Peripheral Arterial Disease, Essay Example

Abstract

A growing health concern for many Americans is Peripheral Arterial Disease (PAD). Affecting multiple arterial circulations, it is often a consequence of systemic disease processes. The burden of this disease typically occurs alongside other cardiovascular risk factors. These may include such factors as diabetes mellitus, (DM), hypertension, smoking or lipid disorders. DM, in particular, is an increasingly important co-factor due to the number of PAD patients with DM continuing to rise. An early manifestation of PAD called intermittent claudication (IC), frequently leads to a reduction in quality of life for patients with limited ambulation. Typical ischemic pain of one or more muscle groups, atypical pain in the body, or no symptoms of pain at all, may be characteristic presentations in a PAD patient with compromised blood flow to their extremities. Arterial occlusion, which causes acute limb ischemia, may also be a life threatening condition associated with PAD.³⁷

Exploring the etiology, risk factors, and clinical manifestations of lower extremity arterial disease will be the focus of this article. This will include PAD as it affects the leg arteries, due to atherosclerosis. Through the understanding of the role of the Acute Care Nurse Practitioner (ACNP) in the treatment options and implications for care, such matters as the frequency of asymptomatic disease, percutaneous intervention, the noninvasive evaluation and management of this disorder through medical therapy, and surgery options will be presented.¹⁰

Introduction

The most typical form of peripheral vascular disease is PAD; characterized by, a partial or absolute failure of the arterial system to transport oxygenated blood to peripheral tissue. ² Lesions and additional symptoms of PAD may occur in both the upper and the lower extremities of the body, however, PAD in general occurs more commonly in the lower extremities. By far, the most common etiology of PAD is atherosclerosis. In the United States, atherosclerotic cardiovascular disease is a rising health concern as witnessed by such issues as the mortality rate due to heart and cerebrovascular diseases. In the elderly population, PAD is a leading cause of morbidity, demonstrating further, the mounting concern for this health problem among that segment of the population.

Epidemiology

PAD and coronary artery disease (CAD) share a number of risk factors. The strongest risk factors for PAD, in addition to age and gender, are hypercholesterolemia, hypertension, hyperhomocystinemia, smoking and diabetes. A 1.5 fold enlarged risk for developing intermittent claudication was conferred by gender, increasing age, and smoking. ³¹  Comparatively, diabetes, and stage 2 or greater hypertension, were connected with more than a 2 fold increase in intermittent claudication, while clinical evidence of coronary artery disease nearly tripled the possibility of IC.¹¹ As well, 20% of symptomatic patients with PAD had diabetes, as revealed by data collected from the Framingham Heart Study. ²⁶ It is obvious that age and gender play a role in the risk factors for PAD; however, the significance of the CAD risk factors exceeds that of age and gender alone for this disease.

Pathophysiology

While atherosclerosis is the leading cause of PAD in patients over 40 years of age, it is essential to note that other causes may include thrombosis, fibromuscular dysplasia, embolism, entrapment, vasculitis, trauma, and cystic adventitial disease. People older than 60 years of age typically have the highest prevalence rate of atherosclerotic PAD. This prevalence rate increases significantly in persons who smoke, and in persons with diabetes mellitus, hypertension, hypercholesterolemia, or hyperhomocysteinemia.³

Research shows that PAD is caused by atherosclerosis. This usually leads to arterial stenosis and occlusions in the chief vessels supplying the lower extremities. To have normal blood flow at rest, and therefore no limb symptoms during this same time period, is emblematic for patients with intermittent claudication. With exercise, the patient may experience occlusive lesions in the arterial supply of the leg muscles, restraining the increase in blood flow. This will result in a divergence between oxygen supply and the muscle metabolic demand that is linked with the indicator of claudication. Another causative factor to the reduced exercise performance of patients with PAD, is the acquired metabolic abnormalities in the muscles of the lower extremities.³⁴

Presentation

The disease progresses from intermittent claudication (IC), which is defined as a pain, ache, cramp, numbness, or a sense of fatigue in the muscles occurring during exercise or walking and relieved by rest, to PAD. The site of claudication is distal to the location of the occlusive lesion. For example, buttock, hip, and thigh discomfort occur in patients with aortoiliac disease, whereas calf claudication develops in patients with femoral-popliteal disease. The elevated incidence of obstructive lesions is more frequently found in the lower extremities of the body than the upper. Improvement is typically observed when the legs are in a dependent position rather than a horizontal resting position. With severe ischemia, rest pain may be persistent.¹³

The majority of patients with PAD have limited exercise performance and walking ability. Reduced physical performance and quality of life are costs associated with PAD. Intermittent claudication is a standard symptom in patients with PAD. IC is indicated by muscle discomfort in a lower limb (mainly calf, thigh, or buttocks), created by exercise and relieved by rest within 10 minutes. Atypical, or even an absence of symptoms in the limbs, may well be linked with walking limitations in patients without classical claudication as well. Classic claudication symptoms may not transpire in patients who have co-morbidities, which prevent ample activity to generate limb symptoms, such as congestive heart failure, severe pulmonary disease and musculoskeletal disease. Also, patients who are so wholly deconditioned that exercise is not performed may not present with classical claudication symptoms. Therefore, if PAD is suspected, patients should be questioned regarding any restrictions they experience throughout exercise that limits their walking capability. ^{4, 34}

Physical examination

Pain: The most widespread symptom of arterial occlusion is pain. It occurs in the distal part, often the toe or feet, as that tissue becomes ischemic. Acute arterial pain differs from chronic arterial pain. Acute arterial pain is usually related to occlusive events and is often described as shooting, throbbing, stabbing or stinging. Patients may be unable to endure a breeze blowing across the skin. As the disease progresses to a more severe degree, frequent physical signs may include thickened nails, hair loss, flat and shiny skin, reduced skin temperature, and pallor or cyanosis of the skin. In patients with critical limb ischemia, ulcers or gangrene may arise. ³⁵

Pulselessness: In chronic arterial disease, the accurateness of pedal pulse palpation is highly erratic. Frequently, the pulses are absent or diminished, indicative but not diagnostic of acute limb injury (ALI). Palpable pulses alone do not rule this out. More useful than the subjective pulse exam, a Doppler is used to assess the presence of the pulse in the absence of a palpable pulse. ³⁴

Pallor: While possibly subject to environmental circumstances, change in color and temperature is a general finding in ALI. These findings are mainly notable when dissimilar from the contra lateral limb. Venous filling may also be slow or deficient. ³⁴ The skin may appear pale and cool on contact as compared to additional areas of the body. Capillary refill should be assessed, with return of color after more than 3 seconds indicating slow arterial circulation. Elevation of the legs and repetitive flexing of the calf muscles generate pallor of the soles of the feet, whereas rubor, secondary to reactive hyperemia, may develop when the legs are dependent. The severity of the ischemia and the attendance of collateral vessels is determined by the time required for rubor to develop, or for the veins in the foot to fill after the patient’s legs are transferred from an elevated to a dependent situation. Severe ischemia in patients may cause the development of peripheral edema since they maintain their legs in a dependent position much of the time. Ischemic neuropathy can result in numbness and hyporeflexia.^{13, 34}

Paresthesia: Numbness occurs in more than half of patients and represents the extreme end of ischemia in chronic occlusive disease. It is necessary to distinguish between diabetic neuropathy and ischemic pain. Diabetic neuropathy is described as tingling, numbness, shooting pain, hot, and cold sensations. Whereas, ischemic pain presents with changes in color, pale or cyanotic coloring, cooler in temperature, shooting, throbbing, stinging, or stabbing pain.

Paralysis: This is suggestive of limb-threatening ischemia and mandates prompt evaluation and consultation with a physician. As such, it is a poor prognostic sign.³⁴

Ulcer and gangrene: Ischemic ulcers or gangrene may well present in patients with critical limb ischemia (CLI). Progression from rest pain into tissue loss is typical of CLI. Gangrene generally affects the digits or, in a patient confined to their bed, the heel. In severe cases, gangrene may possibly entail the distal parts of the forefoot. ³⁴

Diagnostics

Noninvasive Vascular Tests

1. Ankle-brachial indices (ABIs):

The most frequent measure to assess the presence and severity of PAD is the ABI. The ABI offers extrapolative data that are valuable to forecast wound healing as well as limb and patient survival. Having been validated against angiographically confirmed disease and established as being 95% responsive and almost 100% specific, the ABI may be used either as a screening instrument for lower extremity PAD or to observe the efficacy of therapeutic interventions. ^7,14

The ABI is established by dividing the ratio of the systolic blood pressure in the ankle, by the systolic blood pressure in the arm. In order to perform the ABI measurement, a hand-held 5–10 MHz Doppler probe and a blood pressure cuff are required. Measurement is taken by placing the patient in a supine situation for 5 minutes. Following this, the systolic blood pressure is measured in both arms, with the higher rate used as the denominator of the ABI. Measurement of the systolic blood pressure is then taken in the dorsalis pedis and posterior tibial arteries by placing the cuff just over the ankle. The higher rate in each limb is the numerator of the ABI

Based on the ABI, the diagnostic criteria for PAD are interpreted as follows:

Normal if 0.91–1.30

Mild obstruction if 0.70–0.90

Moderate obstruction if 0.40–0.69

Severe obstruction if 0.40

Poorly compressible if 1.30 ³²

Index ranges from 0.91 to 1.30 indicate a normal ankle-brachial reading. A reading above 1.30 is by and large indicative of incompressible tibial arteries. Decreases in the ankle–brachial index are consistent with peripheral arterial disease.

An ankle–brachial index ranging from 0.41 to 0.90 is usually indicative of mild-to-moderate peripheral arterial disease. The presence of severe peripheral arterial disease would be suggested by a reading below 0.40. ^{6, 7}

2. Duplex ultrasound of the extremities:

A valuable instrument with which to establish anatomic position and degree of stenosis of PAD is the duplex ultrasound of the extremities. This is recommended for routine supervision subsequent to femoral-popliteal or femoral-tibialpedal bypass with a venous conduit. Approximately 3, 6, and 12 months following the duplex ultrasound are the suggested minimum supervision intervals, and then yearly following graft placement.

3. Postocclusive reactive hyperemia:

This is performed by occluding arterial flow through the inflation of a blood pressure cuff higher than systolic pressure at the point of the upper thigh or knee for 3 minutes, followed by measurement of the systolic blood pressure at the ankle or calf 15 to 30 seconds after releasing the occlusion. When compared to patients devoid of vascular disease, patients with PAD will exhibit a lower postocclusive ABI and a delayed return to preocclusion pressures. The sensitivity of the postocclusive ABI is >95%. Alternative diagnostic strategies should be used to corroborate the diagnosis of lower extremity PAD for persons presenting with classic claudication, and ABI values in the borderline to above normal ranges (0.91 to >1.30). These alternative methods include the toe-brachial index, ABI after treadmill exercise, segmental systolic blood pressures, or duplex ultrasound.

4. Computed tomographic angiography (CTA):

The use of CTA may be considered in order to establish anatomic location and occurrence of significant stenosis in patients with lower extremity PAD. The CTA may also be considered as an alternate for those patients with contraindications to MRA.

5. Magnetic resonance angiography (MRA):

Selecting patients with lower extremity PAD as candidates for endovascular intervention is more simply managed through the use of the MRA on the extremities. Contrast angiography is suggested for assessment of patients with lower extremity PAD when revascularization is contemplated, as it provides comprehensive information about arterial anatomy.

6. Treadmill Testing:

The main effect that PAD has on acute exercise is the development of claudication pain in the leg musculature as a result of insufficient blood flow. The primary objective of a treadmill test for patients with PAD is to obtain reliable measures of (1) the rate of claudication pain development, (2) the ABI response to exercise, and (3) the presence of coexisting coronary heart disease.Claudication and peripheral hemodynamic measurements obtained from a treadmill test are the primary criteria to assess the effectiveness of an exercise program. The specific claudication variables that are measured to assess the functional severity of PAD include, the distances (or times) to onset and to maximal claudication pain. ABI measurements obtained before and after the treadmill test, in addition to claudication measurements provide a more objective assessment of disease severity. Measurement of the ABI immediately after a treadmill exercise stress test can help diagnose PAD in difficult cases as well as determine the extent of impairment of the peripheral circulation The sensitivity of ABI measured after treadmill walking is >95%. ^{13, 34}

Management

The immediate treatment goal in acute arterial occlusion is to preserve the tissue, to provide pain management, and to save the limb, as well as intervention to restore blood circulation. All patients with PAD need aggressive risk factor modification associated with cardiovascular events in order to: improve limb symptoms, to prevent progression of limb ischemia, to preserve limb viability, for smoking cessation, control of diabetes, hypertension, and hypercholesterolemia, along with dietary restrictions aimed at reducing cholesterol and obesity. Identification of persons with asymptomatic lower extremity PAD should be obtained by way of examination and/or measurement of the ABI, in order that beneficial interventions identified to diminish their amplified risk of MI, stroke, and death may be presented.²²

Intermittent claudication and critical limb ischemia therapies include supportive actions, medications, non-operative interventions, and surgical treatment. Supportive measures include meticulous care of the feet, which must be kept clean and protected against unnecessary drying through the use of moisturizing creams, as well as well-fitting and protective shoes to decrease trauma. As they diminish blood flow to the skin, it is imperative to avoid elastic support hose. Other methods to improve perfusion pressure and ameliorate some of the rest pain, in patients with critical limb ischemia, are to use shock blocks beneath the head of the bed simultaneously with a canopy above the feet. ¹³

Revascularization

Revascularization procedures are generally indicated for patients with disabling, progressive, or severe symptoms of intermittent claudication despite medical therapy, and for those with critical limb ischemia. Non-operative interventions include percutaneous transluminal angiography (PTA), stent placement, and atherectomy. Revascularization (endovascular or surgical) therapy is generally held in reserve for patients whose occupational performance or way of life is compromised by claudication. Also, patients who do not indicate a response to pharmacotherapy and exercise, or patients for whom the risk-benefit relation with revascularization is encouraging may be candidates.²²

Amputation

Overwhelming infection that threatens a patient’s life, rest pain that cannot be controlled, or extensive necrosis that has destroyed the foot, are necessary indications for a major amputation in a patient with CLI. ³³ Only in selected cases is amputation considered as primary therapy for lower-limb ischemia. A considerable risk factor for lower-extremity amputation, particularly in patients with diabetes, is PAD. The factors of age, duration of diabetes, and presence of peripheral neuropathy amplify the risk of PAD, in persons with diabetes. Even after amendment for other identified risk factors and the surplus incidence of diabetes, a higher prevalence of PAD was found in African Americans and Hispanics with diabetes, than non-Hispanic whites. Femoralpopliteal and tibial PAD are more strongly connected with diabetes, whereas further risk factors such as hypertension and smoking are more strongly associated with proximal disease in the aorto-iliofemoral vessels.

As most patients are asymptomatic and many do not report their symptoms, the exact pervasiveness of PAD in persons with diabetes has been difficult to determine. Further to this, screening modalities have not been consistently agreed upon, and pain acuity may be dulled by the existence of peripheral neuropathy. As such, a patient presenting with both diabetes and PAD, may be more liable to present with an ischemic ulcer or gangrene, than a patient with PAD alone. Diabetes mellitus increases The risk of lower extremity PAD due to diabetes mellitus increases by 2 to 4 fold and is characteristically found in 12% to 20% of lower extremity PAD patients. ^{14, 19, 28}

Exercise Rehabilitation

Patients with claudication have noticeable impairment in exercise performance and general functional capacity. Improving mobility and quality of existence are essential treatment goals for patients with peripheral arterial disease. ²⁹Exercise training is not linked with substantial changes in blood flow to the legs, and the changes that do occur do not forecast the clinical response.²¹

Intermittent Claudication: Exercise Therapy (Supervised)

Frequency: 3–5 supervised sessions/week

Duration: 35–50 minutes of exercise/session

Type of exercise: treadmill or track walking

To near-maximal claudication pain

Length: ?6 months

Results: 100%–150% enhancement in maximal walking distance and related improvement in quality-of-life

Risk Factor Modification

Smoking Cessation

The single most significant amendable risk factor for the progression and exacerbation of PAD is cigarette smoking. Tobacco utilization has been linked with increased development of atherosclerosis as well as an increased possibility of amputation in PAD patients. Cessation counseling and avoidance of all tobacco goods are vital as these products are an exceptionally strong etiologic risk factor for lower extremity PAD.¹²

It is estimated that more than 80% of persons with lower extremity PAD are existing or previous smokers. ²⁴ Lower extremity PAD is 2 to 3 times more liable than coronary artery disease to be caused by tobacco use. Smoking has been established as increasing the risk of lower extremity PAD by 2 to 6 fold, and the risk of intermittent claudication by 3 to 10 fold, according to a number of large epidemiological studies.^{1, 6} The quantity of cigarettes smoked per day, in addition to the number of years the patient has smoked, increases the risk of lower extremity PAD in a commanding dose-dependent manner. Primarily, reducing their risk of cardiovascular events, as well as the risk of progression of the disease and potential amputation, are reasons patients should be encouraged to discontinue smoking.

Smoking cessation is considered a first-line treatment among smokers with PAD.¹⁵ Cigarette smoking has been estimated to increase 1.4 fold of PAD for every 10 cigarettes per day. History of stroke was associated with a 1.5 fold increase in the prevalence of PAD, less than previous reports.^{3, 7}

Weight reduction

Counseling for weight reduction should be considered for patients who are overweight (BMI 25-30), or for those who are obese (BMI>30). ⁶

Dyslipidemia

Patients with atherosclerosis decrease the risk of adverse cardiovascular events through treatment of dyslipidemia. Elevated total and low-density lipoprotein (LDL) cholesterol, decreased high-density lipoprotein (HDL) cholesterol, and hypertriglyceridemia are lipid abnormalities related to lower extremity PAD. ¹⁷

Each 10 mg per dL increase in total cholesterol increases the risk of developing lower extremity PAD by about 5% to 10%. ^{27, 28} Total cholesterol levels are commonly elevated in patients with intermittent claudication more so than in those without lower extremity PAD, as revealed through epidemiological studies. Similarly, levels of LDL are higher and HDL levels are lower in patients with lower extremity PAD, than in age-matched controls. ²⁴   Thus, lipid-lowering therapy has benefit for patients with peripheral arterial disease, who often have coexisting coronary and cerebral arterial disease.

The current recommendation for patients with peripheral arterial disease is to achieve a serum LDL cholesterol concentration of less than 100 mg per deciliter and a serum triglyceride concentration of less than 150 mg per deciliter. Statin use has been demonstrated to favorably influence leg functioning, walking performance, ankle-brachial index (ABI) values, symptoms of claudication, and mortality. Target LDL cholesterol levels 70 mg/dL were associated with the lowest rate of overall mortality. Statins have beneficial effects beyond their lipid lowering properties and should be considered in all patients with PAD, irrespective of LDL cholesterol levels.²² therefore, statin should be given as initial therapy¹⁶ to achieve a target low-density lipoprotein (LDL) cholesterol level of 100 mg/dL. ²²

Hypertension

Although the correlation is generally weaker than that with cerebrovascular and coronary artery disease, hypertension is linked with lower extremity PAD. ¹² In the Framingham Heart Study, the risk of intermittent claudication was amplified 2.5 to 4 fold in men and women respectively, owing to hypertension. The risk was proportional to the severity of elevated blood pressure. Management of hypertension is critical for prevention of stroke, myocardial infarction, and congestive heart failure. While antihypertensive therapy may decrease limb perfusion pressure, it may also potentially intensify symptoms of claudication or chronic limb ischemia. Current PAD guidelines recommend using ACE inhibitors in symptomatic PAD patients. ²²

Diabetes

A frequent cardiovascular impediment in patients with diabetes is PAD. Affecting virtually every vascular bed, the pervasive character of diabetes on the atherothrombotic environment of the peripheral vasculature is unique. Owing to the atypical metabolic state accompanying diabetes, changes in the condition of arterial structure and function result. Inflammation has been recognized as both a risk indicator and conceivably a risk factor for atherothrombotic disease states, including PAD.⁵ In addition, levels of CRP are unusually elevated in patients with impaired glucose regulation syndromes, including impaired glucose tolerance and diabetes.

Proportional to the severity and extent of diabetes is the risk of developing lower extremity PAD. There is a 7 to 15 fold more likely rate of diabetic patients with lower extremity PAD undergoing a major amputation, than non-diabetics with lower extremity PAD. The risk of developing CLI is also greater in diabetics than non-diabetics. ²⁵

Aggressive glycemic control, with a hemoglobin A1C goal of 7.0% or as close to 6% as possible, is favored for patients with both diabetes and PAD. A statin should be given as initial therapy; however, niacin is a significant drug due to its ability to increase serum HDL concentrations and lower serum triglyceride concentrations without worsening glucose metabolism in these patients.

Antiplatelet and Anticoagulation Therapy

A long-term prescription of an antiplatelet drug should be prescribed for all symptomatic patients with or without a record of other cardiovascular disease, in order to decrease the risk of cardiovascular morbidity and mortality. ⁷ Antiplatelet therapy with aspirin is effective in preventing secondary events in patients with PAD, including delaying the rate of progression and decreasing the need of peripheral arterial procedures, minimizes the possibility of death from vascular causes, myocardial infarction, and stroke in patients with vascular diseases by 25% . It is also suggested for patients with peripheral arterial disease.³ Aspirin/ASA is successful in PAD patients, who also have medical evidence of other forms of cardiovascular disease (coronary or carotid). Use in PAD patients who do not have clinical evidence of other forms of cardiovascular disease may also be considered.  Also successful in dropping cardiovascular events in a subgroup of patients with symptomatic PAD is Clopidogrel, with or without supplementary clinical evidence of cardiovascular disease.⁹

Vasodilators:

FDA approved drugs pentoxifylline and cilostazol may be used to treat intermittent claudication in some patients. An effective treatment to improve symptoms and augment walking distance in patients with lower extremity PAD, and intermittent claudication (in the absence of heart failure), is Cilostazol given at a dosage of 100 mg orally two times per day. Pentoxifylline at a dosage of 400 mg 3 times per day, may also be considered as second-line alternative treatment to cilostazol to advance walking distance in patients with intermittent claudication.²²

Role of ACNP

Prevention

Peripheral arterial disease (PAD) is a common condition, with a prevalence of up to 20% in populations aged over 65 years. It is associated with a marked increase in cardiovascular risk in patients, both with and without, coexisting coronary artery disease. The risk factors for coronary and peripheral arterial disease are similar, and higher cholesterol concentrations are associated with higher rates of peripheral arterial disease.²³

PAD commonly results from progressive narrowing of arteries in the lower extremities and is a manifestation of systemic atherosclerosis. It is well known that PAD is associated with increased risk of mortality from cardiovascular disease and all causes such as cerebral vascular diseases, renal disease, and diabetic mellitus. PAD carries a cardiovascular risk similar to that of CAD.  Peripheral arterial disease (PAD) is a growing health problem for many Americans. The burden of PAD often occurs along with other cardiovascular risk factors, including diabetes mellitus (DM), low-grade inflammation, hypertension, and lipid disorders. DM, in particular, is an increasingly important co-factor because the number of PAD patients with DM continues to increase. ACNP must be aggressive in the treatment of risk factors in patients with PAD when no other obvious cardiovascular symptoms are present.

It is vital to make a diagnosis of PAD in patients with diabetes, in order to elicit symptoms, avert disability and limb loss, and to categorize a patient with an elevated risk of MI, stroke, and death. Most individuals with this disease are asymptomatic, and the condition is detected during routine physical examination of abnormal pulses, vascular bruits, or an abnormal value for the ankle–brachial index.⁴ Therefore, a focused vascular physical assessment is imperative.

The following are recommendations for ankle-brachial index (ABI) screening used to distinguish peripheral arterial disease in the individual patient.

An ABI should be calculated for:

• All patients who have exertional leg symptoms
• All patients between the age of 50–69, and who have a cardiovascular risk factor (principally smoking or diabetes)
• All patients age 70+ years in spite of of risk-factor status
• All patients with a Framingham risk score of 10%–20%²²

Early detection of PAD and aggressive management of cardiovascular risk factors should reduce the incidence and severity of CLI. Patients with CLI should be referred to a vascular specialist early in the course of their disease to plan for revascularization options.

Aggressive management of risk factor modification and Antiplatelet-drug therapy³⁶ on the part of the ACNP is vital in management and care of PAD and other ischemic events or fatal complications.

Summary

Although PAD may be seen in the absence of clinical CAD, asymptomatic CAD is frequently present in patients with PAD. Every patient presenting with PAD should be considered to have CAD until proven otherwise. Evaluation and treatment for PAD should include evaluation and control of CAD risk factors.

Having a greater burden of metabolic syndrome exacerbates the ambulatory dysfunction of PAD patients limited by intermittent claudication. Patients with PAD, who have more metabolic syndrome components, present with worsened intermittent claudication, physical function, health-related quality of life, and peripheral circulation. Aggressively treating these metabolic syndrome components may be particularly beneficial in managing symptomatology and long-term prognosis of PAD patients.  PAD is a significant health concern in the elderly population, which is likely to continue to increase in future years.

ACNPs have greater responsibility in the conservative management of patients with asymptomatic PAD, as well as patients with intermittent claudication, in order to modify risk factors and improve ambulatory ability. In addition, patients with more severe PAD typically require revascularization of the lower extremities, which may also enter under the purview of the ACNP’s responsibility.

References

ACC/AHA Guidelines for the Management of Patients With … (n.d.). Retrieved September 23, 2010 from http://www.scai.org/asset.axd?id=1e6edd5a-ebeb-4c32-9f71-3a8f56933b78&t=633921667472970000

Access med Creager Mark A, Loscalzo Joseph, “Chapter 243. Vascular Diseases of the Extremities” (Chapter). Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J: Harrison’s Principles of Internal Medicine, 17e: http://www.accessmedicine.com/content.aspx?aID=2880274.

Abbott RD, Rodriguez BL, Petrovitch H, Yano K, Schatz IJ, Popper JS, et al. Ankle brachial blood pressure in elderly men and the risk of stroke: the Honolulu Heart Program. J Clin Epidemiol 2001;54:973-8.

Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomized trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324:71-86. [Erratum, BMJ 2002;324: 141.]

Beckman JA, Creager MA, Libby P: Diabetes atherosclerosis: epidemiology, pathophysiology, and management. JAMA 287:2570–2581, 2002)

Bowlin SJ, Medalie JH, Flocke SA, et al. Epidemiology of intermittent claudication in middle-aged men. Am J Epidemiol 1994;140:418-30.; More than 80% of patients with lower extremity PAD are current or former smokers (40).

Chang CC, Ho SC, Tsai SS, Yang CY. Ischemic heart disease mortality reduction in an arseniasis-endemic area in southwestern Taiwan after a switch in the tap-water supply system. J Toxicol Environ Health A 2004;67:1353-61.

Cheng Susan, Bell Susan M, Zieman Susan J, “Chapter 75. Aging and Atherosclerosis” (Chapter). Halter JB, Ouslander JG, Tinetti ME, Studenski S, High, KP, Asthana S: Hazzard’s Geriatric Medicine and Gerontology, 6ed:

Clagett P, Sobel M, Jackson M, Lip G, Tangelder M, Verhaeghe R. Antithrombotic therapy in peripheral arterial disease: The SeventhACCP Conference on antithrombotic and thrombolytic Chest 2004;126:S609-26.

Clinical features, diagnosis, and natural history of lower … (n.d.). Retrieved from http://www.uptodate.com/patients/content/topic.do?topicKey=~bRhDzg8iotC8ZJ

Criqui MH: Peripheral arterial disease: epidemiological aspects. Vascular Medicine 6 (Supl.1):3–7, 2001.

Criqui MH, Denenberg JO, Langer RD, et al. The epidemiology of peripheral arterial disease: importance of identifying the population at risk. Vasc Med 1997;2:221-6.

Reager Mark A, Loscalzo Joseph, “Chapter 243. Vascular Diseases of the Extremities” (Chapter). Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J: Harrison’s Principles of Internal Medicine, 17e:

Diabetes In Control Dot Com. The FREE weekly newsletter for … (n.d.). Retrieved September 23, 2010 from http://www.diabetesincontrol.com/tyk/192/answer2.shtml

Dormandy JA, Rutherford RB. Management of peripheral arterial disease (PAD). TASC Working Group. TransAtlantic Inter-Society Consensus (TASC). J Vasc Surg 2000;31(1 Pt 2):S1-S296.

Elam MB, Hunninghake DB, Davis KB, et al. Effect of niacin on lipid and lipoprotein levels and glycemic control in patients with diabetes and peripheral arterial disease: the ADMIT study: a randomized trial. JAMA 2000;284:1263-70.

Fowkes FG, Housley E, Riemersma RA, et al. Smoking, lipids, glucose intolerance, and blood pressure as risk factors for peripheral atherosclerosis compared with ischemic heart disease in the Edinburgh Artery Study. Am Journal of Epidemiology 1992;135:331-40.

Hiatt WR. Medical treatment of peripheral arterial disease and claudication. N Engl J Med 2001; 344:1608-21.

Hiatt WR, Hoag S, Hamman RF. Effect of diagnostic criteria on the prevalence of peripheral arterial disease. The San Luis Valley Diabetes Study. Circulation 1995;91:1472-9.

Hirsch AT, Criqui MH, Treat-Jacobson D, Regensteiner JG, Creager MA, Olin JW, et al. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA 2001;286:1317-24.

Hiatt WR, Regensteiner JG, Hargarten ME, Wolfel EE, Brass EP. Benefit of exercise conditioning for patients with peripheral arterial disease. Circulation 1990;81:602-9.

Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006;113: 463-654.

Lee AJ, Price JF, Russell MJ, Smith FB, van Wijk MC, Fowkes FG. Improved prediction of fatal myocardial infarction using the ankle brachial index in addition to conventional risk factors: the Edinburgh Artery Study. Circulation 2004;110:3075-80.

Meijer WT, Hoes AW, Rutgers D, et al. Peripheral arterial disease in the elderly: the Rotterdam Study. Arterioscler Thromb Vasc Biol 1998;18:185-92.

Most RS, Sinnock P. The epidemiology of lower extremity amputations in diabetic individuals. Diabetes Care 1983; 6:87-91.

Murabito JM, D’Agostino RB, Silbershatz H, Wilson WF: Intermittent claudication: a risk profile from the Framingham Heart Study. Circulation 96:44–49, 1997.

Murabito JM, D’Agostino RB, Silbershatz H, et al. Intermittent claudication. A risk profile from The Framingham Heart Study. Circulation 1997;96:44-9.

Newman AB, Siscovick DS, Manolio TA, et al. Ankle-arm index as a marker of atherosclerosis in the Cardiovascular Health Study. Cardiovascular Heart Study (CHS) Collaborative Research Group. Circulation 1993;88:837-45.

Regensteiner JG, Meyer TJ, Krupski WC, Cranford LS, Hiatt WR. Hospital vs. home-based exercise rehabilitation for patients with peripheral arterial occlusive disease. Angiology 1997;48:291-300.

Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH: Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation 97:425–428, 1998

Sanderson KJ, van Rij AM, Wade CR, et al. Lipid peroxidation of circulating low density lipoproteins with age, smoking and in peripheral vascular disease. Atherosclerosis 1995;118:45-51. Erratum in: Atherosclerosis 1996;121:295.

Strandness DE Jr, Bell JW: Peripheral vascular disease: diagnosis and evaluation using a mercury strain gauge. Ann Surg 161 (Suppl. 4):1–35, 1965.

TASC II Inter-Society Consensus Guidelines for the management … (n.d.). Retrieved September 22, 2010 from http://www.tasc-2-pad.org/Client/EN/index.aspx?Composant=Actualite&IDBase=794&Methode=ClientFDetail&Ref=+Amputation

TASC. Management of peripheral arterial disease (PAD). TransAtlantic Inter-Society Consensus (TASC). Eur J Vasc Endovasc Surg 2000;19(Suppl A):Si-xxviii. S1-250.

TASC. Management of Peripheral Arterial Disease (PAD) TransAtlanticIntersociety Consensus (TASC). J Vasc Surg 2000;31(1 part 2):S1-287.

The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Arch Intern Med 1997;157:2413-46. [Erratum, Arch Intern Med 1998;158:573.

Upper extremity peripheral arterial disease. (n.d.). Retrieved September 23, 2010 from http://www.uptodate.com/patients/content/topic.do?topicKey=~iieP_d6L7Ha69m

White C. Intermittent claudication. N Engl J Med 2007;356:1241-50