Cardiology Intensive Board Review, 3 ed.

Peripheral Vascular Disease

Douglas E. Joseph • Hemantha K. Koduri

ANSWERS

1.b. Chronic venous insufficiency. This patient has no history of neuropathy and has intact sensation, making a neurotrophic ulcer often associated with diabetes unlikely. While his glucose is elevated, inadequate information is provided to make the diagnosis of diabetes mellitus. Bilateral leg edema, hyperpigmentation of the ankles, and the location of the ulcer over the medial malleolus (“gaiter distribution”) are findings consistent with a venous stasis wound. Ulcers secondary to arterial disease are usually painful, involve the toes, and are well circumscribed. The information provided suggests adequate arterial supply. Wounds associated with calciphylaxis may be anywhere. They are usually very painful, involve large areas of skin, and are associated with black eschar formation. These wounds are most often seen in patients with renal impairment and hyperparathyroidism, neither of which is true in this case. Nothing in the clinical vignette is suggestive of a brown recluse spider bite.11

2.c. Admit to the hospital for an urgent diagnostic abdominal aortogram with runoff and potential endovascular revascularization. The patient described is suffering from acute critical limb ischemia. The hallmarks of acute limb ischemia are the five “P’s”, which are suggestive of impending tissue necrosis. They are pain, paralysis, paresthesia, pulseless, and pallor and some add poikilothermia (coldness) for a sixth “P.” Our patient exhibits all but paralysis. Based on the Society for Vascular Surgery/International Society for Cardiovascular Surgery classification scheme for clinical categories of acute limb ischemia, her limb is marginally to intermediately threatened. Acute limb ischemia requires prompt diagnosis and intervention to avoid limb loss and life-threatening systemic illness resulting from tissue gangrene.12

3.a. Regular visits with assessment for interval change in symptoms, vascular examination, and ABI measurement beginning in the immediate post-procedure period and at intervals for at least 2 years. Unlike follow-up of autologous vein bypass grafts, well-established evidence-based guidelines for surveillance of post-endovascular revascularization patients do not exist. However, it is considered standard of care to evaluate these patients with interval history, examination, and measurement of the ABI regularly for at least 2 years after their percutaneous revascularization procedure.13

4.e. Warm compresses and nonsteroidal anti-inflammatory drugs for pain. Empiric anticoagulation, including outpatient anticoagulation, for superficial vein thrombosis is not routinely recommended. The clinical scenario may represent HIT and she should have a follow-up platelet count in 2 days. Her prior platelet counts from her recent hospitalization should be evaluated for a drop in platelets of ≥50% from baseline.15

5.e. An aPTT prolongation of 1.5 to 2.0 times the baseline value. Although the recommended range for therapeutic anticoagulation for VTE with a DTI is 1.5 to 2.5 times the baseline, which is not given as an option, published data indicate that anticoagulation with a DTI target aPTT of 1.5 to 2.0 times the baseline is just as efficacious and is associated with less bleeding risk.16

6.c. Normal physiologic cold response. This patient is exhibiting a normal response to prolonged exposure to cold. The diagnosis of Raynaud phenomenon is clinical and includes the presence of pallor or acrocyanosis and pain with cold exposure. Redness of the hands with warming after prolonged cold exposure, without concomitant pain, may be a normal response in a healthy young individual. He should be counseled to wear gloves and report any change in his symptoms, as his family history does predispose him to development of Raynaud phenomenon.17

7.e. Order antinuclear antibodies, erythrocyte sedimentation rate, and perform nailfold capillaroscopy. If all these tests are normal, it is very unlikely that this patient has secondary Raynaud phenomenon and no further testing is necessary.18

8.e. As needed. Although the patient does not have Raynaud phenomenon, he should be encouraged to follow up as needed because of his family history. Patients who have primary Raynaud phenomenon should have clinical follow-up for a minimum of 2 years after diagnosis.17

9.d. Pulmonary arteriogram. An arteriogram is the test most likely to confirm pulmonary artery hypertension in this patient presenting with cor pulmonale, although a right heart catheterization is usually done first. This patient most likely has chronic thromboembolic pulmonary hypertension (CTEPH), a condition seen in otherwise healthy postsplenectomy patients. Other predisposing conditions include history of pulmonary embolism, myeloproliferative disorders, and chronic inflammatory conditions.19

10.c. IV epoprostenol is an effective therapy in patients with advanced disease. Patients with CTEPH may be bridged to pulmonary endarterectomy with IV epoprostenol. The other answers are incorrect. Anticoagulation with a vitamin K antagonist is indicated; however, the INR target of 2.0 to 3.0 is recommended. The Aerosolized Iloprost Randomization (AIR) study did not demonstrate improved exercise capacity with inhaled iloprost. Bosentan does improve exercise capacity and decreases pulmonary vascular resistance, but is not advocated for use in patients with moderate-to-severe hepatic dysfunction.19

11.e. Begin a weight-based unfractionated heparin infusion. Although LMWH may be appropriate as the initial anticoagulant of choice for the treatment of an acute DVT in the ambulatory as well as hospitalized patient, it does not require a bolus. In the setting of the postoperative state where rapid reversal of anticoagulation may be required, unfractionated heparin is favored. An inferior vena cava filter would be an appropriate recommendation if anticoagulation could not be administered at therapeutic levels. Thrombolytic therapy is contraindicated in the setting of recent open heart surgery. Use of a DTI is not indicated for routine anticoagulation.22

12.e. Administration of IV unfractionated heparin intraoperatively with subsequent daily monitoring of platelet counts. The nature of immune response to heparin is anamnestic; this means a second exposure in the absence of positive antibodies is not associated with the development of a clinical hyperacute immune response. Perioperatively, heparin products should be avoided in patients with a history of HIT even with undetectable antiplatelet antibodies prior to cardiac surgery or vascular surgery. Nevertheless, heparin is favored over DTIs in cardiac and vascular surgery because of its reversibility and relative ease of use. Acute HIT is unlikely to occur even in patients who have a remote history of HIT as long as there has been no heparin exposure within the previous 100 days. This recommendation is based on expert opinion (level 1C) and not on randomized controlled trials.15

13.b. Given the clinical circumstances the laboratory finding is of doubtful clinical significance and you advise she should be anticoagulated with a vitamin K antagonist for 3 months with a target INR of 2.0 to 3.0. While the site of thrombosis is somewhat out of the ordinary, it was in the setting of abdominal surgery and was her first episode; therefore, a routine course of 3 months of anticoagulation with a vitamin K antagonist and an INR target of 2.0 to 3.0 is appropriate. All first-episode venous thrombotic events are not treated the same. Patients with malignancy-related thrombosis, idiopathic events, and those with certain thrombophilic conditions such as the antiphospholipid antibody syndrome require a longer duration of therapy relative to patients with transient risk factors for VTE. The MTHFR genetic mutation in the absence of hyperhomocysteinemia is not associated with increased risk of recurrence after discontinuation of anticoagulant therapy and has not been shown to increase thrombogenicity requiring a higher than usual INR target.23

14.d. Fatal pulmonary embolism is a leading cause of maternal mortality in the Western world. Thromboembolism is clearly the leading direct cause of maternal mortality according to the Seventh Report of the Confidential Enquiries into Maternal Deaths in the United Kingdom. The May-Thurner syndrome involves compression of the left iliac vein by the right iliac artery. The greatest teratogenicity of warfarin is seen during weeks 6 through 12. Use of LMWH in pregnant women who have prosthetic heart valves is highly controversial and certainly not the standard of care.24

15.b. Erythromelalgia. The name of this condition is based on three Greek words: erythro meaning red, melos meaning extremity, and algos meaning pain. It is uncommon, affecting about 1 in 40,000. It may be primary or secondary. Primary erythromelalgia is usually bilateral, not associated with gangrene, and patients have normal pulses. Secondary erythromelalgia is often unilateral, can be associated with gangrene, and patients have variable pulses. Secondary erythromelalgia can be associated with medications including bromocriptine, nifedipine, nicardipine, and verapamil. It may also herald the onset of a myeloproliferative disease such as polycythemia vera or essential thrombocythemia.24

16.d. Complete blood count with differential (CBC with diff). Patients with this condition should have a CBC with diff checked periodically for at least 2 to 3 years. It is important for treating physicians to recognize that erythromelalgia can precede the laboratory manifestations of a myeloproliferative disorder by up to 2 to 3 years.28

17.b. Gunther Tulip retrievable vena cava filter. This patient is young and his deep vein thrombosis is situational. He is expected to recover fully with no sequelae; thus he does not require placement of a permanent inferior vena cava filter. Proximal iliac thrombus in the setting of a hospitalized trauma patient following multiple abdominal surgeries is a very high-risk scenario for development of serious, life-threatening VTE. Anticoagulation is the treatment of choice when it can be safely administered; however, when contraindicated an inferior vena cava filter should be placed without delay. Patients with a temporary contraindication for anticoagulants should be reassessed at short intervals and, if circumstances permit, anticoagulants should be instituted for treatment of their VTE and to prevent recurrence. Of the filter types listed, only the Gunther Tulip is approved in the United States for retrieval. The OptEase is also approved for retrieval. The Bird’s Nest filter is the only filter available for use in patients with a so-called megacava (vena cava greater than 28 mm). The Bird’s Nest filter can be placed into an inferior vena cava of up to 42 mm in diameter. The TrapEase, Greenfield, and Simon Nitinol filters were not designed to have the option of retrieval.25

18.d. Surgical evacuation of the hematoma and suture repair of the artery. The patient complains of developing numbness in the setting of developing a large hematoma and pseudoaneurysm. To relieve the compressive effect of the hematoma, prevent irreversible injury, and relieve pain, the most appropriate method of repair in this patient is to evacuate the hematoma. Most small to moderately sized pseudoaneurysms can be treated with either ultrasound-guided compression, thrombin injection, or when very small may be observed for spontaneous resolution. Placement of a femoral compression device (Fem-Stop) is not appropriate in this setting, and bandages should not be wrapped proximally around the thigh as this will cause worsening swelling and pain.26

19.c. Follow up with serial duplex ultrasound scans. The peroneal vein is a calf vein with less propensity for clinically significant sequelae. Anticoagulant therapy for calf vein DVT is controversial. However, in this setting there is a clear contraindication to anticoagulate. Even prophylactic doses of anticoagulants are not advisable in patients with hemorrhagic pericardial effusions status post open heart surgery. Serial ultrasound scans have been studied as an alternative to anticoagulant therapy. If no propagation after several weeks, no anticoagulant therapy is necessary. If propagation occurs, then anticoagulation versus placement of an inferior vena cava should be considered.27

20.b. Thromboangiitis obliterans (TAO, Buerger disease). TAO classically manifests in young, male patients with a recent history of heavy tobacco use. The clinical presentation is consistent with ischemia, beginning distally and involving the small- and medium-sized arteries. Usually the lower extremities are involved, with ischemia or claudication of the feet or legs. Foot or arch claudication is typical. Occasionally, the hands are involved. If the disease progresses with continued exposure to tobacco, patients are at significant risk for progressive ischemia, ulceration, gangrene, and eventually amputation. Antiphospholipid antibody syndrome is certainly possible, but it is not a hereditary condition and most often manifests with venous thrombosis. Takayasu arteritis does not usually present in this way. Nothing is suggestive of atrophie blanche, and premature atherosclerosis presenting in a 25-year-old man with claudication and ischemia would be highly unusual.28

21.b. Cessation of exposure to all forms of tobacco. The strong link between tobacco abuse and TAO is well recognized. There have been suggestions that some patients may demonstrate an abnormal sensitivity to a component of tobacco, which leads to small vessel occlusive disease. It has been shown that patients with TAO have higher tobacco consumption as well as higher carboxyhemoglobin levels than do patients with atherosclerosis.28

22.c. May-Thurner syndrome. Also known as iliac vein compression syndrome, Cockett syndrome, or iliocaval compression syndrome, May-Thurner syndrome is caused by compression of the left common iliac vein by the right common iliac artery and the underlying vertebral body. A history of chronic left lower extremity edema with or without the presence of DVT is suggestive of May-Thurner syndrome, especially in a female population. This phenomenon causes a partial obstruction caused by physical entrapment of the vein under the artery as well as by repetitive pulsatile force resulting in intimal hyperplasia of the vein. It has been estimated that this condition occurs in 2% to 5% of patients who are evaluated for lower extremity venous problems.29

23.c. Venography for thrombus removal and stent placement. May-Thurner syndrome is an anatomical anomaly that results in repeated venous trauma and often subsequent thrombus formation. Removal of thrombus followed by angioplasty, if needed, and placement of a stent is a potentially definitive treatment that could avoid the need for indefinite anticoagulant therapy in the young woman presented in this case.29

24.c. Compression stockings. The importance of edema control is often underestimated for wound healing. This patient has deep system venous reflux. He has no signs of infection complicating the healing of his incision, so antibiotics are unlikely to be helpful. Topical steroids offer no benefit in this case. His ABIs suggest adequate arterial inflow for wound healing. Whirlpool therapy is helpful in select cases, most often when multiple small wounds are present, which need cleansing and gentle debridement. Although the size of the wound is not clearly stated, these wounds are most often small and referral for skin grafting is not indicated.30

25.b. CT venogram of the abdomen and pelvis. Monophasic (loss of respiratory phasicity) flow is suggestive of proximal venous obstruction, especially in a patient with swollen limbs and under high-risk circumstances for VTE. Monophasicity is not specific to thrombosis. Other potential causes include obesity, pregnancy, and a pelvic mass. Respiratory or cardiac dysfunction may also produce an abnormal venous flow pattern.31

26.b. Begin alteplase 100 mg IV over 2 hours. The patient presented has a clinically massive pulmonary embolism with hemodynamic compromise; thus thrombolytic therapy is indicated.32

27.b. Atrial arrhythmia. There have been many laboratory, ECG, and echocardiogram findings shown to be predictive of mortality and prognosis. Right ventricular dysfunction, particularly when accompanied by hypotension, is predictive of pulmonary embolism–related hospital mortality. Elevated serum troponin and elevated brain natriuretic peptide have also been shown to predict an increased risk of death. Additional findings associated with a poorer prognosis include atrial arrhythmia, right bundle branch block, inferior Q waves and precordial T-wave inversions, and ST-segment changes. The other distracters have not been shown to predict prognosis.

28.b. Begin enoxaparin 1 mg/kg subcutaneous injections every 12 hours. Cancer patients are at a sixfold increased risk of developing VTE. Patients with active cancer make up about 20% of all new VTE diagnosed in the community. The risk, however, varies somewhat with cancer type, and those that incur a higher risk include malignant brain tumors and adenocarcinoma of the ovary, pancreas, colon, stomach, lung, prostate, and kidney. Several studies have demonstrated a benefit to treatment with LMWH when compared with coumadin in this patient population. One study, which compared dalteparin with coumadin, reported 27 of 336 patients in the LMWH group had recurrent VTE when compared with 53 of 336 in the coumadin group in a 6-month follow-up period. There was no increased risk of bleeding in the LMWH group.33,34

29.e. Proceed with placement of an inferior vena cava filter. The patient has a proximal DVT with a contraindication for anticoagulation. This scenario represents an absolute indication for the placement of an inferior vena cava filter. Pneumatic compression stockings are indicated for the prevention of VTE but not for treatment. Serial duplex ultrasound scans may be an acceptable strategy for management of isolated acute calf vein thrombosis but not for proximal DVT. IV unfractionated heparin or enoxaparin 1 mg/kg subcutaneous injections would be appropriate treatment options if the patient did not have a recent gastrointestinal bleed requiring transfusion.35

30.c. Order bilateral ABI measurements in the vascular laboratory at rest and following an exercise protocol. The patient in the clinical vignette presented with classic intermittent claudication symptoms suggestive of PAD. A normal resting ABI does not rule out PAD in a patient presenting with ambulatory symptoms.36 Performing the test following exercise often unmasks significant disease revealing markedly lower ABI values. Exercise may be an appropriate suggestion but it will not help to establish the diagnosis of this patient’s presenting problem. It would be premature to refer this patient for intervention. Pseudoclaudication may present similarly, but this patient has risk factors for PAD; therefore, a post exercise ABI would be the most appropriate next step in their workup. Repeating the resting ABI in 6 months is not likely to provide new information.

31.c. Less than 100 mg/dL. The most recent practice guidelines for the management of PAD, updated in March 2013, recommend a target LDL of less than 100 mg/dL for patients with an established diagnosis of PAD.36

32.c. Less than 130/80 mmHg. The most recent practice guidelines for the management of PAD, updated in March 2013, recommend a target blood pressure of less than 140/90 mmHg for patients with PAD. The guidelines recommend a lower target, less than 130/80 mmHg, for patients with PAD and concomitant diabetes mellitus or renal insufficiency.36

33.e. None of the above. Thiazide diuretics, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and β-adrenergic blockers are all acceptable medications to achieve blood pressure targets in patients with PAD.36

34.c. Every 6 to 12 months. According to the appropriate use criteria published by the intersocietal committee on peripheral vascular testing and the American College of Cardiology Foundation/American Heart Association practice guidelines for PAD, patients with an asymptomatic AAA measuring 4.0 to 5.4 cm should have surveillance imaging every 6 to 12 months in the first year.36,37

35.d. 5.5 cm or greater. The patient should be referred for repair once the infrarenal AAA reaches a diameter of 5.5 cm or greater due to an increased risk of spontaneous rupture.36 Surveillance imaging is advised at regular intervals for aneurysms less than 5.5 cm.

36.e. All of the above groups are appropriate to screen for an AAA. According to the appropriate use criteria published by intersocietal committee on peripheral vascular testing all of the groups listed are appropriate for AAA screening.37

37.a. Four weeks after the intervention. All patients should get a baseline carotid duplex ultrasound within 4 weeks after a carotid artery stenting or endarterectomy procedure.37

38.b. Every 12 months. It is recommended to repeat carotid duplex ultrasound every 12 months after the first year following carotid artery stenting to assess for evidence of in-stent restenosis.37

39.c. Popliteal artery aneurysm. Shown is a transverse and longitudinal image of a large popliteal artery aneurysm containing mural thrombus. The appearance is not suggestive of an abscess, Baker cyst, lymph node, or lipoma.

40.d. 50%. A large number of patients with a popliteal artery aneurysm will also have an AAA. Furthermore, 50% of patients with a popliteal artery aneurysm will have an aneurysm of the contralateral popliteal artery.38

41.e. Refer for repair of the aneurysm. Popliteal artery aneurysms measuring greater than 2.5 cm are at risk for thrombosis, embolism, or rupture and therefore should be repaired.36 Popliteal artery aneurysms measuring less than 2.5 cm are imaged at regular intervals.

42.b. Thromboembolism. Popliteal artery aneurysms most commonly cause thromboembolism that can lead to popliteal artery occlusion or painful distal embolic lesions. Rupture of popliteal artery aneurysms occurs infrequently.38,39

43.d. Pseudoaneurysm. The spectral Doppler waveform shown is a typical to-and-fro signal seen within the neck of the pseudoaneurysm. The incidence of pseudoaneurysm complicating percutaneous arterial procedures ranges between 0.2% and 0.5%. Patients typically present post catheter-based procedure with a painful pulsatile mass. When small these may resolve spontaneously, while others require intervention such as ultrasound-guided thrombin injection or surgical repair.5

44.c. Subclavian artery stenosis. Color Doppler imaging shows significant color aliasing, spectral broadening, and turbulent high-velocity flow within the subclavian artery. It is important to recognize severe subclavian artery stenosis prior to coronary artery bypass surgery in which the internal mammary artery may be utilized. Severe subclavian artery stenosis can lead to retrograde flow in the internal mammary artery predisposing to early graft failure. In an aneurysm usually the velocities are decreased.

45.c. Warfarin skin necrosis. Pictured is a large erythematous lesion with surrounding violaceous borders. Given the history of several days of high doses of warfarin without parental anticoagulation makes warfarin skin necrosis the most correct response. Heparin skin necrosis has been described but usually occurs at the site of subcutaneous injections.

HIT can rarely be associated with necrotic skin lesions but in this case her platelets remained stable. A vasculitis can cause skin necrosis but is unlikely in the given scenario.

46.d. Aortic valve stenosis. The waveforms in the bilateral internal carotid and vertebral arteries have a Tardus-Parvus morphology. They have a blunted and slow upstroke, suggesting more proximal or central narrowing. In this patient, these findings along with a systolic murmur are suggestive of aortic valve stenosis.

47.d. Saddle pulmonary embolism. This patient has a pulmonary embolism involving both main pulmonary arteries. Massive and submassive pulmonary embolism can cause an increase in troponin and B-type natriuretic peptide as seen in acute myocardial infarction. The image shown illustrates a filling defect within the main pulmonary artery at the bifurcation. There are no findings suggestive of aortic dissection, pneumonia, or interstitial fibrosis.

48.c. Carotid intima-media thickness. According to the latest American College of Cardiology/American Heart Association cardiovascular risk assessment guidelines, there is insufficient evidence available to recommend use of carotid intima-media thickness, ApoB, albuminuria, glomerular filtration rate, or cardiorespiratory fitness in cardiovascular risk assessment. There is adequate evidence to recommend use of high-sensitivity C-reactive protein, ABI, coronary artery calcium score, and a family history of premature cardiovascular disease for refinement of cardiovascular risk assessment.40

REFERENCES

1.Dziewas R, Konrad C, Drager B, et al. Cervical artery dissection. J Neurol. 2003;250(10):1179–1184.

2.Mafee MF, Raofi B, Kumar A, et al. Glomus faciale, glomus jugulare, glomus tympanicum, glomus vagale, carotid body tumors, and simulating lesions. Role of MR imaging. Radiol Clin North Am. 2000;38(5):1059–1076.

3.Wilgis EF. Evaluation and treatment of chronic digital ischemia. Ann Surg. 1981;193(6):693–698.

4.Slovut DP, Olin JW. Fibromuscular dysplasia. N Engl J Med. 2004;350 (18):1862–1871.

5.Ferguson JD, Whatling PT, Martin V, et al. Ultrasound guided percutaneous thrombin injection of iatrogenic femoral artery pseudoaneurysms after coronary angiography and intervention. Heart. 2001;85(4):e5.

6.Kelm M, Perings SM, Jax T, et al. Incidence and clinical outcome of iatrogenic femoral arteriovenous fistulas, implications for risk stratification and treatment. J Am Coll Cardiol. 2002;40(2):291–297.

7.McEllistrem RF, O’Toole DP, Keane P. Post cannulation radial artery aneurysm—a rare complication. Can J Anaesth. 1990;37:907–909.

8.Podlaha J, Holub R, Konecny Z, et al. 20 year experience with operations for popliteal artery aneurysm. BMJ/Bratisl Lek Listy. 2005;106(12): 421–422.

9.TASC Guidelines. Management of PAD. J Vasc Surg. 2000;31:S1–S296.

10.Criqui MH, Fronek A, Klauber MR, et al. The sensitivity, specificity, and predictive value of traditional clinical evaluation of peripheral arterial disease: results from noninvasive testing in a defined population. Circulation. 1985;71:516–522.

11.Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower 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). Circulation. 2006;21(113):e471–e486.

12.Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower 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). Circulation. 2006;21(113):e525–e557.

13.Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower 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). Circulation. 2006;21:e527–e533.

14.Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower 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). Circulation. 2006;21(113):e547–e557.

15.Warkentin TE, Greinacher A. Review heparin-induced thrombocytopenia: recognition, treatment, and prevention: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126;311S–317S.

16.Warkentin TE, Greinacher A. Heparin-induced thrombocytopenia: recognition, treatment, and prevention: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126;311–337.

17.Wigley FM. Raynaud’s phenomenon. N Engl J Med. 2002;347:1001–1008.

18.Creager MA, Dzau VJ, Loscalzo J. Vascular Medicine: A Companion to Braunwald’s Heart Disease. Philadelphia, PA: Elsevier Health Sciences; 2006:689–706.

19.Hoeper MM, Mayer E, Simonneau G, et al. Chronic thromboembolic pulmonary hypertension. Circulation. 2006;113:2011–2020.

20.Ely JW, Osheroff JA, Chambliss ML, et al. Approach to leg edema of uncertain etiology. J Am Board Fam Med. 2006;19:148–160.

21.Eberhardt RT, Raffetto JD. Chronic venous insufficiency. Circulation. 2005;111:2398–2409.

22.Buller HR, Agnelli G, Hull RD, et al. Antithrombotic therapy for venous thromboembolic disease: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126:401S–428S.

23.Bates SM, Greer IA, Hirsh J, et al. See use of antithrombotic agents during pregnancy: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy, Section 5.0. Chest. 2004;126:627S–644S.

24.Young JR, Olin JW, Bartholomew JR, eds. Peripheral Vascular Diseases, 2nd ed. St. Louis, MO: Mosby; 1996:614–617.

25.Hann CH, Streiff MB. The role of vena cava filters in the management of venous thromboembolism. Blood Rev. 2005;19:179–202.

26.Creager MA, Dzau VJ, Loscalzo J, eds. Vascular Medicine: A Companion to Braunwald’s Heart Disease. Philadelphia, PA: Saunders; 2006:159–160.

27.The Sixth ACCP Conference on Antithrombotic and Thrombolytic Therapy: evidence-based guidelines. Chest Suppl. 2001;119:176S–193S.

28.Creager MA, Dzau VJ, Loscalzo J, eds. Vascular Medicine: A Companion to Brunwald’s Heart Disease. Philadelphia, PA: Saunders; 2006:641–654.

29.Cil BE, Akpinar E, Karcaaltincaba M, et al. Case 76: May-Thurner syndrome. Radiology. 2004;233:361–365.

30.Takahaski PY, Kiemele LJ, Jones JP. Wound care for elderly patients: advances and clinical applications for practicing physicians. Mayo Clin Proc. 2004;79:260–267.

31.Dewald CL, Jensen CC, Park YH, et al. Vena cavography with CO2 versus iodinated contrast material for IVC filter placement: a prospective evaluation. Radiology. 2000;216:752–756.

32.The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: evidence-based guidelines. Chest Suppl. 2004;126:413S.

33.Lee AYY, Levine MN, Baker RI, et al. Low-molecular-weight heparin versus coumadin for the prevention of recurrent venous thromboembolism in patients with cancer. N Engl J Med. 2003;349:146–153.

34.The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: evidence-based guidelines. Chest Suppl. 2004;126:371S.

35.Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141:e419S–e494S.

36.Anderson JL, Halperin JL, Albert NM, et al. Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:1425–1443.

37.Mohler III ER, Gornik HL, Gerhard-Herman M, et al. ACCF/ACR/AIUM/ASE/ASN/ICAVL/SCAI/SCCT/SIR/SVM/SVS 2012 appropriate use criteria for peripheral vascular ultrasound and physiological testing part I: arterial ultrasound and physiological testing. J Am Coll Cardiol. 2012;60:242–276.

38.Huang Y, Gloviczki P, Noel AA, et al. Early complications and long-term outcome after open surgical treatment of popliteal artery aneurysms: is exclusion with saphenous vein bypass still the gold standard? J Vasc Surg. 2007;45:706–713.

39.Dawson I, Sie RB, van Bockel JH, et al. Atherosclerotic popliteal aneurysm. Br J Surg. 1997; 84:293–299.

40.Goff Jr DC, Lloyd-Jones DM, Bennett G, et al. 2013 ACC/AHA guideline on the assessment of cardiovascular risk. J Am Coll Cardiol. 2013. doi:10.1016/j.jacc.2013.11.005