Peripheral arterial disease

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Rim Halaby

Peripheral arterial disease is commonly divided in the Fontaine stages, introduced by Dr. René Fontaine in 1954. There’s another classification created by Rutherford consisting of three grades and six categories. In addition, the American College of Cardiology/American Heart Assocommon iliac arterytion (ACC/AHA) uses a symptoms-based classification (absence of symptoms, claudication, critical limb ischemia and acute limb ischemia) in their guidelines. TASC (Trans Atlantic Inter-Society Consensus) morphological consensus is used to guide the choice between endovascular and surgical revarscularization in the management of patients with peripheral artery disease.

• Stage I: Asymptomatic
• Stage II a: Claudication after walking a distance that exceeds 200 meters
• Stage II b: Claudication after walking a distance inferior to 200 meters
• Stage III: Ischemia rest pain
• Stage IV: Ulceration or tissue loss (gangrene)^[1]

• Grade 0, Category 0: Asymptomatic
• Grade I, Category 1: Mild claudication
• Grade I, Category 2: Moderate claudication
• Grade I, Category 3: Severe claudication
• Grade II, Category 4: Ischaemia rest pain
• Grade III, Category 5: Minor tissue loss
• Grade IV, Category 6: Major tissue loss^[2]

Shown below is an image showing the difference between Fontaine’s and Rutherford’s classification:

• Absence of symptoms
• Claudication
• Critical/chronic limb ischaemia
• Acute limb ischaemia

• TASC (Trans Atlantic Inter-Society Consensus) morphological consensus is used to guide the choice between endovascular and surgical revarscularization in the management of the patients with peripheral artery disease.

• TASC type A iliac lesions:
  • Single stenosis less than 3 cm of the common iliac artery or external iliac artery (unilateral/bilateral)
• TASC type B iliac lesions:
  • Single stenosis 3 to 10 cm in length, not extending into the common femoral artery, or
  • Total of 2 stenoses less than 5 cm long in the common iliac artery and/or external iliac artery and not extending into the common femoral artery, or
  • Unilateral common iliac artery occlusion
• TASC type C iliac lesions:
  • Bilateral 5- to 10-cm-long stenosis of the common iliac artery and/or external iliac artery, not extending into the common femoral artery, or
  • Unilateral external iliac artery occlusion not extending into the common femoral artery, or
  • Unilateral external iliac artery stenosis extending into the common femoral artery, or
  • Bilateral common iliac artery occlusion
• TASC type D iliac lesions:
  • Diffuse, multiple unilateral stenoses involving the common iliac artery, external iliac artery, and common femoral artery (usually more than 10 cm long), or
  • Unilateral occlusion involving both the common iliac artery and external iliac artery, or
  • Bilateral external iliac artery occlusions, or
  • Diffuse disease involving the aorta and both iliac arteries, or
  • Iliac stenoses in a patient with an abdominal aortic aneurysm orother lesion requiring aortic or iliac surgery^[3]

• TASC type A femoropopliteal lesions:
  • Single stenosis less than 3 cm of the superficial femoral artery or popliteal artery
• TASC type B femoropopliteal lesions:
  • Single stenosis 3 to 10 cm in length, not involving the distal popliteal artery, or
  • Heavily calcified stenoses up to 3 cm in length, or
  • Multiple lesions, each less than 3 cm (stenoses or occlusions), or
  • Single or multiple lesions in the absence of continuous tibial runoff to improve inflow for distal surgical bypass
• TASC type C femoropopliteal lesions:
  • Single stenosis or occlusion longer than 5 cm, or
  • Multiple stenoses or occlusions, each 3 to 5 cm in length, with or without heavy calcification
• TASC type D femoropopliteal lesions:
  • Complete common femoral artery or superficial femoral artery occlusions or complete popliteal and proximal trifurcation occlusions^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Rim Halaby

Peripheral arterial disease (PAD) is most commonly a manifestation of atherosclerosis resulting from vascular inflammation. Other uncommon causes should be suspected when the PAD occurs at a young age and in the context of a positive history. Uncommon causes include degenerative diseases (Marfan’s syndrome and Ehlers-Danlos syndrome), dysplastic disorders (fibromuscular dysplasia), inflammatory diseases (arteritis) and hypercoagulable states.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Arterial dissection
• Atheroembolism
• Atherosclerosis
• Thromboangiitis obliterans
• Thromboembolism
• Thrombosed aneurysm

Cardiovascular	Arterial dissection, arteriomegaly, arteritis, atheroembolism, atherosclerosis, Buergers disease, cystic adventitial disease, Erdheim cystic medial necrosis, fibromuscular dysplasia, hypertension, Leriche’s syndrome, multifocal fibrosclerosis, Sneddon syndrome, Takayasu’s arteritis, temporal arteritis, thromboangiitis obliterans, thromboembolism, thrombosed aneurysm, vasculitis
Chemical / poisoning	Ergot use
Dermatologic	Sneddon syndrome, vasculitis
Drug Side Effect	Ergot use
Ear Nose Throat	No underlying causes
Endocrine	Diabetes
Environmental	Smoking
Gastroenterologic	No underlying causes
Genetic	Deafness peripheral neuropathy and arterial disease, Ehlers-Danlos syndrome, heterozygous familial hypercholesterolemia, Marfan’s syndrome, neurofibromatosis, pseudoxanthoma elasticum
Hematologic	Hypercoagulable state, thrombophilia, thrombosis
Iatrogenic	Radiation arteritis, radiation fibrosis, surgery, thrombosis
Infectious Disease	No underlying causes
Musculoskeletal / Ortho	No underlying causes
Neurologic	Neurofibromatosis, Sneddon syndrome
Nutritional / Metabolic	Hyperlipidemia, homocysteinemia, lipoproteinemia
Obstetric/Gynecologic	No underlying causes
Oncologic	Cancer, tumor
Opthalmologic	Sneddon syndrome
Overdose / Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal / Electrolyte	No underlying causes
Rheum / Immune / Allergy	Buergers disease, retroperitoneal fibrosis, Sneddon syndrome, thromboangiitis obliterans, vasculitis
Sexual	No underlying causes
Trauma	Iliac endofibrosis (athletic injury), limb trauma, popliteal artery entrapment syndrome
Urologic	Retroperitoneal fibrosis
Dental	No underlying causes
Miscellaneous	Obesity

• Arterial dissection
• Arteriomegaly
• Arteritis
• Atheroembolism
• Atherosclerosis
• Buergers disease
• Cancer
• Cystic adventitial disease
• Deafness peripheral neuropathy and arterial disease
• Diabetes ^[1]
• Ehlers-Danlos syndrome
• Erdheim cystic medial necrosis
• Ergot use
• Fibromuscular dysplasia
• Heterozygous familial hypercholesterolemia
• Homocysteinemia
• Hypercoagulable state
• Hyperlipidemia
• Hypertension
• Iliac endofibrosis (athletic injury)
• Leriche’s syndrome
• Limb trauma
• Lipoproteinemia
• Marfan’s syndrome
• Multifocal fibrosclerosis
• Neurofibromatosis
• Obesity
• Popliteal artery entrapment syndrome
• Pseudoxanthoma elasticum
• Radiation arteritis
• Radiation fibrosis
• Retroperitoneal fibrosis
• Sneddon syndrome
• Surgery
• Takayasu’s arteritis
• Temporal arteritis
• Thromboangiitis obliterans
• Thromboembolism
• Thrombophilia
• Thrombosis
• Tumor
• Thrombosed aneurysm
• Vasculitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Rim Halaby

The most important disorder that peripheral arterial disease and the associated symptom of claudication must be distinguished from is pseudoclaudication caused by lumbar spinal stenosis. Intermittent claudication (IC) must also be differentiated from lower extremity pain caused by non-vascular etiologies that may include neurologic, musculoskeletal and venous pathologies. Given the diversity in and the severity of symptoms among patients with peripheral arterial disease, there is a long list of disorders that peripheral arterial disease must be distinguished from. In fact, the false-positive diagnosis rates of peripheral arterial disease are estimated to be around 44% and the false-negative rates are estimated to be around 19%.

• Arteritis (Takayasu, giant cell)
• Aortic coarctation
• Aortic dissection
• Baker’s cyst
• Chronic compartment syndrome
• Cystic adventitial disease
• Deconditioning
• Degenerative joint disease (hip, back, knee)
• Embolic disease
• Fibromuscular dysplasia
• Myopathy
• Popliteal artery entrapment syndrome
• Popliteal vein compression
• Retroperitoneal fibrosis
• Spinal stenosis
• Thromboangiitis obliterans
• Venous claudication

Cardiovascular	Arteritis (Takayasu, giant cell) • Aortic coarctation • Aortic dissection • Claudication due to venous congestion (Venous claudication) • Deep vein thrombosis • Compartment Syndrome • Embolic disease • Fibromuscular dysplasia • Thromboangiitis obliterans
Chemical / poisoning	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	Pseudoxanthoma elasticum
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	No underlying causes
Musculoskeletal / Ortho	Arthritis • Compartment Syndrome • Baker’s cyst • Degenerative joint disease • Myopathy • Popliteal artery entrapment syndrome • Popliteal artery entrapment syndrome • Spinal stenosis
Neurologic	Compartment Syndrome • Spinal stenosis • Spondylolisthesis
Nutritional / Metabolic	No underlying causes
Oncologic	No underlying causes
Opthalmologic	No underlying causes
Overdose / Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal / Electrolyte	No underlying causes
Rheum / Immune / Allergy	Arthritis
Trauma	No underlying causes
Miscellaneous	No underlying causes

It is important to know the typical presentation of claudication so that it can be differentiated from the symptoms of other disorders.

• Claudication pain is a cramp- like pain that is always induced by exercise at a constant distance that the patient walks.
• Claudication pain can be either unilateral or bilateral.
• Claudication pain is relieved by rest.

Claudication caused by the peripheral arterial disease must be differentiated from the pseudoclaudication caused by lumbar spinal stenosis.^[2] Lumbar spinal stenosis is due to nerve root compression by herniated disks or osteophytes and the pain typically follows the dermatome of the affected root.

• The pain usually begins immediately upon walking and may be felt in the calf or in the lower leg and it is associated sometimes with numbness and paresthesias.
• The pain is not quickly relieved by rest and may even be present at rest.
• A sensation of pain running down the back of the leg as well as a history of back problems may be present.
• In patients with cauda equina syndrome, upright positioning aggravates the narrowing of the spinal canal and therefore causes the symptoms.
• Symptoms are usually associated with walking; nevertheless, upright standing may produce pain, weakness or discomfort in the hips, thighs and buttocks.
• Symptoms are alleviated by sitting or flexing the lumbar spine forward as opposed to standing, which alleviates pain caused by IC.

Venous claudication occurs in patients with chronic venous insufficiency and those who develop post-thrombotic syndrome after deep venous thrombosis. Baseline venous hypertension in the obstructed veins worsens with exercise.

• Venous claudication produces a tight bursting pressure in the limb following exercise, usually worse in the thigh and uncommonly in the calf.
• It is usually associated with venous edema in the leg.
• Venous claudication tends to improve with cessation of exercise but total resolution takes much longer time than the resolution of intermittent claudication (IC).
• Leg elevation helps in relieving the symptoms.

Chronic compartment syndrome is an uncommon cause of exercise-induced leg pain. It results from thickened fascia, muscular hypertrophy or when external pressure is applied to the leg. It tends to occur in young athletes who develop increased pressure within a fixed compartment which compromises the perfusion and the function of the tissues within that space. Intracompartmental pressure testing before and after exercise is the diagnostic test of choice.

• Chronic compartment syndrome presents as tight bursting pressure in the calf or foot after endurance sports or other robust exercise.
• Pain subsides slowly with rest.

• Osteoarthritis in joints is typically worse in the morning or at the initiation of movement.
• The degree of pain varies day to day and does not cease upon stopping exercise or standing.
• The pain improves after sitting, lying down, or leaning against an object to alleviate weight-bearing on the joint.
• The pain may be affected by weather changes, and may be present at rest.

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Editors-in-Chief: C. Michael Gibson; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [1]; Rim Halaby

The prevalence of peripheral arterial disease varies considerably depending on the definition of PAD as well as on the age of the studied population. The overall prevalence of peripheral arterial disease in the general population is 12–14%. The prevalence of PAD is higher in the elderly and affects up to 20% of patients over the age of 70 years.

• The overall prevalence of peripheral vascular disease in the general population is 12–14%, affecting up to 20% of those over 70.^[1][2]
• The incidence of symptomatic disease increases with age. It starts at about 0.3% per year for men aged 40–55 years and some studies have shown it to rise to about 1% per year for male patients aolder than 75 years.^[3][4]
• 70%–80% of the patients are asymptomatic and very few patients will ever require revascularisation or amputation.
• Peripheral vascular disease affects 1 in 3 diabetics older than 50.^[5]
• Approximately 6.5 million people in America have PVD.^[6] Despite its prevalence and cardiovascular risk implications, only 25 percent of PAD patients are undergoing treatment.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Rim Halaby

The risk factors associated with peripheral artery disease are similar to those associated with coronary artery disease. They can be classified as traditional and non traditional. Another way to classify the risk factors is depending on their level of risk: high risk factors (tobacco and diabetes), moderate risk factors (hypertension and hyperhomocysteinemia) and low risk factors (hypercholesterolemia). Some risk factors are modifiable, like hypertension, whereas others are not.

• The prevalence of PAD increases with age.
• The risk for lower-extremity peripheral arterial disease varies with age depending on other co-existing risk factors:
  • Age less than 50 years:
    • Risk factors: diabetes and one other atherosclerosis risk factor (smoking, dyslipidemia, hypertension, or hyperhomocysteinemia).
  • Age 50 to 69 years:
    • Risk factors: smoking or diabetes.
  • Age 70 years and older:
    • Risk factors: similar to other atherosclerotic diseases.
• Younger patients with PAD tend to have poorer overall long-term outcomes, as well as a higher number of failed bypass surgeries leading to amputation, compared with their older counterparts.^[1]

• Cigarette smoking is the single most modifiable risk factor for the development of PAD; in fact, smoking increases the risk of PAD 4-fold and accelerates the onset of PAD symptoms by nearly a decade.
  • The association between smoking and PAD is about twice as strong as that between smoking and coronary artery disease.
  • An apparent dose-response relationship exists between the pack-year history and PAD risk.
• Compared with their nonsmoking counterparts, smokers with PAD have poorer survival rates and are more likely to progress to critical limb ischemia, and twice as likely to progress to amputation, and also have reduced arterial bypass graft patency rates.
• Individuals who are able to stop smoking are less likely to develop rest pain and have improved survival.^[1]

• Diabetes mellitus confers a 1.5-fold to 4-fold increase in the risk of developing symptomatic or asymptomatic PAD and is associated with an increased risk of cardiovascular events and early mortality among individuals with PAD.
  • Diabetes is a stronger risk factor for PAD in women than in men.
  • The prevalence of PAD is higher in African Americans and Hispanics with diabetes than in non-Hispanic whites with diabetes.
• In patients with diabetes, the prevalence and extent of PAD also appears to correlate with the age of the individual and the duration and severity of his or her diabetes.
  • There is a 28% increase of PAD for every percentage-point increase in hemoglobin A1c.
• PAD prevalence is also increased in individuals with impaired glucose tolerance.

• Late, progressive and more severe presentation as a result initial asymptomatic nature of PAD in diabetics
• Occlusive disease in the tibial arteries
• Impaired wound healing due to microangiopathy and neuropathy
• Higher risk for ischemic ulceration and gangrene.^[1]

• Abnormalities in vascular smooth muscle cells
• Endothelial cell dysfunction
• Elevated blood pressure
• Impaired fibrinolytic function
• Increased levels of triglycerides, cholesterol, and other blood lipids
• Increased vascular inflammation
• Increased in platelet aggregation
• Tobacco use

• Elevations in total cholesterol, LDL cholesterol, very low-density lipoprotein (VLDL) cholesterol, and triglycerides are all independent risk factors for PAD.
  • There is 10% increased risk of developing PAD for every 10-mg/dL rise in total cholesterol.
• Elevations in high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I appear to be protective
• The form of dyslipidemia seen most frequently in patients with PAD is the combination of a reduced HDL cholesterol level and an elevated triglyceride level (commonly present in patients with the metabolic syndrome and diabetes).^[1]

• Hypertension has been reported in as 50-92% of patients with PAD.
• Patients with PAD and hypertension are at greatly increased risk of stroke and myocardial infarction independently of other risk factors.

• PAD has been shown to be disproportionately prevalent in black and Hispanic populations

• There is an association between PAD and chronic kidney disease independently from diabetes, hypertension, ethnicity and age. This association might be related to the increased vascular inflammation and markedly elevated plasma homocysteine levels seen in chronic kidney disease.
• The prevalence of an abnormal ABI (< 0.90) is much higher in patients with end-stage renal disease than in those with chronic kidney disease, ranging between 30% and 38%.

• Genetic predisposition to PAD is supported by observations of increased rates of cardiovascular disease (including PAD) in “healthy” relatives of patients with intermittent claudication.
• To date, no major gene for PAD has been detected.

• Hypercoagulable state, caused by altered levels of D-dimer, homocysteine or lipoprotein a, is an uncommon risk factor for PAD.
• Hepercoagulable state is suspected in younger persons who lack traditional risk factors, patients with a strong family history of premature atherosclerosis, and individuals in whom arterial revascularization fails for no apparent technical reason.
  • Hyperhomocysteinemia is associated with premature atherosclerosis and appears to be a stronger risk factor for PAD than for CAD.^[1]

• An association between abdominal obesity and PAD has been reported, although it is unclear whether any association exists between PAD and body mass index (BMI)
• The lack of association between PAD and BMI can be explained by the tendency of smokers (those at an increased risk for PAD) have lower BMIs than nonsmokers. Also, many of the individuals at risk for PAD are elderly males, who generally have lower BMIs as well.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]; Rim Halaby

Synonyms and keywords: Ankle-brachial index; ankle brachial index; ABI; ankle-arm index; ankle-brachial blood pressure index, ankle-arm ratio; Winsor index

A resting ankle brachial index (ABI) is the screening study of choice in a patient who has suspected lower extremity peripheral arterial disease. The ankle brachial index is an indicator of atherosclerosis and it provides prognostic information even in the absence of any symptoms of peripheral arterial disease. It is defined as the ratio of the ankle blood pressure divided by the highest brachial blood pressure. An ankle branchial index should be obtained if a patient has one or more of the following characteristics: 1) exertional claudication; 2) presence of nonhealing wounds; 3) age over 50 with a history of smoking or diabetes or 4) age over 65.

• The ABI is a screening test for the assessment of the presence of PAD. Studies in 2006 suggests that an abnormal ABI may be an independent predictor of mortality, as it reflects the burden of atherosclerosis.^[1][2]

• The blood pressure in the ankle is higher than that in the arms because the blood pressure wave gets amplified as it propagates away from the heart causing the systolic blood pressure to increase and the diastolic pressure to decrease. In fact, two factors are involved in the amplification of the blood pressure distally from the heart:
  • Retrograde wave reflection from resistant distal arterioles that adds up to the antegrade blood pressure wave.
  • Remodelling and increased stiffness of the blood vessels in the legs as evidenced by increased wall thickening and and unchanged inner radius, secondary to the increased hydrostatic pressure while walking.^[3]
• It should be noted that the ABI varies by age, ethnicity, gender, and height:^[4]
  • ABI is expected to increase with aging as the arterial stiffness increase.
  • Taller individuals are expected to have a higher ABI because the blood pressure waves must propagate longer distances away from the heart.
  • Women have an ABI that is almost 0.7 less than that of men.^[3]

• The pressures in the posterior tibial artery and dorsalis pedis artery in the feet and the brachial artery at the elbow are estimated. A Doppler probe is used, through a device called the Pulse Volume Recorder (some variances may apply depending on the physician), to monitor the pulse while a sphygmomanometer (blood pressure cuff) is inflated above the artery. The cuff is deflated and the pressure at which the pulse returns is recorded. The blood pressures are measured after 10 minutes of rest.

The USPSTF stated^[5]:

• “The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for PAD and CVD risk with the ABI in asymptomatic adults. (I statement).”

The American College of Cardiology/American Heart Association states^[6]:

• Age ≥65 y
• Age 50–64 y, with risk factors for atherosclerosis (e.g., diabetes mellitus, history of smoking, hyperlipidemia, hypertension) or family history of PAD (63)
• Age <50 y, with diabetes mellitus and 1 additional risk factor for atherosclerosis
• Individuals with known atherosclerotic disease in another vascular bed (e.g., coronary, carotid, subclavian, renal, mesenteric artery stenosis, or AAA)

• The ABI is the ratio of the ankle to the highest brachial blood pressure and an ABI of greater than 0.9 is considered normal, suggesting that there is no significant peripheral vascular disease affecting the vessels of the legs.

• ABI should be measured in both legs in all new patients with PAD of any severity to confirm the diagnosis and establish a baseline.

• 0.9 to 1.3: Normal
• 0.5 to 0.7: Moderate
• < 0.50: Severe
• ≥ 1.4: Poorly compressible vessels
  • A value greater than 1.4 is considered abnormal, and suggests calcification of the walls of the arteries and noncompressible vessels, reflecting severe peripheral vascular disease.

• The exercise ABI is done by having the patient stand on their toes repeatedly. The ABI is rechecked after exercise. This test is done if the patient has symptoms with exercise. However, patients with peripheral artery disease can have normal ABI at rest; however, they show abnormal ABI measurements after stress exercise.
• During exercise, the systolic pressure increases causing an increase in the pressure difference beyond the diseased vessel. Hence, the ABI will decrease. An abnormal result is a drop of > 20% on ABI in one minute, despite a normal ABI at rest.
• Patients who can not tolerate the treadmill exercise can do the tip toe exercise as an alternative.

• 0.5 to 0.9: Mild
• 0.15 to 0.8: Moderate
• < 0.15: Severe^[7]

• Exercise tolerance less than 5 minutes: Moderate
• Exercise tolerance less than 3 minutes: Severe^[8]

• When the vessels are stiff, as in the case of diseases like diabetes, the ABI index is inaccurate in the evaluation of the severity of the arterial occlusive diseases.
• Toe-brachial index is a reliable alternative when the vessels are stiff and non compressible.
• The normal range for the toe-brachial pressure index is values more than 0.70.^[9]

• Segmental pressure examinations is basically applying the same ABI principle but on different parts of the extremities.

Shown below is a table summarizing the interpretation of the ABI values and the appropriate actions to be taken accordingly:

ABI value	Interpretation	Action	Nature of ulcers, if present
Above 1.2	Abnormal Vessel hardening from PVD	Refer routinely	Venous ulcer use full compression bandaging
1.0 – 1.2	Normal range	None
0.9 – 1.0	Acceptable
0.8 – 0.9	Some arterial disease	Manage risk factors
0.5 – 0.8	Moderate arterial disease	Routine specialist referral	Mixed ulcers use reduced compression bandaging
Under 0.5	Severe arterial disease	Urgent specialist referral	Arterial ulcers no compression bandaging used

• Normal ABI in the presence of symptoms: No change in the mortality rate
• ABI < 0.85: 10% five year mortality rate
• ABI < 0.4: 50% one year mortality rate

Class I

“1. The Doppler method should be used to measure the SBP in each arm and each ankle for the determination of the ABI. (Level of Evidence: A) ”

“2. The cuff size should be appropriate with a width at least 40% of the limb circumference. (Level of Evidence: B) ”

“3. The ankle cuff should be placed just above the malleoli with the straight wrapping method. (Level of Evidence: B) ”

“4. Any open lesion with the potential for contamination should be covered with an impermeable dressing. (Level of Evidence: C) ”

Class III (No Benefit)

“1. The use of the cuff over a distal bypass should be avoided (risk of bypass thrombosis).(Level of Evidence: C)”

Class I

“1. Each clinician should adopt the following sequence of limb pressure measurement for the ABI at rest: first arm, first PT artery, first DP artery, other PT artery, other DP artery, and other arm.(Level of Evidence: C ”

“2. After the measurement of systolic pressures of the 4 limbs, if the SBP of the first arm exceeds the SBP of the other arm by >10 mm Hg, the blood pressure of the first arm should be repeated, and the first measurement of the first arm should be disregarded. (Level of Evidence: C) ”

Class I

“1. The ABI of each leg should be calculated by dividing the higher of the PT or DP pressure by the higher of the right or left arm SBP. (Level of Evidence: A) ”

“2. When ABI is used as a diagnostic tool to assess patients with symptoms of PAD, the ABI should be reported separately for each leg. (Level of Evidence: C) ”

“3. When the ABI is used as a prognostic marker of cardiovascular events and mortality, the lower of the ABIs of the left and right leg should be used as the prognostic marker of cardiovascular events and mortality. The exception to this recommendation is the case of noncompressible arteries. (Level of Evidence: C) ”

Class IIa

“1. For any situation, when the ABI is initially determined to be between 0.80 and 1.00, it is reasonable to repeat the measurement. (Level of Evidence: B) ”

Class I

“1. In the case of clinical suspicion based on symptoms and clinical findings, the ABI should be used as the first line noninvasive test for the diagnosis of PAD. (Level of Evidence: A) ”

“2. An ABI <0.90 should be considered the threshold for confirming the diagnosis of lower extremity PAD. (Level of Evidence: A) ”

“3. When the ABI is >0.90 but there is clinical suspicion of PAD, post-exercise ABI or other noninvasive tests, which may include imaging, should be used. (Level of Evidence: A) ”

“4. When the ABI is >1.40 but there is clinical suspicion of PAD, a toe-brachial index or other noninvasive tests, which may include imaging, should be used. (Level of Evidence: A) ”

Class IIa

“1. It is reasonable to consider a post-exercise ankle pressure decrease of >30 mm Hg or a post-exercise ABI decrease of >20% as a diagnostic criterion for PAD. (Level of Evidence: A) ”

Class III (No Benefit)

“1. The ABI should not be used alone to follow revascularized patients. (Level of Evidence: C)”

Class IIa

“1. An ABI decrease of >0.15 over time can be effective to detect significant PAD progression. (Level of Evidence: B) ”

Class I

“1. Individuals with an ABI <0.90 or >1.40 should be considered at increased risk of cardiovascular events and mortality independently of the presence of symptoms of PAD and other cardiovascular risk factors. (Level of Evidence: A) ”

Class IIa

“1. The ABI can be used to provide incremental information beyond standard risk scores in predicting future cardiovascular events. (Level of Evidence: A) ”

“1. Subjects with an ABI between 0.91 and 1.00 are considered “borderline” in terms of cardiovascular risk. Further evaluation is appropriate. (Level of Evidence: A) ”

Class I

“1. The resting ABI should be used to establish the lower extremity PAD diagnosis in patients with suspected lower extremity PAD, defined as individuals with 1 or more of the following: exertional leg symptoms, nonhealing wounds, age 65 years and older, or 50 years and older with a history of smoking or diabetes.[13][14][15](Level of Evidence: B)”

“2. The ABI should be measured in both legs in all new patients with PAD of any severity to confirm the diagnosis of lower extremity PAD and establish a baseline.[16][17][18](Level of Evidence: B)”

“3. The toe-brachial index should be used to establish the lower extremity PAD diagnosis in patients in whom lower extremity PAD is clinically suspected but in whom the ABI test is not reliable due to noncompressible vessels (usually patients with long-standing diabetes or advanced age).[19][20][21][22][23] (Level of Evidence: B)”

“4. Leg segmental pressure measurements are useful to establish the lower extremity PAD diagnosis when anatomic localization of lower extremity PAD is required to create a therapeutic plan.[24][25][26][27] (Level of Evidence: B)”

“5. ABI results should be uniformly reported with noncompressible values defined as greater than 1.40, normal values 1.00 to 1.40, borderline 0.91 to 0.99, and abnormal 0.90 or less.[28] (Level of Evidence: B)”

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] Aarti Narayan, M.B.B.S [3]; Rim Halaby

Most patients with peripheral arterial disease (PAD) have a benign course, with the majority of patients being asymptomatic. However, clinical manifestations may progress rapidly in smokers, patients with diabetes and patients with chronic renal failure. Peripheral arterial disease is associated with complications that include ischemic leg pain at rest, ulceration and gangrene. In addition, the mortality rate among patients with peripheral arterial disease is higher than that of the general population. Mortality is mainly due to concomitant coronary artery disease and cerebrovascular disease rather than to the peripheral arterial disease itself.

• Patients with peripheral arterial disease can be asymptomatic, have non critical symptoms or have critical symptoms that include ischemic leg pain, leg ulcers and gangrene. In fact, 20% to 50% of patients with peripheral arterial disease are asymptomatic.^[1]
• The need of revascularization and amputation is relatively low. Lifestyle modifications and medical management is sufficient to treat asymptomatic to mild PAD. However, severe ischemia requires revascularization surgeries as definitive treatment.
• The progression of non critical claudication symptoms is as follows:
  • Symptoms remain stable in 70-80% of patients within five years.
  • Symptoms worsen in 10-20% of patients within five years and can include rest pain, ulcers and gangrene.
  • Symptoms progress to critical limb ischemia in 1-2% within five years.^[2]

Below is an image summarizing the natural history of PAD. To note is that mortality in PAD is related to associated cardiovascular disease rather than PAD per se:

• Patients with PAD are at a higher risk for major cardiovascular events, especially myocardial infarction (MI), stroke and death which are related to the atherosclerotic pathophysiological basis of PAD and not directly related to PAD itself.
• Patients limb-related complications directly linked to the PAD may include:
  • Blood clots or emboli that block off small arteries
  • Lower extremity ulcers
  • Gangrene
  • Need for amputation.

• Amputation:

• The rate of amputation is relatively low in patients with PAD and it is estimated to be almost 1% per year.
• Patients who do not quit smoking have two fold higher risk of amputation than patients who quit smoking.
• Patients who have diabetes have 25% risk of amputation within 10 years.
• Patients who present with acute critical limb ischemia have 10 to 30% risk of amputation within 30 days.^[3]

• Patients with peripheral arterial disease have a 15 to 30 % five year mortality rate, which is two to six times higher than that of the general population.
• The mortality associated with the peripheral vascular disease is rarely directly related to the disease itself but it is rather related to the co-existing coronary and cerebrovascular diseases.^[3]
  • Presence of peripheral arterial disease in a patient correlates strongly with a higher cardiovascular and cerebrovascular mortality rate.^[4]
  • 30 to 50% of the patients with symptomatic PAD have evidence of coronary artery disease, whereas 15% to 25% of symptomatic PAD patients have evidence of significant carotid artery stenosis.^[5]
• Patients with PAD have a twofold to fourfold increase in the risk of all-cause mortality and a threefold to sixfold increase in the risk of cardiovascular death compared to patients without PAD.
• All patients with PAD should be targeted with the same secondary prevention goals as patients with coronary artery disease.

Shown below is an image depicting the overlap between peripheral artery disease, cardiovascular disease and cerebrovascular disease:

• Severity of symptoms:

• Non critical claudication: 15-30% five year mortality rate
• Critical claudication (Limb rest pain, ulcers, gangrene): 25% one year mortality rate

• ABI:

• Normal ABI in the presence of symptoms: no change in the mortality rate
• ABI < 0.85: 10% five year mortality rate
• ABI < 0.4: 50% one year mortality rate

• Tobacco use:

• Two fold increase in mortality

• Diabetes:

• Increase in all causes of mortality

• Location of the arterial occlusive disease:

• Aorticoliliac: 73% five year survival
• Femoral: 80% five year survival^[2]

Shown below is a table depicting the five year primary patency rates in affected vessels following angioplasty with or without stenting versus that following bypass grafting:

Location	Angioplasty ± Stenting	Bypass grafting
Distal aorta/proximal common iliac artery	51 – 88%	80 – 90%
Distal common iliac artery	56 – 65%	Vein: 60 – 75%, Synthetic: 55 – 62%
Proximal external iliac artery	40 – 56%	Vein: 60 – 70%, Synthetic: 55 – 62%
Distal external iliac artery	10 – 40%	Vein: 50 – 60%, Synthetic: 10 – 15%

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