Peripheral Artery Disease
The recommendations in this chapter arose from issues concerning the symptomatic expression of peripheral artery disease (PAD), assessment of PAD’s severity, and consistency with other listings. Not all symptomatic patients with PAD present with intermittent claudication. Some symptoms are atypical, and the most severe cases present not with claudication, but with rest pain. In terms of assessing impairment severity, the ankle-brachial index (ABI) is a good test, but in some instances it needs to be augmented or replaced by other testing techniques. In addition, because hemodynamic severity as measured by ABI and other techniques is not strongly associated with degree of symptoms or functional limitation, evidence of functional limitation consistent with severe PAD should also be required. Logically, and for consistency with other cardiovascular listings, three hospitalizations within 1 year for PAD should be a way to meet the functional criterion. Also, for consistency with other listings, the functional limitation for PAD should be the same as that defined for the musculoskeletal system, that is, inability to ambulate effectively.
Peripheral artery disease1 (PAD) is a condition that occurs when arteries outside the heart and brain become narrowed or obstructed. The
most common cause of PAD is a buildup of plaque inside the arteries, called atherosclerosis, which reduces the flow of blood to the extremities. Most people with early PAD do not experience symptoms. However, if left untreated, PAD may progress to the point that the muscles are starved for oxygen when a person uses them to walk or climb stairs. The resulting pain, called claudication, is usually intermittent, that is, it goes away when the person stops exercising. In more severe cases of PAD, the person may experience pain even when resting, and leg or foot wounds may not heal normally. In a small percentage of cases, the circulation of blood may become so reduced that severe ischemic muscle damage results, and amputation may be required.
Medically, PAD is of grave concern because it is a strong sign of systemic atherosclerosis and thus a high risk of a heart attack, ischemic stroke, and vascular death. The risk of heart attack is 20 to 60 percent higher, the risk of stroke is 40 percent higher, and the risk of death from coronary heart disease is two to six times higher than in people without PAD (Hirsch et al., 2006). Several studies have shown that the more severe the symptoms of PAD, the higher the mortality rate due to heart attack or stroke (Belch et al., 2003).
PAD itself rarely causes death (unless an ischemic limb is untreated for too long), but it can cause substantial morbidity and disability. Individuals with PAD have a reduced peak exercise capacity that limits their range of physical functioning. For example, they have less capacity to walk than otherwise similar individuals without PAD. If they have progressed to intermittent claudication, they have substantial limitations on their capacity to walk. In severe cases, claudication, muscle weakness or numbness, ischemic leg pain at rest, or ulceration will interfere with a person’s ability to work.
According to the National Health and Nutrition Examination Survey (NHANES), approximately 5 percent of U.S. adults ages 40 or older (more than 5 million individuals) had PAD (defined as an ankle-brachial index [ABI] of less than 0.90 in either leg) for the period 1999 to 2002 (PauloseRam et al., 2005). Of these, approximately one-fourth had moderate to severe PAD, defined as an ABI less than 0.70 in either leg. These rates went up sharply with age and were higher among men than women, among non-Hispanic blacks than among non-Hispanic whites or Mexican Americans, and in individuals with diabetes than nondiabetic individuals. A more recent systematic review of U.S. prevalence, that included NHANES findings
and was corrected for biases—such as not including persons with previous revascularization or a high ABI (i.e., an ABI greater than 1.4), found a PAD prevalence of 8.5 million in 2000 (Allison et al., 2007).
The majority of individuals with PAD are asymptomatic. According to several large population studies, the prevalence of symptomatic PAD (i.e., claudication) by age group is about 0.6 percent for those ages 30 to 39, 1.2 percent for those ages 40 to 49, 2.3 percent for those ages 50 to 59, and 3.2 percent for those ages 60 to 64. Prevalence increases sharply among older individuals—to 6 percent among those ages 64 to 69 and 7 percent among those ages 70 to 74 (Norgren et al., 2007).
Intermittent claudication is approximately twice as common among PAD patients with diabetes. PAD in nondiabetic patients also progresses more quickly and is more likely to involve distal vessels, and the need for amputation because of critical leg ischemia is 5 to 10 times higher (Norgren et al., 2007).
DIAGNOSTIC CRITERIA AND METHODS
The physical examination of patients presenting with pain during exercise includes checking for abnormal leg pulses, for bruits, and for cool or ulcerated skin. However, physical examination findings are not sufficient for a diagnosis of PAD, even combined with a history of risk factors, such as smoking, high blood pressure, or high cholesterol (Criqui et al., 1985; Khan et al., 2006).
The definitive method or “gold standard” for diagnosing PAD is contrast angiography because of its ability to provide detailed information about arterial anatomy. However, contrast angiography is invasive and carries some risk. Therefore, the American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the management of patients with PAD recommend that contrast angiography be used only when revascularization is contemplated (Class I Recommendation, Level of Evidence: B) (Hirsch et al., 2006).
Short of situations in which revascularization is being considered, the ACC/AHA guidelines indicate that “Patients with vascular disorders can usually be assured that an accurate anatomic diagnosis will be made with modern noninvasive vascular diagnostic techniques (e.g., ankle- and toe-brachial indices, segmental pressure measurements, pulse volume recordings, duplex ultrasound imaging, Doppler waveform analysis, and exercise testing)” and that “these tests will usually provide adequate information for creation of a therapeutic plan.” When required, these physiological and anatomic data can be supplemented by use of magnetic resonance angiography (MRA), computed tomography angiography (CTA), and selective use of invasive aortic and lower extremity angiographic techniques (Hirsch et al., 2006:e490).
Ankle-Brachial and Toe-Brachial Indexes
The most common method to establish or rule out a diagnosis of lower extremity PAD is the ABI because it is reasonably accurate, has good sensitivity and excellent specificity, and is easy to perform, inexpensive, and noninvasive. The ABI is the ratio of systolic blood pressure at the ankle to the systolic blood pressure in the brachial artery of the upper arm. Normal ABI values are between 1.00 and 1.40.2 Abnormal ABI values are 0.90 or less (values of 0.91 through 0.99 are considered to be borderline) (Hirsch et al., 2006). An ABI of 0.90 usually indicates vessel blockage in a major vessel of at least 50 percent (Dormandy et al., 1999).
ABI values of 0.41 to 0.90 are considered to represent mild to moderate PAD. Values of 0.40 or less indicate severe PAD and a high risk of amputation due to critical limb ischemia (Hirsch et al., 2006). A 20 percent or greater decrease in the ABI after exercise is also diagnostic for PAD, and the more severe the disease, the longer it takes for the ankle pressure to return to normal after exercise (Gerhard-Herman et al., 2006).
Studies of the sensitivity, specificity, and accuracy of the ABI as a tool to diagnose peripheral artery blockage of 50 percent or more, using contrast angiography as the standard, have found that the ABI has a sensitivity of 72 to 95 percent, specificity of 96 to 100 percent, positive predictive value of 90 to 100 percent, negative predictive value of 96 to 99 percent, and overall accuracy of 98 percent (Hirsch et al., 2006). In unselected populations, sensitivity is about 80 percent and specificity is about 96 percent (higher values are from studies that compare extremes: patients scheduled for intervention with young healthy controls) (Criqui and Ninomiya, 2006).
The highest brachial and ankle blood pressure readings are used in clinical practice and are required by the current listing for PAD. However, two recent studies have found that the ABI based on the average pressure in each ankle has the strongest statistical association with leg function (Allison et al., 2010; McDermott et al., 2000). One of the studies, the Multi-Ethnic Study of Atherosclerosis (MESA), compared three ways to measure ankle pressure in a given leg to compute the ABI: (1) the higher of the dorsalis pedis artery and posterior tibial artery pressures, (2) the lower of the dorsalis pedis artery and posterior tibial artery pressures, and (3) the mean of these two ankle pressures (Allison et al., 2010). The prevalence of PAD in the study population was three times higher using the lower pressure than
using the higher pressure. The MESA study also calculated the sensitivity and specificity of the alternative ABIs in predicting several subclinical measures of atherosclerosis (e.g., coronary artery calcium, thickness of carotid artery plaque) and several risk factors (e.g., smoking, dyslipidemia). The finding was that using the ABI based on the lower pressure reading is more sensitive, but less specific than the ABI based on the higher pressure (the average of the two pressures was intermediate). In other words, using the higher pressure reading results in a specificity of 98 to 99 percent, which results in few false positives. However, the lower sensitivity leads to more false negatives. On the other hand, while using the lower pressure value is more sensitive, it is less specific and results in more false positives.
The major limitation of the ABI as a diagnostic test is its inability to obtain accurate results with incompressible arteries due to medial calcification, which can occur in patients with conditions such as diabetes or chronic kidney disease. When the ABI is greater than or equal to 1.40, the toe-brachial index (TBI) should be used because arteries in the toes are much less likely to be calcified. The TBI procedure is similar to the ABI procedure except that it is performed with a photoplethysmograph infrared light sensor and a very small blood pressure cuff placed around the toe. A TBI less than 0.70 is sufficient to diagnose PAD (Hirsch et al., 2006). Ischemic rest pain is common when toe pressures are less than 30 mm Hg (Rutherford et al., 1997). A case-control study of 56 men with stable claudication and toe pressures less than 40 mm Hg found that 34 percent progressed to rest pain, ulceration, or gangrene over 31 months, compared with 9 percent of age-, sex-, and race-matched controls, and that those with diabetes had the highest incidence of deterioration (Bowers et al., 1993).
The ABI has been in use in clinical practice for some time, but it remains more likely to be found in a specialized vascular laboratory than in primary care settings (Mohler et al., 2004). This test is relatively inexpensive and can be done in 15 minutes or less by a trained nurse (Criqui et al., 2008; Pearson et al., 2009). Nevertheless, two-thirds of the participants in a recent program to implement the ABI measurement in primary care outpatient clinics had not measured the ABI of patients prior to participation. They reported that moderate to major barriers to administering the ABI included time constraints (56 percent), lack of reimbursement (45 percent), and limited staff availability (45 percent) (Mohler et al., 2004).
The TBI is rarely measured in primary care because measurement of toe pressure is more time consuming and technically difficult and requires additional equipment (Brooks et al., 2001).
Other Diagnostic Methods
Other noninvasive, inexpensive, and relatively safe diagnostic methods that provide diagnostic discrimination include segmental pressure measurements, pulse volume recordings, duplex ultrasonography, Doppler waveform analysis, and ABI after exercise testing (Hirsch et al., 2006). Segmental pressure measurements help to identify the location of arterial blockages. Pulse volume recording is another useful technique for diagnosing PAD, especially in people with incompressible arteries. Continuous-wave Doppler ultrasound measurements of blood flow with duplex imaging are useful in assessing PAD severity and location. Pulse volume recording and Doppler ultrasound are often used to assess the results of revascularization.
Exercise treadmill tests are used to diagnose PAD, provide objective evidence of the degree of the functional limitations of PAD, identify any non-PAD exercise limitations, and determine the safety of prescribing an exercise program, as well as to measure the response to therapy. According to the ACC/AHA guidelines, a standardized exercise protocol should be used with a motorized treadmill to measure pain-free walking distance and maximal walking distance. Generally, the treadmill should be programmed to provide a progressive workload beginning at a less intense level than used for healthy individuals and patients with coronary heart disease, such as the Gardner-Skinner, Hiatt, or Naughton protocols. ABI values should be determined before and after the test to ensure that the claudication symptoms are due to PAD and not to other causes (Hirsch et al., 2006). A decrease in ABI of 15 to 20 percent is diagnostic of PAD (Norgren et al., 2007).
Treadmill testing is not suitable for patients who, due to age or other reasons, are not able to exert themselves enough to allow reliable results. In such cases, a 6-minute walk test may be used to obtain an objective assessment of functional limitation and response to therapy (Hirsch et al., 2006). Another useful exercise test is the “heel rise test,” where the patient repeatedly raises up on his or her toes with hands outstretched against a wall for balance. The drop in ankle pressure with this test correlates quite highly with that seen during a standard treadmill test (Amirhamzeh et al., 1997; McPhail et al., 2001).
MRA and CTA, as with contrast angiography, could be used to diagnose PAD, but they are expensive; are usually done with intravenous
contrast, which is invasive; and are considered to be most useful for identifying patients who are suitable candidates for endovascular or surgical revascularization (Hirsch et al., 2006).3
Clinical guidelines for diagnosis and management of PAD in the United States were first issued by ACC and AHA in 2005 (Hirsch et al., 2006), although clinicians previously accepted the idea that they should aggressively treat PAD symptoms to reduce functional loss, increase quality of life, and decrease rates of amputation. Also well recognized was the idea that aggressive risk factor modification was needed to lower the incidence of cardiovascular events, especially heart attack and stroke, stemming from the systemic atherosclerosis that a diagnosis of PAD strongly signals (Belch et al., 2003).
The 2005 ACC/AHA guidelines emphasize the reduction of atherosclerotic risk factors, such as smoking, diabetes, high cholesterol, hypertension, lack of exercise, and poor diet (Hirsch et al., 2006). These steps are prescribed primarily to reduce the likelihood of a heart attack or stroke, but they may also slow atherosclerosis of the lower limbs, and thus slow, halt, or reverse the progressive loss of functional capacity and the development of critical limb ischemia and limb loss.
Ideally, patients with PAD should be treated aggressively for their underlying atherosclerosis. Treatment includes smoking cessation, taking antihypertensive and lipid-lowering medications, controlling diabetes when present, and taking blood-thinning medications such as aspirin or clopidogrel.4 Therapies known to improve the effects of claudication specifically on functional capacity (e.g., exercise tolerance or walking distance) include smoking cessation, supervised walking exercise, medication, and if indicated, revascularization through angioplasty or surgery. Specific findings include the following:
Patients with intermittent claudication who stop smoking are much less likely to progress to rest pain (Jonason and Bergström, 1987) or critical leg ischemia (Hobbs and Bradbury, 2003). However, a meta-analysis did not find that smoking cessation improved maximal treadmill walking distance (Girolami et al., 1999).
The ACC/AHA guidelines recommend that individuals with PAD who smoke should be advised to stop smoking and be offered comprehensive smoking cessation interventions, including behavior modification therapy, nicotine replacement therapy, or bupropion (Class I Recommendation, Level of Evidence: B) (Hirsch et al., 2006).
Many studies have shown that supervised exercise training doubles pain-free walking distance and maximal walking time on average (Hirsch et al., 2007; Watson et al., 2008). The ACC/AHA guidelines recommend a program of supervised exercise training as an initial treatment modality for patients with intermittent claudication. The supervised exercise training should be performed for a minimum of 30 to 45 minutes, at least 3 times per week, for 12 or more weeks (Class I Recommendation, Level of Evidence: A) (Hirsch et al., 2006). However, few such programs exist because of lack of reimbursement by health insurers.
Cilostazol, a phosphodiesterase inhibitor, was approved by the Food and Drug Administration (FDA) in 1999 for the treatment of claudication after it was shown in six controlled clinical trials to increase pain-free and maximal constant-load treadmill walking distances by 65 to 98 percent and 40 to 76 percent, respectively (Regensteiner et al., 2002). The same meta-analysis found that patients on cilostazol reported significantly greater gains in community walking distances and speeds according to the Walking Impairment Questionnaire than did patients on placebo.
The ACC/AHA guidelines agree that cilostazol (100 mg orally two times per day) is an effective therapy to improve symptoms and increase walking distance in patients with lower extremity PAD and intermittent claudication. Therefore, the guidelines recommend that a therapeutic trial of cilostazol should be considered in all patients with lifestyle-limiting claudication (Class I Recommendation, Level of Evidence: A). Cilostazol cannot be used in patients with heart failure, however, because of possible adverse side effects (Hirsch et al., 2006).
Pentoxifylline (400 mg three times per day) may be considered as second-line alternative therapy to cilostazol to improve walking distance in patients with intermittent claudication, although improvement has been shown to be better with cilostazol (Class IIb Recommendation, Level of Evidence: A) (Hirsch et al., 2006). No other medications are recommended at this time, or have been approved by FDA, although a number are being developed and tested.
The most common side effects of cilostazol are gastrointestinal complaints, including nausea or change in stool characteristics
(approximately 15 percent for each), headache (approximately 30 percent), and palpitations (9 percent). Side effects usually lessen with continued use (Carman and Fernandez, 2006). A study of long-term effects of cilostazol did not find increased mortality or serious bleeding events (Hiatt et al., 2008b). The most common side effects of pentoxifylline are also gastrointestinal (Carman and Fernandez, 2006).
The absolute gains in distance from medication are modest. For example, patients taking cilostazol were able to walk an average of 100 additional meters on a graded treadmill test before they were forced to stop by symptoms (350 instead of 250 meters) (Regensteiner et al., 2002).
Revascularization should be considered for patients with severe, lifestyle-limiting symptoms, such as severe claudication or rest pain despite medical therapy for 3 months. Endovascular procedures (e.g., percutaneous angioplasty and stents) are usually effective, but open surgical procedures (e.g., bypass or endarterectomy) are indicated in certain patients (Hirsch et al., 2007).
According to the ACC/AHA guidelines for PAD, endovascular procedures are indicated for individuals with a vocational or lifestyle-limiting disability because of intermittent claudication when clinical features suggest a reasonable likelihood of symptomatic improvement with endovascular intervention and (1) there has been an inadequate response to exercise or pharmacological therapy or (2) there is a very favorable risk–benefit ratio (e.g., focal aortoiliac occlusive disease) (Class I Recommendation, Level of Evidence: A) (Hirsch et al., 2006).
Surgical revascularization for claudication is rarely indicated. Patients are initially treated with an endovascular intervention, and bypass surgery is an option only if that fails. According to the guidelines, surgical interventions are indicated for individuals with claudication symptoms who have a significant functional disability that is vocational or lifestyle limiting, who are unresponsive to exercise or pharmacotherapy, and who have a reasonable likelihood of symptomatic improvement (Class I Recommendation, Level of Evidence: B) (Hirsch et al., 2006).
Blood carries oxygen and nutrients needed for the body to live and function. PAD results in reduced blood flow to the muscles and nerves of the lower extremities. In advanced cases, the reduced flow of blood can cause muscle pain, weakness, and numbness when an individual walks or even,
in more severe cases, when an individual is at rest. A person with advanced PAD may also develop leg ulcers that will not heal. In the most severe instances, the muscles may die and the lower leg or foot must be amputated. The resulting limitations on mobility may become severe enough to prevent an individual with PAD from engaging in substantial gainful activity.
PAD and Work
An intensive literature search found neither research on the participation of persons with PAD in the workforce generally, nor more detailed analyses of workforce participation by ABI score or by any other objective laboratory test result or medical finding. This lack of research on the employment effects of PAD may be explained by its relatively low prevalence in the working-age population. Furthermore, most people who have PAD are asymptomatic, and many people with ischemic symptoms think these are due to aging or other medical conditions and do not report them.
An article on the impact of surgery for PAD on returning to work examined a retrospective follow-up study in Finland of 67 middle-aged patients (mean equals 53 years). Of those, 63 had a positive outcome based on vascular criteria. Of the 50 patients not yet retired at the time of the surgery, 41 returned to work. After 10 years, only 9 of the 41 who had returned to work were still working. Of the rest, 13 had retired (most due to the progression of PAD), and 19 had died. A preoperative ABI less than or equal to 0.50 or less was associated with increased risk of death but not with the rate of return to work (Peräkylä et al., 1994).
PAD and Functional Limitation
In the absence of research on the predictors of employment of those with PAD, its impact on functions that are plausibly related to work, such as exercise tolerance or ability to walk a certain distance or speed, must serve as proxies for work disability. A number of studies have examined the association between ABI and various measures of functional ability (Eberhardt et al., 2005; McDermott et al., 1998, 2002, 2007, 2009; Selvin and Hirsch, 2008). A few studies have looked at the association of PAD with measures of peak exercise capacity on a treadmill (Hiatt et al., 1990).
These studies consistently found that patients with PAD are functionally impaired and that the degree of functional limitation increased as clinical measures of impairment worsened. The studies found, for example, that:
Less than 40 percent of the participants with an ABI lower than 0.40 could walk continuously for 6 minutes compared with more
than 95 percent of those with an ABI between 1.00 and 1.50 (McDermott et al., 2002);
Patients with abnormal (less than 0.90) ABIs walked significantly shorter distances than those with normal ABIs (McDermott et al., 1998);
The hazard ratios for losing the ability to walk one-quarter mile or walk up and down one flight of stairs without assistance more than 5 years from diagnosis were 4.16 for severe PAD (ABI less than 0.50), 3.82 for moderate PAD (ABI between 0.50 and 0.69), and 3.22 for mild PAD (ABI between 0.70 and 0.89) (McDermott et al., 2009); and
The NHANES 1999–2004 survey found that 51 percent of individuals ages 60 and older with an ABI less than 0.90 reported difficulty walking for a quarter mile, walking up 10 steps without resting, or walking from one room to another on the same level, compared with 33 percent of those in the same age group overall (Selvin and Hirsch, 2008).
Studies have also found that the impact of PAD on health-related quality of life is substantial. In one study, the impact was comparable to that of other cardiovascular conditions, although PAD patients were most affected by calf pain while other cardiovascular patients were most affected by chest pain, shortness of breath, and palpitations (Regensteiner et al., 2008).
Although ABI and other measures of hemodynamic severity are clearly associated with functional capacity, especially at the very low and high ends of the scale, they are not strong predictors of functional limitations. For example, the correlation of ABI at rest with walking ability on a treadmill of a given individual is low (Hiatt et al., 1988). This is probably due to a number of factors, including individual differences in comorbidities, muscle pathology, leg blood flow, and conditioning (Brass et al., 2004: McDermott et al., 2001). As a result, some patients with a low ABI will have little walking impairment, while others with a higher ABI will have marked walking impairment (Hirsch et al., 2006). In this situation, ABI or other blood pressure measure is not sufficient to sharply differentiate claimants who are unable to work from those who are able to work without additional evidence of functional limitations consistent with incapacity to work.
The listing for PAD requires the existence of intermittent claudication plus specified test results based on ankle or toe blood pressure readings (Box 8-1). This results in four sublistings for PAD. The first, 4.12A, requires intermittent claudication and a resting ABI less than 0.50. The second,
Current Listing for Peripheral Arterial Disease
4.12 Peripheral arterial disease, as determined by appropriate medically acceptable imaging (see 4.00A3d, 4.00G2, 4.00G5, and 4.00G6), causing intermittent claudication (see 4.00G1) and one of the following:
SOURCE: SSA, 2008.
4.12B, is applied when a claimant has intermittent claudication and the ABI is at 0.50 or higher (but rarely if it is 0.80 or higher). Sublisting 4.12B is met if there is intermittent claudication and systolic blood pressure at the ankle drops by half or more during a treadmill exercise test and does not recover for 10 minutes or longer.
The third and fourth sublistings were added when the PAD listing was revised in 2006. Sublisting 4.12C requires intermittent claudication and resting toe systolic blood pressure of less than 30 mm Hg (the normal range is 80 to 110), and sublisting 4.12D requires intermittent claudication and resting toe/brachial systolic blood pressure to be less than 0.40 (the normal range is greater than or equal to 0.7). The inclusion of toe pressures addressed the fact that the ankle blood pressure readings are not a valid measure of PAD in individuals with abnormally stiff ankle arteries because of medial arterial calcification or other causes.
The PAD listing must also be read in conjunction with part 4.00G, “Evaluating Peripheral Vascular Disease,” of the introductory section to the cardiovascular system:
The serious effects of PAD are delineated in 4.00G1 (“What is peripheral vascular disease?”): “you may have pain in your calf after walking a distance that goes away when you rest (intermittent
claudication); at more advanced stages, you may have pain in your calf at rest or you may develop ulceration or gangrene.”
4.00G2 (“How do we assess limitations resulting from PVD?”) indicates that the Social Security Administration (SSA) will assess the claimant’s limitations based on symptoms together with physical findings, Doppler studies, other appropriate noninvasive studies, or angiographic findings (the last if they are already in the medical record, because SSA will not pay for invasive tests due to risk and cost).
4.00G5 (“When will we purchase exercise Doppler studies for evaluating peripheral arterial disease?”) outlines the policies regarding the purchase of exercise Doppler studies. SSA will pay for an exercise Doppler study if one has not been done or if it is needed to determine if the claimant meets sublisting 4.12B, and a disability determination services (DDS) medical consultant, “preferably one with experience in the care of patients with cardiovascular disease,” determines the test would not be risky or would otherwise be contraindicated. SSA requires the exercise test to be performed on a treadmill at 2 mph on a 12 percent grade for up to 5 minutes. Blood pressures at the ankle are measured after exercise and the time required for the systolic blood pressure to return to or near to the preexercise level is determined.
4.00G6 (“Are there any other studies that are helpful in evaluating PAD?”) lists recording ultrasound Doppler unit and strain-gauge plethysmography as additional tests useful in evaluating the severity of PAD, especially if there is small vessel disease or medial arterial calcification.
4.00G7 (“How do we evaluate PAD under 4.12?”) and 4.00G8 (“How are toe pressures measured?”) describe the acceptable techniques for taking systolic blood pressures at the ankle and toe and determining ankle-brachial and toe-brachial indexes.
4.00G9 (“How do we use listing 4.12 if you have had a peripheral graft?”) says that current severity after peripheral grafting is based on Doppler studies measuring the flow of blood through the bypass vessel, not findings that precede the bypass surgery.
CONCLUSIONS AND RECOMMENDATIONS
The fundamental conclusion regarding evaluation of PAD disability is that hemodynamic measures such as the ABI do not adequately distinguish between individuals able to work and individuals unable to work. Individuals with an ABI less than 0.50, for example, will have a range of ability to function. Some individuals will be able to work despite intermittent clau-
dication, and others will be unable even though they do not report typical symptoms of intermittent claudication. At the same time, some patients with PAD who have an ABI greater than 0.50 can have a severe walking impairment that limits their ability to work. Adopting more severe values, that is, an ABI less than 0.4, would make the PAD listing more specific, but would increase the number of false negatives, thus increasing the number of legitimate claimants having to go through Steps 4 and 5 to be allowed. Alternatively, adopting an ABI greater than 0.50 would be more sensitive and reduce the number of claims going through Steps 4 and 5, but there would be more false positives.
The basic recommendation for improving the PAD listing as an early screening tool is to supplement the medical diagnostic and severity requirements with evidence of severe functional limitations. Because PAD’s path to disability is functional limitations on mobility, the committee recommends using the criteria for lower body disability used in the musculoskeletal listings. The committee also recommends some clarifications in and medical updates of listing 4.12.
Appropriate PAD Diagnostic Techniques
Listing 4.12 currently requires a diagnosis of PAD based on “appropriate medically acceptable imaging,” which is defined in the introductory section to the cardiovascular system listings as a technique to diagnose and evaluate PAD that is widely accepted as accurate by the medical community.5 The ACC/AHA PAD guidelines list a number of acceptable methods for diagnosis besides the ABI, including duplex ultrasound imaging, Doppler waveform analysis, CTA, MRA, and contrast angiography (Hirsch et al., 2006), which all have high sensitivity and specificity (Collins et al., 2007). In practice, however, a diagnosis of PAD is usually based on the ABI, and the other diagnostic methods are reserved for cases in which further evaluation is needed to make the diagnosis and determine appropriate medical management or to help guide decisions to intervene invasively.
Technically, the Doppler techniques used to determine ankle and toe blood pressures do not produce images. Similarly, the techniques used to record waveforms do not produce images. Also, although duplex ultrasonography images the leg arteries with B-mode ultrasound, it also measures flow velocity with pulsed Doppler, and the latter technique—which is not imaging—is often the main basis for a diagnosis of PAD.
The committee was informed that SSA considers Doppler studies to be appropriate medically acceptable imaging. However, to eliminate confusion, the committee recommends that the phrase “appropriate medically acceptable imaging” in 4.12 be revised to say “appropriate medically acceptable testing.” This revision would also be consistent with the ACC/AHA PAD guidelines, which also consider another nonimaging modality, treadmill exercise testing with or and without preexercise and postexercise ABIs, to be an appropriate diagnostic technique (see Recommendation 8-1a).
Appropriate PAD Symptom Requirements
Current listing 4.12 requires “intermittent claudication,” which is calf pain that develops from walking that goes away soon after the claimant stops walking (4.00G1). Intermittent claudication is considered to be the classic symptom of PAD. It is an appropriate listing requirement because it is usually associated with severe functional limitations on ability to walk and climb stairs. However, other symptoms in the absence of intermittent claudication can also indicate inability to engage in any gainful activity. For example, some individuals with an ABI less than 0.50 experience atypical leg symptoms that are as disabling as symptoms of intermittent claudication (McDermott et al., 2001). In addition, individuals may apply to SSA for disability benefits with advanced-stage symptoms that have succeeded an earlier period of intermittent claudication. These include rest pain (i.e., constant leg pain), ulceration, or gangrene. These are appropriately mentioned in the introductory section to the cardiovascular system listings, but they are not in the PAD listing as an alternative to intermittent claudication.6
The committee understands that if a claimant has atypical leg pain attributable to PAD that limits walking, but meets the other requirements of 4.12 (e.g., an ABI less than 0.50), a finding of medical equivalence could be made. In this case, the atypical leg pain would substitute for the missing finding of “intermittent claudication.” Similarly, if the claimant’s PAD has already progressed beyond intermittent claudication to rest pain, ulcers, or gangrene, but otherwise satisfies the requirements of 4.12, a finding of medical equivalence would be possible.
The committee recommends that, rather than rely on equivalence, a broader set of symptoms be permitted to meet the listing than intermittent claudication alone (see Recommendation 8-1b).
Add Treatment Requirement
Treatments for PAD exist (described above) that reduce symptoms and increase mobility and quality of life. These include supervised physical rehabilitation, medications, and, if indicated, angioplasty or bypass surgery. The committee recommends that a requirement that the applicant be on a regimen of prescribed treatment be added to the listing (see Recommendation 8-1c).
PAD Severity Requirements
Listing 4.12 currently requires one of four test results: (1) an ABI less than 0.50, (2) a TBI less than 0.40, (3) a resting toe systolic pressure less than 30 mm Hg, or (4) a drop in resting ankle systolic pressure of at least 50 percent during exercise on a treadmill that requires at least 10 minutes to recover to the preexercise level.
The committee discussed the ABI values that currently meet the PAD listing. For evaluating disability, SSA strongly prefers clinical tests that are very sensitive (which would screen in the highest percentage of claimants unable to work as possible) and very specific (which would screen out as many individuals who can work as possible). As with all clinical screening tests, however, there is a trade-off between sensitivity and specificity. In this case, the higher the ABI, the more claimants unable to work will meet the Listings and be allowed, but also the more claimants who can work will be allowed. For example, if an ABI less than or equal to 0.90 met the listing, it would be highly sensitive because the vast majority of those with PAD and unable to work would be allowed. This gain would come at the cost of specificity, however, because many individuals with PAD who could work would be included. Similarly, if the listing required an ABI less than or equal to 0.10, the specificity would be very near, if not equal to, 100 percent, but the sensitivity would be very low, because only a small proportion of those unable to work would be allowed. There would be no false positives, but this would make the listing ineffective as an administrative device for speeding decisions on obvious allowances.
Because some individuals with an ABI less than 0.50 can work, the committee considered recommending a decrease in the ABI requirement in the PAD listing to less than 0.40. An ABI less than 0.40 is the point at which critical leg ischemia becomes a danger, potentially requiring an endovascular or surgical intervention soon, if not immediately, to prevent gangrene and amputation. Virtually everyone with this ABI score has severe leg pain and substantial muscle weakness, severely limiting mobility and stamina. Although this test result requirement would be very specific, the decrease in sensitivity would mean that more individuals who actually met
the listing would not be allowed at Step 3 and would have to go through Steps 4 and 5 to be allowed. This would defeat the purpose of the Listings, which is to reduce the percentage of claimants going through Steps 4 and 5 who ultimately will be allowed.
The committee also discussed setting a higher ABI cut-off value, such as 0.70, at which point leg symptoms begin to be common. This would make the listing very sensitive, probably allowing most claimants truly unable to work because of PAD, and it would require fewer Step 4 and 5 determinations. However, it would also reduce specificity and allow more false positives, which would undermine the credibility of the disability program.
Unfortunately, the literature search found no studies of the sensitivity and specificity of an ABI less than 0.50 (or of any other ABI value) for predicting the functional status, however measured, nor of employment status, of working-age individuals. However, based on personal clinical observations by some committee members and logical extrapolation from studies of functional status of individuals with various ABI values, the committee recommends retaining the current ABI value of less than 0.50 to meet the listing, but requiring additional information about the functioning of the claimant (see Recommendation 8-1d).
Also, the PAD listing could be simplified by folding Criteria B, C, and D into a new, broader criterion, in which tests other than the ABI can be used to establish listing-level severity. These include the TBI, Doppler waveforms, duplex ultrasonography, MRA, CTA, contrast angiography, and graded treadmill tests. The basis for this change is the relative lack of evidence that toe pressures or changes in ankle pressure during exercise are predictive of functional status. The current introductory section to the cardiovascular system, which dates from 2006, notes that medical standards for evaluating exercise toe pressures do not exist, which is still the case. Given that TBI and toe systolic pressure results require interpretation by DDS medical consultants and consultative examiners, SSA might broaden as well the range of tests that can be used to establish listing-level severity (see Recommendation 8-1e). This criterion would apply to claimants with an ABI of 0.50 or greater or with evidence of medical calcification due to diabetes or other causes.
Addition of Functional Assessment of PAD
The committee concludes that an ABI less than 0.50 constitutes a reasonable trade-off between sensitivity and specificity, but it is not totally accurate. Although an ABI less than 0.50 is an indicator of severe PAD, and most individuals with that ABI will be unable to work because of immobility due to leg pain and muscle weakness, some individuals will be able to work. At the same time, some claimants with ABIs of 0.50 or more will
be too functionally limited by pain and weakness to work. Therefore, an ABI less than 0.50 is neither 100 percent sensitive nor specific for inability to work.
The committee concludes that, to increase sensitivity without significantly decreasing specificity, the ABI and other clinical signs should be augmented with an assessment of function. PAD is disabling when it impinges on an individual’s mobility and severely limits or precludes his or her ability to fulfill effectively normal life roles, including the ability to engage in gainful employment. This is equivalent to the requirement in the musculo-skeletal system listings that a claimant be unable to ambulate effectively (Box 8-2). For consistency within the Listings, the committee recommends that SSA apply the same standard in evaluating PAD (see Recommendation 8-1f, below) or accept a history of three hospitalizations within a 12-month period as evidence of listing-level limitations on capacity to work.
1.00 Musculoskeletal System
B.2.b.What we mean by inability to ambulate effectively.
(1) Definition. Inability to ambulate effectively means an extreme limitation of the ability to walk; i.e., an impairment(s) that interferes very seriously with the individual’s ability to independently initiate, sustain, or complete activities. Ineffective ambulation is defined generally as having insufficient lower extremity functioning ... to permit independent ambulation without the use of a hand-held assistive device(s) that limits the functioning of both upper extremities.
(2) To ambulate effectively, individuals must be capable of sustaining a reasonable walking pace over a sufficient distance to be able to carry out activities of daily living. They must have the ability to travel without companion assistance to and from a place of employment or school. Therefore, examples of ineffective ambulation include, but are not limited to, the inability to walk without the use of a walker, two crutches or two canes, the inability to walk a block at a reasonable pace on rough or uneven surfaces, the inability to use standard public transportation, the inability to carry out routine ambulatory activities, such as shopping and banking, and the inability to climb a few steps at a reasonable pace with the use of a single hand rail. The ability to walk independently about one’s home without the use of assistive devices does not, in and of itself, constitute effective ambulation.
SOURCE: SSA, 2008.
RECOMMENDATION 8-1. The requirement for diagnostic evidence of peripheral artery disease (PAD) should be based on appropriate medically acceptable testing, and evidence of listing-level PAD should be based on an ankle-brachial index (ABI) of less than 0.50 or other test results consistent with severe PAD, combined with a requirement that, despite prescribed treatment, (1) leg pain interferes with mobility consistent with the musculoskeletal system listings, or (2) there have been three hospitalizations due to PAD within a 12-month period. Specifically,
Recommendation 8-1a. The word imaging in the phrase “appropriate medically acceptable imaging” currently in 4.12 should be replaced by the word testing or other term broader than imaging, because nonimaging tests such as Doppler techniques are commonly used to diagnose PAD and also to assess its severity.
Recommendation 8-1b. The current requirement in listing 4.12 for the presence of intermittent claudication should be changed to require that “leg pain” caused by PAD be present because the definition of intermittent claudication excludes too many individuals with disabling leg symptoms.
Recommendation 8-1c. Listing 4.12 should require that the applicant be on a regimen of prescribed treatment because therapies exist that can improve functional capacity.
Recommendation 8-1d. Criterion A in listing 4.12—an ABI of less than 0.50—should be retained, coupled with a new requirement for evidence of a severe limitation, such as an extreme functional limitation on effective mobility or three hospitalizations for PAD within a 12-month period (see Recommendation 8-1f).
Recommendation 8-1e. Current criteria B, C, and D in listing 4.12 should be replaced by a new criterion B that an appropriate test or tests be consistent with severe PAD, when the ABI is 0.50 or greater or there is evidence of medial calcification of the ankle arteries. These tests should include the toe-brachial index, Doppler waveforms, duplex ultrasonography, magnetic resonance angiography, computed tomography angiography, contrast angiography, and graded treadmill tests. These test results should be coupled with a new requirement for evidence of a severe functional limitation on mobility or a history of three hospitalizations due to PAD within a 12-month period (see Recommendation 8-1f).
Recommendation 8-1f. Criterion A or new criterion B should be necessary but not sufficient to establish listing-level impairment unless there is also evidence of a severe limitation on mobility, for example, as defined in the musculoskeletal system listings (i.e., “inability to ambulate effectively”) or there is a history of three hospitalizations due to PAD within a 12-month period.
Allison, M. A., E. Ho, J. O. Denenberg, R. D. Langer, A. B. Newman, R. R. Fabsitz, and M.H. Criqui. 2007. Ethnic-specific prevalence of peripheral arterial disease in the United States. American Journal of Preventive Medicine 32(4):328–333.
Allison, M. A., V. Aboyans, T. Granston, M. M. McDermott, A. Kamineni, H. Ni, and M. H. Criqui. 2010. The relevance of different methods of calculating the ankle-brachial index: The multi-ethnic study of atherosclerosis. American Journal of Epidemiology 171(3):368–376. http://aje.oxfordjournals.org/cgi/reprint/171/3/368 (accessed June 4, 2010).
Amirhamzeh, M. M., J. H. Chant, J. L. Rees, L. J. Hands, R. J. Powell, and W. B. Campbell. 1997. A comparative study of treadmill tests and heel raising exercise for peripheral arterial disease. European Journal of Vascular and Endovascular Surgery 13(3):301–305.
Ankle Brachial Index Collaboration. 2008. Ankle brachial index combined with Framingham Risk Score to predict cardiovascular events and mortality: A meta-analysis. Journal of the American Medical Association 300(2):197–208. http://jama.ama-assn.org/cgi/reprint/300/2/197 (accessed June 4, 2010).
Belch, J. J. F., E. J. Topol, G. Agnelli, M. Bertrand, R. M. Califf, D. L. Clement, M. A. Creager, J. D. Easton, J. R. Gavin III, P. Greenland, G. Hankey, P. Hanrath, A. T. Hirsch, J. Meyer, S. C. Smith, F. Sullivan, M. A. Weber, and Prevention of Atherothrombotic Disease Network. 2003. Critical issues in peripheral arterial disease detection and management: A call to action. Archives of Internal Medicine 163(8):884. http://archinte.ama-assn.org/cgi/reprint/163/8/884 (accessed June 4, 2010).
Bowers, B. L., R. J. Valentine, S. I. Myers, A. Chervu, and G. P. Clagett. 1993. The natural history of patients with claudication with toe pressures of 40 mm Hg or less. Journal of Vascular Surgery 18(3):506–511. http://download.journals.elsevierhealth.com/pdfs/journals/0741-5214/PII074152149390269R.pdf (accessed June 4, 2010).
Brass, E. P., W. R. Hiatt, and S. Green. 2004. Skeletal muscle metabolic changes in peripheral arterial disease contribute to exercise intolerance: A point-counterpoint discussion. Vascular Medicine 9(6):293–301. http://vmj.sagepub.com/content/9/4/293.long (accessed July 28, 2010).
Brooks, B., R. Dean, S. Patel, B. Wu, L. Molyneaux, and D. K. Yue. 2001. TBI or not TBI: That is the question. Is it better to measure toe pressure than ankle pressure in diabetic patients? Diabetic Medicine 18(7):528–532. http://www3.interscience.wiley.com/cgi-bin/fulltext/118991958/PDFSTART (accessed June 4, 2010).
Carman, T. L., and B. B. Fernandez Jr. 2006. Contemporary management of peripheral arterial disease: II. Improving walking distance and quality of life. Cleveland Clinic Journal of Medicine 73(Suppl 4):S38–S44. http://www.ccjm.org/content/73/Suppl_4/S38.full.pdf (accessed June 4, 2010).
Collins, R., J. Burch, G. Cranny, R. Aguiar-Ibáñez, D. Craig, K. Wright, E. Berry, M. Gough, J. Kleijnen, and M. Westwood. 2007. Duplex ultrasonography, magnetic resonance angiography, and computed tomography angiography for diagnosis and assessment of symp-
tomatic, lower limb peripheral arterial disease: Systematic review. BMJ 334(7606):1257. http://www.bmj.com/cgi/reprint/334/7606/1257 (accessed June 4, 2010).
Criqui, M. H., and J. Ninomiya. 2006. The epidemiology of peripheral arterial disease. In Vascular medicine: A companion to Braunwald’s heart disease, edited by M. A. Creager, V. J. Dzau, and J. Loscalzo. Philadelphia, PA: Saunders. Pp. 223–238.
Criqui, M. H., A. Fronek, M. R. Klauber, E. Barrett-Connor, and S. Gabriel. 1985. The sensitivity, specificity, and predictive value of traditional clinical evaluation of peripheral arterial disease: Results from noninvasive testing in a defined population. Circulation 71(3):516–522. http://circ.ahajournals.org/cgi/reprint/71/3/516 (accessed June 4, 2010).
Criqui, M. H., M. J. Alberts, F. G. Fowkes, A. T. Hirsch, P. T. O’Gara, and J. W. Olin. 2008. Atherosclerotic Peripheral Vascular Disease Symposium II: Screening for atherosclerotic vascular diseases: Should nationwide programs be instituted? Circulation 118(25):2830–2836. http://circ.ahajournals.org/cgi/reprint/118/25/2830 (accessed June 4, 2010).
Dormandy, J., L. Heeck, and S. Vig. 1999. The natural history of claudication: Risk to life and limb. Seminars in Vascular Surgery 12(2):123–137.
Eberhardt, M. S., S. Saydah, R. Paulose-Ram, and M. Tao. 2005. Mobility limitation among persons aged ≥ 40 years with and without diagnosed diabetes and lower extremity disease—United States, 1999–2002. Morbidity & Mortality Weekly Report 54(46):1183–1186.
Gerhard-Herman, M., J. A. Beckman, and M. A. Creager. 2006. Vascular laboratory testing. In Vascular medicine: A companion to Braunwald’s heart disease, edited by M. A. Creager, V. J. Dzau, and J. Loscalzo. Philadelphia, PA: Saunders. Pp. 146–165.
Girolami, B., E. Bernardi, M. H. Prins, J. W. Ten Cate, R. Hettiarachchi, P. Prandoni, A. Girolami, and H. R. Büller. 1999. Treatment of intermittent claudication with physical training, smoking cessation, pentoxifylline, or nafronyl: A meta-analysis. Archives of Internal Medicine 159(4):337–345. http://archinte.ama-assn.org/cgi/reprint/159/4/337 (accessed June 4, 2010).
Hiatt, W. R., D. Nawaz, J. G. Regensteiner, and K. F. Hossack. 1988. The evaluation of exercise performance in patients with peripheral vascular disease. Journal of Cardiopulmonary Rehabilitation 8(12):525–532.
Hiatt, W. R., J. G. Regensteiner, M. E. Hargarten, E. E. Wolfel, and E. P. Brass. 1990. Benefit of exercise conditioning for patients with peripheral arterial disease. Circulation 81(2):602–609. http://circ.ahajournals.org/cgi/reprint/81/2/602 (accessed June 4, 2010).
Hiatt, W. R., J. Goldstone, S. C. Smith Jr., M. McDermott, G. Moneta, R. Oka, A. B. Newman, and W. H. Pearce. 2008a. Atherosclerotic Peripheral Vascular Disease Symposium II: Nomenclature for vascular diseases. Circulation 118(25):2826–2829. http://circ.ahajournals.org/cgi/reprint/118/25/2826 (accessed June 4, 2010).
Hiatt, W. R., S. R. Money, and E. P. Brass. 2008b. Long-term safety of cilostazol in patients with peripheral artery disease: The CASTLE study (Cilostazol: A Study in Longterm Effects). Journal of Vascular Surgery 47(2):330–336. http://download.journals.elsevierhealth.com/pdfs/journals/0741-5214/PIIS0741521407016096.pdf (accessed June 4, 2010).
Hirsch, A. T., Z. J. Haskal, N. R. Hertzer, C. W. Bakal, M. A. Creager, J. L. Halperin, L. F. Hiratzka, W. R. Murphy, J. W. Olin, J. B. Puschett, K. A. Rosenfield, D. Sacks, J. C. Stanley, L. M. Taylor Jr., C. J. White, J. White, R. A. White, E. M. Antman, S. C. Smith Jr., C. D. Adams, J. L. Anderson, D. P. Faxon, V. Fuster, R. J. Gibbons, S. A. Hunt, A. K. Jacobs, R. Nishimura, J. P. Ornato, R. L. Page, and B. Riegel. 2006. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic). Circulation 113(11):e463–e654. http://circ.ahajournals.org/cgi/reprint/113/11/e463 (accessed June 4, 2010).
Hirsch, A. T., H. Kalsi, and T. W. Rooke. 2007. Peripheral arterial diseases. In Cardiovascular Medicine, 3rd Ed., edited by J. T. Willerson, H. J. J. Wellens, J. N. Cohn, and
D. R. Holmes Jr. London: Springer, Pp. 1681–1703 (Chapter 78). http://www.springer-link.com/content/k44p86174748xl18/fulltext.pdf (accessed June 4, 2010).
Hobbs, S. D., and A. W. Bradbury. 2003. Smoking cessation strategies in patients with peripheral arterial disease: An evidence-based approach. European Journal of Vascular and Endovascular Surgery 26(4):341–347.
Jonason, T., and R. Bergström. 1987. Cessation of smoking in patients with intermittent claudication: Effects on the risk of peripheral vascular complications, myocardial infarction and mortality. Acta Medica Scandinavica 221(3):253–260.
Khan, N. A., S. A. Rahim, S. S. Anand, D. L. Simel, and A. Panju. 2006. Does the clinical examination predict lower extremity peripheral arterial disease? Journal of the American Medical Association 295(5):536–546. http://jama.ama-assn.org/cgi/reprint/295/5/536 (accessed June 4, 2010).
McDermott, M. M., K. Liu, J. M. Guralnik, S. Mehta, M. H. Criqui, G. J. Martin, and P. Greenland. 1998. The ankle brachial index independently predicts walking velocity and walking endurance in peripheral arterial disease. Journal of the American Geriatrics Society 46(11):1355–1362.
McDermott, M. M., M. H. Criqui, K. Liu, J. M. Guralnik, P. Greenland, G. J. Martin, and W. Pearce. 2000. Lower ankle/brachial index, as calculated by averaging the dorsalis pedis and posterior tibial arterial pressures, and association with leg functioning in peripheral arterial disease. Journal of Vascular Surgery 32(6):1164–1171. http://download.journals.elsevierhealth.com/pdfs/journals/0741-5214/PIIS0741521400653016.pdf (accessed June 4, 2010).
McDermott, M. M., P. Greenland, K. Liu, J. M. Guralnik, M. H. Criqui, N. C. Dolan, C. Chan, L. Celic, W. H. Pearce, J. R. Schneider, L. Sharma, E. Clark, D. Gibson, and G. J. Martin. 2001. Leg symptoms in peripheral arterial disease: Associated clinical characteristics and functional impairment. Journal of the American Medical Association 286(13):1599–1606. http://jama.ama-assn.org/cgi/reprint/286/13/1599 (accessed June 4, 2010).
McDermott, M. M., P. Greenland, K. Liu, J. M. Guralnik, L. Celic, M. H. Criqui, C. Chan, G. J. Martin, J. Schneider, W. H. Pearce, L. M. Taylor, and E. Clark. 2002. The ankle brachial index is associated with leg function and physical activity: The walking and leg circulation study. Annals of Internal Medicine 136(12):873–883. http://www.annals.org/content/136/12/873.full.pdf+html (accessed June 4, 2010).
McDermott, M. M., J. M. Guralnik, L. Tian, L. Ferrucci, K. Liu, Y. Liao, and M. H. Criqui. 2007. Baseline functional performance predicts the rate of mobility loss in persons with peripheral arterial disease. Journal of the American College of Cardiology 50(10):974–982. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645658/pdf/nihms45550.pdf (accessed June 4, 2010).
McDermott, M. M., J. M. Guralnik, L. Tian, K. Liu, L. Ferrucci, Y. Liao, L. Sharma, and M. H. Criqui. 2009. Associations of borderline and low normal ankle-brachial index values with functional decline at 5-year follow-up: The WALCS (Walking and Leg Circulation Study). Journal of the American College of Cardiology 53(12):1056–1062.
McPhail, I. R., P. C. Spittell, S. A. Weston, and K. R. Bailey. 2001. Intermittent claudication: An objective office-based assessment. Journal of the American College of Cardiology 37(5):1381–1385. http://content.onlinejacc.org/cgi/reprint/37/5/1381.pdf (accessed June 4, 2010).
Mohler, E. R., III, D. Treat-Jacobson, M. P. Reilly, K. E. Cunningham, M. Miani, M. H. Criqui, W. R. Hiatt, and A. T. Hirsch. 2004. Utility and barriers to performance of the ankle-brachial index in primary care practice. Vascular Medicine 9(4):253–260. http://vmj.sagepub.com/cgi/reprint/9/4/253 (accessed June 4, 2010).
Norgren, L., W. R. Hiatt, J. A. Dormandy, M. R. Nehler, K. A. Harris, F. G. Fowkes, and TASC II Working Group. 2007. Inter-society consensus for the management of peripheral arterial disease (TASC II). Journal of Vascular Surgery 45(Suppl 1):S5–S67. http://download.journals.elsevierhealth.com/pdfs/journals/0741-5214/PIIS0741521406022968.pdf (accessed June 4, 2010).
Paulose-Ram, R., Q. Gu, M. Eberhardt, E. Gregg, L. Geiss, and M. Engelgau. 2005. Lower extremity disease among persons aged ≥ 40 years with and without diabetes—United States, 1999–2002. Morbidity & Mortality Weekly Report 54(45):1158–1160. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5445a4.htm (accessed June 4, 2010).
Pearson, T., G. Kukulka, and Z. Ur Rahman. 2009. Ankle brachial index measurement in primary care setting: How long does it take? Southern Medical Journal 102(11):1106–1110.
Peräkylä, T. K., M. Lepäntalo, R. Lassila, J. A. Pietilä, and O. Lindfors. 1994. Ability to work after arterial surgery for chronic incapacitating ischaemia of the lower limb in middle-aged patients. European Journal of Surgery 160(8):425–429.
Regensteiner, J. G., J. E. Ware Jr., W. J. McCarthy, P. Zhang, W. P. Forbes, J. Heckman, and W. R. Hiatt. 2002. Effect of cilostazol on treadmill walking, community-based walking ability, and health-related quality of life in patients with intermittent claudication due to peripheral arterial disease: Meta-analysis of six randomized controlled trials. Journal of the American Geriatrics Society 50(12):1939–1946. http://www3.interscience.wiley.com/cgi-bin/fulltext/121434226/PDFSTART (accessed June 4, 2010).
Regensteiner, J. G., W. R. Hiatt, J. R. Coll, M. H. Criqui, D. Treat-Jacobson, M. M. McDermott, and A. T. Hirsch. 2008. The impact of peripheral arterial disease on health-related quality of life in the Peripheral Arterial Disease Awareness, Risk, and Treatment: New Resources for Survival (PARTNERS) Program. Vascular Medicine 13(1):15–24. http://vmj.sagepub.com/cgi/reprint/13/1/15 (accessed June 4, 2010).
Rehring, T. F., B. G. Sandhoff, R. S. Stolcpart, J. A. Merenich, and H. W. Hollis Jr. 2005. Atherosclerotic risk factor control in patients with peripheral arterial disease. Journal of Vascular Surgery 41(5):816–822.
Rutherford, R. B., J. D. Baker, C. Ernst, K. W. Johnston, J. M. Porter, S. Ahn, and D. N. Jones. 1997. Recommended standards for reports dealing with lower extremity ischemia: Revised version. Journal of Vascular Surgery 26(3):517–538. http://download.journals.elsevierhealth.com/pdfs/journals/0741-5214/PIIS0741521497700454.pdf (accessed June 4, 2010).
Selvin, E., and A. T. Hirsch. 2008. Contemporary risk factor control and walking dysfunction in individuals with peripheral arterial disease: NHANES 1999–2004. Atherosclerosis 201(2):425–433. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771432/pdf/nihms82490.pdf (accessed June 4, 2010).
SSA (Social Security Administration). 2008. Listing of impairments—Adult listings (Part A). Disability evaluation under Social Security (Blue Book). http://www.socialsecurity.gov/disability/professionals/bluebook/AdultListings.htm (accessed July 22, 2010).
Watson, L., B. Ellis, and G. C. Leng. 2008. Exercise for intermittent claudication. Cochrane Database Systematic Reviews 8(4):CD000990.