Peripheral Arterial Disease

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Chapter 55

Peripheral Arterial Disease

1. What are the key components of the vascular physical examination?

    According to the American College of Cardiology/American Heart Association (ACC/AHA) guidelines on peripheral arterial disease (PAD), the key components of the vascular physical examination include the following:

image Blood pressure measurements in both arms

image Carotid pulse palpation for upstroke and amplitude, and auscultation for bruits

image Auscultation of the abdomen and flank for bruits

image Palpation of the abdomen for aortic pulsation and its maximal diameter

image Palpation of brachial, radial, ulnar, femoral, popliteal, dorsalis pedis, and posterior tibial pulses; pulse intensity is scored as follows: 0, absent; 1, diminished; 2, normal; 3, bounding

image Performance of the Allen test when knowledge of hand perfusion is needed

image Auscultation of the femoral arteries for the presence of bruits

image Inspection of the feet for color, temperature, and integrity of the skin, and for ulcers

image Observation of other findings suggestive of severe PAD, including distal hair loss, trophic skin changes, and hypertrophic nails

2. Can the location of the patient’s lower extremity claudication help to localize the site of occlusive disease?

    The answer is a qualified yes. Because the pathophysiology of claudication is complex, there is not a perfect correlation between anatomic site of disease and location of symptoms. However, in general, the following statements can be made:

3. What noninvasive tests are used in the assessment of lower limb claudication?

image Ankle-brachial index (ABI): The ankle-brachial index is the ankle systolic pressure (as determined by Doppler) divided by the brachial systolic pressure. An abnormal index is less than 0.90. The sensitivity is approximately 90% for diagnosis of PAD. (See Question 4 for further details.)

image Pulse volume recordings (PVRs): Pulse volume recordings measure changes in volume of toes, fingers, or parts of limbs that occur with each pulse beat as blood flows into or out of the extremity. A toe-to-brachial index of less than 0.6 is abnormal, and values of less than 0.15 are seen in patients with rest pain (toe pressures of less than 20 mm Hg).

image Duplex ultrasonography: Duplex ultrasonography is a noninvasive method of evaluating arterial stenosis and blood flow. This method can localize and quantify the degree of stenosis. Ultrasonography is dependent on operator skill.

image Transcutaneous oxygen tension measurements: These measurements are useful in assessing tissue viability for wound healing. Measurements greater than 55 mm Hg are considered normal and less than 20 mm Hg are associated with nonhealing ulcers.

image Exercise testing: This testing determines treadmill walking time and preexercise and postexercise ABI. In those without significant PAD, the ABI is unchanged after exercise. In patients with PAD, the ABI falls after exercise. This test is more sensitive for detecting disease than a resting ABI alone.

4. What is the ABI?

    The ABI is the ratio of systolic blood pressure at the level of the ankle to the systolic blood pressure measured at the level of the brachial artery. More specifically, blood pressure is measured in both brachial arteries (with the higher systolic blood pressure being used) and is measured using a Doppler instrument with a blood pressure cuff on the lower calf, in both posterior tibial and dorsalis pedis arteries. Pulse wave reflections in healthy persons should result in higher blood pressures in the ankle vessel pressure (10-15 mm Hg higher than in the brachial arteries), and thus a normal ABI should be greater than 1.00. Using a diagnostic threshold of 0.90 to 0.91, several studies have found the sensitivity of the ABI to be 79% to 95% and the specificity to be 96% to 100% to detect stenosis of 50% or more reduction in lumen diameter.

    Experts emphasize that the ABI is a continuous variable below 0.90. Values of 0.41 to 0.90 are considered to be mildly to moderately diminished; values of 0.40 or less are considered to be severely decreased. An ABI of 0.40 or less is associated with an increased risk of rest pain, ischemic ulceration, or gangrene. Patients with long-standing diabetes or end-stage renal disease on dialysis and elderly patients may have noncompressible leg arterial segments caused by medial calcification, precluding assessment of the ABI. These patients are best evaluated using digital pressures and with assessment of the quality of the arterial waveform in the PVR studies. A system for interpretation of the ABI is given in Table 55-1.

TABLE 55-1

INTERPRETATION OF THE ANKLE-BRACHIAL INDEX

ABI Interpretation
>1.30 Noncompressible
1.00-1.29 Normal
0.91-0.99 Borderline (equivocal)
0.41-0.90 Mild to moderate PAD
0.00-0.40 Severe PAD

ABI, Ankle-brachial index; PAD, peripheral arterial disease.

Modified from Hiatt WR: Medical treatment of peripheral arterial disease and claudication, N Engl J Med 344:1608-1621, 2001.

5. What are the recommended medical therapies and lifestyle interventions in patients with lower extremity PAD?

    A supervised exercise regimen is recommended as the initial treatment modality for patients with intermittent claudication. Supervised exercise training is recommended over unsupervised exercise training. Cilostazol treatment can lead to a modest increase in exercise capacity. Because agents with similar biologic effects have been shown to increase mortality in patients with heart failure, this drug should not be used in patients with heart failure. Smoking cessation must be strongly emphasized to the patient. Other measures include general secondary prevention interventions. Recommended medical therapies and lifestyle interventions in patients with lower extremity PAD are summarized in Box 55-1. An algorithm for the management of patients with suspected peripheral arterial disease is presented in Figure 55-1.

Box 55-1   RECOMMENDED MEDICAL THERAPIES AND LIFESTYLE INTERVENTIONS IN PATIENTS WITH LOWER EXTREMITY PERIPHERAL ARTERIAL DISEASE

image Statin treatment to lower LDL level to <70-100 mg/dL

image Antihypertensive therapy to lower blood pressure to <140/90 mm Hg (<130/80 mm Hg in patients with diabetes or those with chronic kidney disease)

image Patients with PAD should be offered smoking cessation interventions.

image Antiplatelet therapy is indicated to reduce the risk of MI, stroke, or vascular death.

image Supervised exercise training is the recommended initial treatment modality for intermittent claudication.

image Cilostazol (100 mg orally twice a day) is recommended to improve symptoms and increase walking distance in patients with intermittent claudication. (Cilostazol should not be used in patients with heart failure.)

ACE, Angiotensin-converting enzyme; β-blocker; beta-adrenergic blocking agent; LDL, low-density lipoprotein; MI, myocardial infarction; PAD, peripheral arterial disease.

Modified from Hirsch AT, Haskal ZJ, Hertzer NR, et al: ACC/AHA guidelines for the management of patients with peripheral arterial disease, J Am Coll Cardiol 47(6):1239-1312, 2006.

6. What are the interventional treatment options for patients with claudication?

    Claudication that severely interferes with quality of life or employment should be treated. Endovascular and open surgical reconstruction have both been extensively used for this purpose. Endovascular options are less invasive, typically performed on an outpatient basis, and are associated with lower complication rates. Open surgical options are more durable and best suited for good risk or young patients. Outcomes of either type of intervention are vascular-bed dependent. Iliac stenting has been associated with 5-year patency rates that in most cases are only slightly inferior to that of their open counterparts. Endovascular intervention in the infrainguinal segment, however, is associated with inferior patency, particularly when compared to open bypass using venous conduit.

7. What is critical limb ischemia (CLI) and how is it graded clinically?

    Whereas claudication is produced by decreased perfusion to the muscles upon increased demand, CLI refers to inadequate tissue perfusion at rest and is manifested as rest pain or tissue loss. Patients with CLI have multilevel disease that typically involves iliac, femoral, and tibial arteries. Due to extent of the disease and the coexistent comorbidities, the management of the patient with CLI involves substantial judgment. Hybrid procedures that include simultaneous open and endovascular components, multiple debridements, and extensive rehabilitation therapy programs are fairly typical. Best results are achieved with multidisciplinary approaches that involve interventionalists, surgeons, internists, podiatrists, and infectious disease and endocrine specialists, among others. Isolated vessel-based intervention in the absence of a grand plan for overall patient management should be discouraged, as most of these patients benefit from coordinated treatment in centers familiar with the intricacies and the issues surrounding the management of CLI. One widely used scheme for classifying limb ischemia is given in Table 55-2.

TABLE 55-2

CLINICAL CATEGORIES OF CHRONIC LIMB ISCHEMIA

Grade Category Clinical Description
  0 Asymptomatic, not hemodynamically correct
I 1 Mild claudication
  2 Moderate claudication
  3 Severe claudication
II 4 Ischemic rest pain
  5 Minor tissue loss: nonhealing ulcer, focal gangrene with diffuse pedal ulcer
III 6 Major tissue loss extending above transmetatarsal level, functional foot no longer salvageable

From Rutherford RB, Baker JD, Ernst C, et al: Recommended standards for reports dealing with lower extremity ischemia: revised version, J Vasc Surg 26:517, 1997.

8. What are the main complications of open and endovascular infrainguinal interventions?

    Complications of open interventions include cardiac events, respiratory complications, bleeding, wound infection, hernias, and graft failure. Complications associated with endovascular procedures include access site hematoma, bleeding or pseudoaneurysm, vessel rupture, contrast-induced nephropathy or anaphylactic reactions, recurrent stenosis or occlusion, and radiation-related patient injury. Thrombolytic treatment in particular is associated with increased risk of intracavitary, extremity, or intracranial bleeding, which is heavily dependent on the thrombolytic dose and duration of administration.

9. What are the causes of renal artery stenosis (RAS)?

    Approximately 90% of all renal arterial lesions are due to atherosclerosis. Atherosclerotic-related lesions usually affect the ostium and the proximal 1 cm of the main renal artery.

    Fibromuscular dysplasia (FMD) is the next most common cause. Although it classically occurs in young women, it can affect both genders at any age. Less common causes of renovascular hypertension include renal artery aneurysms, Takayasu arteritis, atheroemboli, thromboemboli, William syndrome, neurofibromatosis, spontaneous renal artery dissection, arteriovenous malformations (AVMs) or fistulas, retroperitoneal fibrosis, and prior abdominal radiation therapy.

10. What are ACC/AHA class I indications for the referral for diagnostic study to identify clinically significant RAS?

    Clinical scenarios that are recognized as class I indications for the performance of a diagnostic study to identify RAS include the following:

11. What are the main indications for RAS percutaneous revascularization?

    Most ACC/AHA indications for percutaneous revascularization are class IIa recommendations, meaning the procedure is reasonable.

    Class I (Indicated):

Class IIa (Reasonable):

12. What are the most common types of visceral artery aneurysms?

    Visceral artery aneurysms are an uncommon form of vascular disease whose pathogenesis and natural history remain incompletely characterized. Their typical presentation involves rupture or erosion into an adjacent viscus, resulting in life-threatening hemorrhage. Nearly 22% of reported visceral artery aneurysms present with rupture, resulting in an 8.5% mortality rate. The distribution of aneurysms among the visceral vessels includes the splenic artery (60%), hepatic artery (20%), superior mesenteric artery (5.5%), celiac artery (4%), gastric and gastroepiploic arteries (4%), jejunal, ileal, colic (3%), pancreaticoduodenal and pancreatic arteries (2%), gastroduodenal artery (1.5%), and inferior mesenteric artery (<1%). Typical indication for treatment include size more than 2 cm and childbearing age in a female patient, because rupture is common during pregnancy and is associated with very high maternal and fetal mortality

13. In general, when should patients with an infrarenal or juxtarenal abdominal aortic aneurysm (AAA) undergo repair?

    Current recommendations are that patients with an infrarenal or juxtarenal AAA should undergo repair when the aneurysm measures 5.5 cm or greater (although it is also a class IIa recommendation that it can be beneficial to repair aneurysms 5.0 to 5.4 cm in diameter). Patients with infrarenal or juxtarenal AAA measuring 4.0 to 5.4 cm in diameter should be monitored by ultrasound or computed tomography (CT) scans every 6 to 12 months. In those with AAA smaller than 4.0 cm, ultrasound examination every 2 to 3 years is felt to be reasonable.

14. What are the relative pros and cons of the treatment options for patients with infrarenal AAA that meets size criteria for repair?

    The traditional open AAA repair has been compared to endovascular infrarenal AAA repair (EVAR) extensively with three large multicenter trials, two in Europe and one in the US. EVAR is associated with lower perioperative mortality and complication rates, particular respiratory complications. However, it also implies the need for long-term follow-up with serial CT scans to assess the endograft and confirm the absence of endoleak or migration. The impact of this follow-up protocol in terms of impact on renal function and radiation-related injury is unclear at present. The survival benefit of EVAR disappeared in all studies after 2 to 3 years of follow-up. Open AAA repair has the additional issue of postoperative late ventral hernia development, which appears to occur in approximately 15% to 20% of patients.

15. What are the anatomic eligibility criteria for endovascular infrarenal AAA repair?

    These include the following:

As device platforms evolve, more challenging anatomies are routinely treated today with endovascular means. In addition, fenestrated and branched devices, and advanced “snorkel” techniques have enabled physicians to successfully treat juxtarenal and thoracoabdominal aneurysms in high-risk patients with endovascular means.

16. What are the primary indications for treatment of extracranial carotid artery occlusive disease?

    In very general terms, indications for intervention are as follows:

Controversy surrounds the overall topic of interventional treatment of asymptomatic carotid artery occlusive disease. The notion that maximizing medical treatment can be as good as intervention with respect to stroke prevention has been gaining acceptance; however, high-quality data to support it are scarce.

17. What are the relative indications for carotid endarterectomy (CEA) and carotid artery stenting (CAS)?

    Carotid stenting indications include the following:

CEA and CAS have been compared in four large randomized controlled trials that are listed in the references section and the reader is encouraged to review their results. CAS appears to be associated with higher stroke but lower myocardial event rates, and no extracranial nerve damage. The topic of first-line treatment in the management of symptomatic carotid artery occlusive disease is somewhat controversial at present, with two slightly conflicting society guideline statements. There is agreement that in the treatment of asymptomatic carotid artery occlusive disease, CEA should be the treatment of choice.

18. What are possible causes of lower limb arterial disease and ischemia or claudication in young patients?

    Atherosclerosis tends to primarily affect older persons; however, it can manifest in younger patients who have familial hyperlipidemic syndromes, Buerger disease (thromboangiitis obliterans), or hypercoagulable disorders. Popliteal entrapment syndrome is an anatomic abnormality in which the popliteal artery gets compressed, either by an abnormal muscle band or because it has taken an abnormal (medial) course behind the knee and is compressed by a normal gastrocnemius muscle. Popliteal adventitial cystic disease is also in the differential diagnosis of claudication in young patients; it produces a popliteal stenosis that gives a classic “scimitar sign” on angiography. Exercise-induced compartment syndrome may produce similar symptoms of leg pain with exercise that is relieved by rest.

19. What is fibromuscular dysplasia (FMD)?

    Fibromuscular dysplasia (FMD), formerly called fibromuscular fibroplasia, is a group of nonatherosclerotic, noninflammatory arterial diseases that can affect almost any artery but most commonly involves the renal arteries. Histologic classification discriminates three main subtypes: intimal, medial, and perimedial, which may be found in a single patient. Angiographic classification includes the following:

20. What is Buerger disease?

    Buerger disease, more appropriately called thromboangiitis obliterans, is a disease of small- and medium-sized arteries, as well as veins and nerves. Buerger disease is a nonatherosclerotic disease, instead caused by inflammatory processes and thrombosis.

    Clinically, it presents most commonly with ischemia of the digits and hand, arm, feet, or calf claudication. Ischemic ulcers may also occur. It occurs almost exclusively in tobacco users, and the only true “treatment” is smoking cessation. The presence of “corkscrew” collaterals is a pathognomonic angiographic finding.

21. What is Takayasu arteritis?

    Takayasu arteritis is a vasculitis of unknown cause, primarily affecting the aorta and its primary branches. It is more common in Asian populations and predominantly affects women. Over time, it can lead to narrowing or occlusion of the aorta and its branches, such as the subclavian artery. Clinically, patients most commonly manifest upper arm claudication but may also develop neurologic symptoms as a result of vertebrobasilar ischemia.

22. What is May-Thurner syndrome?

    Iliocaval compression, or May-Thurner syndrome (MTS), was initially described as the development of spurs in the left iliac vein as a consequence of compression from the contralateral right common iliac artery against the lumbar vertebra. The pathogenesis of MTS is not completely understood, but it is theorized that it may be a combination of both mechanical compression and arterial pulsations by the right iliac artery that leads to the development of intimal hypertrophy within the wall of the left common iliac vein. This can lead to potential endothelial changes and thrombus formation. Patients with MTS tend to be young women in the second to fourth decade of life who develop the syndrome after periods of prolonged immobilization or pregnancy. Patients may have a history of several days or more of persistent, unexplained pain and swelling of the left thigh and calf. Duplex ultrasound characteristically may reveal left common iliac vein thrombosis. Management of symptomatic MTS in association with deep vein thrombosis may involve catheter-directed thrombolysis, anticoagulation, and potentially iliocaval stenting.

Bibliography, Suggested Readings, and Websites

1. Blankensteijn, J.D., de Jong, S.E., Prinssen, M., et al. Two-year outcomes after conventional or endovascular repair of abdominal aortic aneurysms. N Engl J Med. 2005;352:2398–2405.

2. Brott, T.G., Halperin, J.L., Abbara, S., et al, JASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease: executive summary. Circulation 2011;124:489–532 Stroke 42:e4120–e463, 2011; and J Am Coll Cardiol 57:1002–1044, 2011

3. Brott, T.G., Hobson, R.W., 2nd., Howard, G., et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. New Engl J Med. 2010;363:11–23.

4. Eckstein, H.H., Ringleb, P., Allenberg, J.R., et al. Results of the stent-protected angioplasty versus carotid endarterectomy (space) study to treat symptomatic stenoses at 2 years: a multinational, prospective, randomised trial. Lancet Neurol. 2008;7:893–902.

5. Greenhalgh, R.M., Brown, L.C., Kwong, G.P., Powell, J.T., Thompson, S.G. Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: Randomised controlled trial. Lancet. 2004;364:843–848.

6. Hiatt, W.R. Medical treatment of peripheral arterial disease and claudication. N Engl J Med. 2001;344:1608–1621.

7. Hirsch, A.T., Haskal, Z.J., Hertzer, N.R., et al. ACC/AHA guidelines for the management of patients with peripheral arterial disease. J Am Coll Cardiol. 2006;47:1239–1312.

8. Norgren, L., Hiatt, W.R., Dormandy, J.A., et al. Inter-society consensus for the management of peripheral arterial disease (tasc ii). Eur J Vasc Endovasc Surg. 2007;33(Suppl 1):S1–S5.

9. Lederle, F.A., Freischlag, J.A., Kyriakides, T.C., et al. Outcomes following endovascular vs open repair of abdominal aortic aneurysm: A randomized trial. JAMA. 2009;302:1535–1542.

10. Mas, J.L., Trinquart, L., Leys, D., et al. Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial: results up to 4 years from a randomised, multicentre trial. Lancet Neurol. 2008;7:885–892.

11. Murad, M.H., Shahrour, A., Shah, N.D., et al. A systematic review and meta-analysis of randomized trials of carotid endarterectomy vs stenting. J Vasc Surg. 2011;53:792–797.

12. Norgren, L., Hiatt, W.R., Dormandy, J.A., et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). Eur J Vasc Endovasc Surg. 2007;33(Suppl 1):S1–S75.

13. Ricotta, J., AbuRahma, A., Ascher, E., et al. Updated Society for Vascular Surgery guidelines for management of extracranial carotid disease. J Vasc Surg. 2011;54:832–836.

14. Ringleb, P.A., Allenberg, J., Bruckmann, H., et al. 30 day results from the space trial of stent-protected angioplasty versus carotid endarterectomy in symptomatic patients: a randomised non-inferiority trial. Lancet. 2006;368:1239–1247.

15. Sacco, R.L., Adams, R., Albers, G., et al. AHA/ASA guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack. Stroke. 2006;37:577–617.

16. White, C.J., Jaff, M.R., Haskal, Z.J., et al. Indications for renal arteriography at the time of coronary arteriography: a science advisory from the American Heart Association Committee on Diagnostic and Interventional Cardiac Catheterization, Council on Clinical Cardiology, and the Councils on Cardiovascular Radiology and Intervention and on Kidney in Cardiovascular Disease. Circulation. 2006;114:1892–1895.

17. Yadav, J.S., Wholey, M.H., Kuntz, R.E., et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. New Engl J Med. 2004;351:1493–1501.

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