in the superficial femoral artery, stent placement showed no advantage over angioplasty with bail-out stent placement. 35 , 36

Technology has improved, however, and a recent randomized trial involving 104 patients with severe claudication showed significantly higher patency rates at 1 year for lesions in the superficial femoral artery that were treated with stent placement than for lesions treated with PTA and bail-out stent placement (63% vs. 37%); the maximal walking distance and the ankle–brachial index were also significantly better in the stent group at 1 year. There were no major complications in either group. 37

A randomized trial of drug-coated (sirolimus) stents in the superficial femoral artery failed to show a reduction in the risk of restenosis as compared with the risk associated with bare-metal stents. 38 Use of stents covered with polytetrafluoroethylene (PTFE), developed to seal arterial perforations or to exclude aneurysmal segments, was compared with the use of PTA alone in a randomized trial, and there was no significant difference in 1-year patency rates (50% and 45%, respectively); however, major adverse events were more frequent in the group that received PTFE-covered stents (8.2% vs. 4.0%). 39


Adjunctive Angioplasty


Adjunctive angioplasty techniques such as atherectomy, cryotherapy, and the use of a cutting balloon (a balloon with microtomes attached to its surface, which make shallow incisions in the surface of the lesion when the balloon is inflated) have not been tested in meaningful comparative trials in patients with femoral artery disease; the only available data that show the benefit of these approaches is from single-center studies and uncontrolled registries. 40 , 41 , 42 Laser angioplasty has not been shown to be superior to conventional PTA or stent placement. 43 , 44 , 45 Given the substantial additional expense of these approaches, more evidence of their efficacy is needed before widespread adoption can be justified.

Trials of brachytherapy (use of a catheter to deliver radiation to the lesion) for preventing restenosis in the superficial femoral artery after percutaneous PTA have had inconsistent results. 46 , 47 In one trial, the use of external-beam radiation (at a dose of 14 Gy) after PTA significantly reduced the rate of restenosis at 1 year after PTA, 48 but these results require confirmation. The use of gene or cellular therapies in peripheral arterial disease has not resulted in a clear clinical benefit in small studies 49 ; larger, controlled clinical trials are needed to establish whether there is any role for these therapies in patients with claudication.


Follow-up after Percutaneous Interventions


It is common to measure the ankle–brachial index within a week after a percutaneous intervention has been performed in order to establish a new baseline. Patients are often reevaluated at 3-month intervals for the first year (when the risk of restenosis is highest); these assessments include a detailed history taking, examination, and ankle–brachial index measurements; the value of a walking program and risk-factor modification should be reinforced during these visits. However, data on the optimal approach to follow-up are lacking.




Comprehensive guidelines for the management of peripheral arterial disease have recently been published by an expert multidisciplinary committee organized by the American College of Cardiology (ACC) and the American Heart Association (AHA). 9 The TransAtlantic Inter-Society Consensus, representing multiple international specialty societies, has also published guidelines for the management of peripheral arterial disease that are in general agreement with the ACC–AHA document ( Table 4 ). 27

The ACC–AHA guidelines recommend endovascular therapy for patients whose condition interferes with their job performance or lifestyle and who have had an inadequate response to exercise or pharmacologic therapy, as long as the clinical features suggest a reasonable likelihood of symptomatic improvement and the risk–benefit ratio is very high. 9 The recommendations in this article are in agreement with the ACC–AHA guidelines.



  1. Selvin E, Erlinger TP. Prevalence of and risk factors for peripheral arterial disease in the United States: results from the National Health and Nutrition Examination Survey, 1999-2000. Circulation 2004;110:738-743. 
  2. Pasternak RC, Criqui MH, Benjamin EJ, et al. Atherosclerotic Vascular Disease Conference: Writing Group I: epidemiology. Circulation 2004;109:2605-2612. 
  3. Hiatt WR. Medical treatment of peripheral arterial disease and claudication. N Engl J Med 2001;344:1608-1621. 
  4. McDermott MM, Kerwin DR, Liu K, et al. Prevalence and significance of unrecognized lower extremity peripheral arterial disease in general medicine practice. J Gen Intern Med 2001;16:384-390. 
  5. McDermott MM, Liu K, Greenland P, et al. Functional decline in peripheral arterial disease: associations with the ankle brachial index and leg symptoms. JAMA 2004;292:453-461. 
  6. Kannel WB, Skinner JJ Jr, Schwartz MJ, Shurtleff D. Intermittent claudication: incidence in the Framingham Study. Circulation 1970;41:875-883. 
  7. Muluk SC , Muluk VS, Kelley ME, et al. Outcome events in patients with claudication: a 15-year study in 2777 patients. J Vasc Surg 2001;33:251-257. 
  8. Aquino R, Johnnides C, Makaroun M, et al. Natural history of claudication: long-term serial follow-up study of 1244 claudicants. J Vasc Surg 2001;34:962-970. 
  9. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary 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. J Am Coll Cardiol 2006;47:1239-1312. 
  10. Schmieder FA, Comerota AJ. Intermittent claudication: magnitude of the problem, patient evaluation, and therapeutic strategies. Am J Cardiol 2001;87:3D-13D. 
  11. Ouwendijk R, de Vries M, Pattynama PM, et al. Imaging peripheral arterial disease: a randomized controlled trial comparing contrast-enhanced MR angiography and multi-detector row CT angiography. Radiology 2005;236:1094-1103. 
  12. Gradinscak DJ, Young N, Jones Y, O'Neil D, Sindhusake D. Risks of outpatient angiography and interventional procedures: a prospective study. AJR Am J Roentgenol 2004;183:377-381. 
  13. Singh H, Cardella JF, Cole PE, et al. Quality improvement guidelines for diagnostic arteriography. J Vasc Interv Radiol 2002;13:1-6. 
  14. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003;289:2560-2572. [Erratum, JAMA 2003;290:197.] 
  15. Hankey GJ, Norman PE, Eikelboom JW. Medical treatment of peripheral arterial disease. JAMA 2006;295:547-553. 
  16. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med 2000;342:145-153. [Erratum, N Engl J Med 2000;342:748, 1376.] 
  17. Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324:71-86. [Erratum, BMJ 2002;324:141.] 
  18. CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet 1996;348:1329-1339. 
  19. Strandness DE Jr, Dalman RL, Panian S, et al. Effect of cilostazol in patients with intermittent claudication: a randomized, double-blind, placebo-controlled study. Vasc Endovascular Surg 2002;36:83-91. 
  20. Dawson DL, Cutler BS, Hiatt WR, et al. A comparison of cilostazol and pentoxifylline for treating intermittent claudication. Am J Med 2000;109:523-530. 
  21. Leng GC, Fowler B, Ernst E. Exercise for intermittent claudication. Cochrane Database Syst Rev 2000;2:CD000990-CD000990. 
  22. Bendermacher BL, Willigendael EM, Teijink JA, Prins MH. Supervised exercise therapy versus non-supervised exercise therapy for intermittent claudication. Cochrane Database Syst Rev 2006;2:CD005263-CD005263. 
  23. Gardner AW, Poehlman ET. Exercise rehabilitation programs for the treatment of claudication pain: a meta-analysis. JAMA 1995;274:975-980.
  24. Holm J, Arfvidsson B, Jivegard L, et al. Chronic lower limb ischaemia: a prospective randomised controlled study comparing the 1-year results of vascular surgery and percutaneous transluminal angioplasty (PTA). Eur J Vasc Surg 1991;5:517-522. 
  25. Wilson SE, Wolf GL, Cross AP. Percutaneous transluminal angioplasty versus operation for peripheral arteriosclerosis: report of a prospective randomized trial in a selected group of patients. J Vasc Surg 1989;9:1-9. 
  26. Clark TW, Groffsky JL, Soulen MC. Predictors of long-term patency after femoropopliteal angioplasty: results from the STAR registry. J Vasc Interv Radiol 2001;12:923-933. 
  27. Norgren L, Hiatt WR, Dormandy JA, Nehler MR, Harris KA, Fowkes FGR. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). Eur J Vasc Endovasc Surg 2007;33:Suppl:S1-S75. 
  28. Lundgren F, Dahllof AG, Lundholm K, Schersten T, Volkmann R. Intermittent claudication -- surgical reconstruction or physical training? A prospective randomized trial of treatment efficiency. Ann Surg 1989;209:346-355. 
  29. Feinglass J, McCarthy WJ, Slavensky R, Manheim LM, Martin GJ. Functional status and walking ability after lower extremity bypass grafting or angioplasty for intermittent claudication: results from a prospective outcomes study. J Vasc Surg 2000;31:93-103. 
  30. Perkins JM, Collin J, Creasy TS, Fletcher EW, Morris PJ. Exercise training versus angioplasty for stable claudication: long and medium term results of a prospective, randomised trial. Eur J Vasc Endovasc Surg 1996;11:409-413. 
  31. Whyman MR, Fowkes FG, Kerracher EM, et al. Is intermittent claudication improved by percutaneous transluminal angioplasty? A randomized controlled trial. J Vasc Surg 1997;26:551-557. 
  32. Spronk S, Bosch JL, Veen HF, den Hoed PT, Hunink MG. Intermittent claudication: functional capacity and quality of life after exercise training or percutaneous transluminal angioplasty -- systematic review. Radiology 2005;235:833-842. 
  33. de Vries SO, Visser K, de Vries JA, Wong JB, Donaldson MC, Hunink MG. Intermittent claudication: cost-effectiveness of revascularization versus exercise therapy. Radiology 2002;222:25-36. 
  34. Scheinert D, Scheinert S, Sax J, et al. Prevalence and clinical impact of stent fractures after femoropopliteal stenting. J Am Coll Cardiol 2005;45:312-315. 
  35. Vroegindeweij D, Vos LD, Tielbeek AV, Buth J, Bosch HC. Balloon angioplasty combined with primary stenting versus balloon angioplasty alone in femoropopliteal obstructions: a comparative randomized study. Cardiovasc Intervent Radiol 1997;20:420-425. 
  36. Muradin GS, Bosch JL, Stijnen T, Hunink MG. Balloon dilation and stent implantation for treatment of femoropopliteal arterial disease: meta-analysis. Radiology 2001;221:137-145. 
  37. Schillinger M, Sabeti S, Loewe C, et al. Balloon angioplasty versus implantation of nitinol stents in the superficial femoral artery. N Engl J Med 2006;354:1879-1888. 
  38. Duda SH, Bosiers M, Lammer J, et al. Sirolimus-eluting versus bare nitinol stent for obstructive superficial femoral artery disease: the SIROCCO II trial. J Vasc Interv Radiol 2005;16:331-338. 
  39. Food and Drug Adminstration, Center for Devices and Radiological Health. Gore Viabahn endoprosthesis: summary of safety and effectiveness. PMA application no. P040037.
  40. Suri R, Wholey MH, Postoak D, Hagino RT, Toursarkissian B. Distal embolic protection during femoropopliteal atherectomy. Catheter Cardiovasc Interv 2006;67:417-422. 
  41. 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 2004;15:1391-1397. 
  42. Laird JR, Biamino G, McNamara T, et al. Cryoplasty for the treatment of femoropopliteal arterial disease: extended follow-up results. J Endovasc Ther 2006;13:Suppl 2:II-52.
  43. Visona A, Perissinotto C, Lusiani L, et al. Percutaneous excimer laser angioplasty of lower limb vessels: results of a prospective 24-month follow-up. Angiology 1998;49:91-98. 
  44. Scheinert D, Laird JR Jr, Schroder M, Steinkamp H, Balzer JO, Biamino G. Excimer laser-assisted recanalization of long, chronic superficial femoral artery occlusions. J Endovasc Ther 2001;8:156-166. 
  45. Wissgott C, Scheinert D, Rademaker J, Werk M, Schedel H, Steinkamp HJ. Treatment of long superficial femoral artery occlusions with excimer laser angioplasty: long-term results after 48 months. Acta Radiol 2004;45:23-29. 
  46. Diehm N, Silvestro A, Do DD, et al. Endovascular brachytherapy after femoropopliteal balloon angioplasty fails to show robust clinical benefit over time. J Endovasc Ther 2005;12:723-30.
  47. Wolfram RM, Budinsky AC, Pokrajac B, Potter R, Minar E. Endovascular brachytherapy: restenosis in de novo versus recurrent lesions of femoropopliteal artery -- the Vienna experience. Radiology 2005;236:338-342. [Erratum, Radiology 2006;239:613.] 
  48. Therasse E, Donath D, Lesperance J, et al. External beam radiation to prevent restenosis after superficial femoral artery balloon angioplasty. Circulation 2005;111:3310-3315. 
  49. Lederman RJ, Mendelsohn FO, Anderson RD, et al. Therapeutic angiogenesis with recombinant fibroblast growth factor-2 for intermittent claudication (the TRAFFIC study): a randomised trial. Lancet 2002;359:2053-2058. 
Copyright 2006 © Dr. Jonathan D. Marmur. All rights reserved.