Peripheral Arterial Disease

Transcription

1 Peripheral Arterial Disease 28 C. Huie Lin and Jasvindar Singh Importance of peripheral arterial disease (PAD) has been increasingly recognized: Prevalence of the disease may be as high as 29% in patients with risk factors.1 PAD is associated with 4% to 5% per year risk of myocardial infarction (MI), cerebrovascular accident (CVA), and vascular death.1 This chapter will primarily focus on vascular disease processes that lead to ischemia of the lower extremity, kidney, and carotid artery territories. PAD consists of a group of disorders that lead to progressive stenosis, occlusion, or aneurysmal dilation of the aorta and its noncoronary branch arteries, including the carotid artery, upper extremity, visceral, and lower extremity arterial branches. Lower Extremity Peripheral Arterial Disease GENERAL PRINCIPLES Classification Patients with lower extremity PAD range from those who are asymptomatic to those with acute limb-threatening emergencies. The clinician must differentiate between the severity of symptoms in deciding on further workup and the urgency of a treatment plan. Lower extremity PAD is commonly defined by presentation: Asymptomatic Claudication Critical limb ischemia (CLI) Acute limb ischemia (ALI) Epidemiology Prevalence of PAD has been estimated at 3% to 10% of the population, based on ankle brachial testing. This increases to 15% to 20% in persons aged greater than 70 years.2 In a high-risk patient population aged greater than 50 to 69 years with a history of cigarette smoking or diabetes, the prevalence of PAD is estimated at 29%.3 Etiology The most common cause of PAD is atherosclerosis (Table 28-1). Risk Factors The major cause of lower extremity PAD is atherosclerosis, with identified risk factors of smoking, diabetes, hypertension, hyperlipidemia, hyperhomocysteinemia, and family history of coronary artery disease (CAD) _ch28_p indd /02/14 9:31 PM

2 Diagnosis 339 TABLE 28-1 ETIOLOGY OF PERIPHERAL ARTERIAL DISEASE Atherosclerosis Connective tissue diseases Marfan syndrome Ehlers Danlos syndrome Dysplastic disease Fibromuscular dysplasia Vasculitic diseases Large vessels: Giant-cell (temporal) arteritis, Takayasu arteritis Medium-sized vessels: Kawasaki disease, polyarteritis nodosa Small vessel disease (arterioles and microvessels), Wegener granulomatosis, microscopic polyangiitis, Churg Strauss syndrome, Henoch Schönlein purpura, cryoglobulinaemic vasculitis Thromboangiitis obliterans (Buerger disease) Prothrombotic diseases Vasospastic diseases Cigarette smoking is a significant dose-dependent contributor to the development of lower extremity PAD. More than 80% of patients are current or former smokers, and a cigarette smoker is two to three times more likely to have lower extremity PAD than detectable CAD. 1 Associated Conditions Although PAD can cause significant morbidity, the shared pathophysiology and risk factors between PAD and CAD mean that the majority of these patients will die from cardiovascular diseases such as MI or ischemic stroke. Patients with lower extremity PAD have a twofold to sixfold increased risk of death due to coronary heart disease events and are four to five times more likely to have a stroke or transient ischemic attack (TIA). 1 DIAGNOSIS Clinical Presentation Asymptomatic lower extremity PAD: Limb function is not necessarily normal. Patients may not have classic exertional limb discomfort but may have less typical symptoms, such as decreased walking speed or poor balance. Claudication: Claudication symptoms are due to exercise-induced ischemia. Symptoms of chronic lower extremity atherosclerotic occlusion are variable but are frequently described as reproducible cramping or fatigue with walking, with resolution shortly after rest.

3 340 PERIPHERAL ARTERIAL DISEASE Symptoms may occur anywhere in the lower extremity, including buttocks, thighs, or calves. Critical limb ischemia: CLI is limb pain that occurs at rest (rest pain) or impending limb loss that is caused by severe compromise of blood flow to the affected extremity. This term should be used to describe all patients with chronic pain at rest, ulcers, or gangrene attributable to objectively proven arterial occlusive disease. Acute limb ischemia: ALI is caused by a sudden decrease in limb perfusion that threatens tissue viability. Symptoms occur as a result of thrombosis of an atherosclerotic plaque or a lower extremity embolism, frequently of cardiac or aortic origin. The typical symptoms and signs of ALI include the six P s: pain, paralysis, paresthesias, pulselessness, pallor, and polar (cold). History Asymptomatic patients aged 50 years with cardiovascular risk factors and all patients 70 years should be asked about walking impairment, rest pain, and nonhealing wounds. If positive, further testing should be initiated. Claudication can be confused with pseudoclaudication from spinal stenosis. Classically, limb discomfort associated with spinal stenosis is not reliably reproduced with exertion; it is exacerbated by standing and relieved only by sitting. CLI usually presents with rest pain that is worse while lying in a supine position. Patients with CLI will often maintain limbs in a dependent position and are frequently unable to walk. As described above, typical symptoms and signs of ALI include the six P s: pain, paralysis, paresthesias, pulselessness, pallor, and polar (cold). Physical Examination Visualization: Capillary refill Nonhealing wounds or ulcers Livedo reticularis (for atheroembolization) Calf atrophy Alopecia over the dorsum of the foot Auscultation and palpation: Bruits over major vascular beds as well as palpation of peripheral pulses over the femoral, popliteal, posterior tibial, and dorsalis pedis arteries (Figure 28-1). The presence of a bruit or a thrill only describes turbulent flow but does not confirm arterial stenosis. In addition, both the volume and the quality of the peripheral pulses should be noted. Elevation-dependency test: This is a screening maneuver, which can be performed by elevating the lower extremities to 60 degrees above horizontal while the patient is supine. Development of pallor in the sole of the foot indicates arterial disease in that extremity. After the patient is sitting upright with legs hanging off the examination table, delayed return of color and venous engorgement in either lower extremity may confirm inadequate circulation. With more advanced disease, a deep red color develops along with dependent edema, so-called dependent rubor. Diagnostic Testing All patients with symptomatic claudication should undergo measurement of the ankle-brachial index (ABI) to confirm the diagnosis and to establish a baseline result (Figure 28-2). 1,2,4-6

4 Diagnosis 341 Renal Artery Celiac Trunk Superior Mesenteric Artery Common Iliac Artery External Iliac Artery Common Femoral Artery Inferior Mesenteric Artery Superficial Femoral Artery Popliteal Artery Anterior Tibial Artery Peroneal Artery Posterior Tibial Artery Dorsalis Pedis Artery FIGURE Diagram of major branches of lower extremity peripheral arterial anatomy. Advanced age and diabetes mellitus contribute to vessel rigidity and make the ABI test less reliable. When this occurs, a toe-brachial index (TBI) can be used instead. n Toe pressures <30 mmhg indicate ischemia, impaired wound healing, and increased risk of amputation. n An ABI <0.9 and a TBI of <0.7 are considered diagnostic of lower extremity PAD. n For the purposes of coronary risk estimation and lipid management, an ABI <0.90 is considered a coronary risk equivalent even in asymptomatic patients. 7 If the resting ABI is normal and clinical suspicion is high, ABI can be repeated after exercise or plantar flexion test. While standing, the patient raises his or her heels off the ground, standing on tip-toe and then returns to the normal position. When symptoms develop or after 50 repetitions, the ABI is repeated. Segmental limb pressure examination may be helpful to further identify the location and extent of lower extremity PAD. Cuffs are placed on the upper thigh, lower thigh, and upper calf. A drop of 20 mmhg in the systolic pressure between segments is consistent with arterial stenosis. Pulse volume recordings use pneumoplethysmography to identify changes in pulse contour and amplitude. In the presence of arterial disease, the slope flattens, the pulse width widens, and the dicrotic notch is lost. Duplex ultrasonography: Duplex ultrasonography combines Doppler velocity and waveform analysis with gray-scale visualization of the arterial wall. A normal waveform is triphasic, with forward flow in cardiac systole followed by a brief flow reversal in early diastole followed by forward flow in late diastole.

5 342 PERIPHERAL ARTERIAL DISEASE Performing pressure measurements and calculating the ankle-brachial index Pressure at right or left arm Formula Right ankle Highest right ankle pressure (mmhg) = brachial index Highest arm pressure (mmhg) Left ankle = brachial index Highest left ankle pressure (mmhg) Highest arm pressure (mmhg) Example Highest ankle pressure 92 mmhg Moderate = = 0.56 = Highest brachial pressure 164 mmhg obstruction Pressure at posterior tibial and dorsalis pedis arteries in right and left ankle Interpretation of calculated index Above 0.90 normal mild obstruction moderate obstruction severe obstruction To calculate the ankle-brachial index, systolic pressures are determined in both arms and both ankles with the use of a hand-held Doppler instrument. The highest readings for the dorsalis pedis and posterior tibial arteries are used to calculate the index. FIGURE Performing pressure measurements and calculating the anklebrachial index. (From White C. Intermittent claudication. N Engl J Med 2007;356: , with permission.) With arterial stenosis, distal blood flow velocities increase. In severe stenosis, the flow-reversal component is absent as well (Figure 28-3). 8 The degree of stenosis is determined by combining waveform analysis and measurement of the peak systolic velocity. For specific anatomic delineation to guide revascularization, additional imaging with computed tomography (CT), magnetic resonance angiography (MRA), or digital subtraction angiography can be used. Digital subtraction angiography (Figure 28-4) remains the gold standard test but it is invasive and carries risks related to the use of contrast and radiation exposure. CT angiography is rapid and noninvasive but carries similar contrast and radiation risks. Calcium found in atherosclerotic lesions can create so-called blooming artifacts, rendering images less accurate. MRA carries fewer risks and gives detailed information, although prior stent placement can affect image quality. TREATMENT The primary goal should be prevention of the development of PAD through risk-factor modification, especially smoking cessation. 1,2,5,6

6 Treatment 343 A B FIGURE Doppler arterial waveforms from patients without (A) and with (B) PAD. In the setting of PAD, the peak systolic velocity increases and the diastolic flow reversal is lost. (From Begelman SM, Jaff MR. Noninvasive diagnostic strategies for peripheral arterial disease. Cleve Clin J Med 2006;73:S22-S29, with permission.) When prevention fails, early detection and lifestyle modification, along with medical and, in some cases, mechanical reperfusion therapy should be combined to maintain and improve quality of life and to avoid limb- and life-threatening progression. Medications Antiplatelet therapy: 1,2,5,6,9 Aspirin (75 to 325 mg daily) or Clopidogrel (75 mg daily)

7 344 PERIPHERAL ARTERIAL DISEASE A B C D FIGURE Lower extremity peripheral arterial disease angiography and percutaneous intervention. (A) Severe hazy lesion in the ostial right common iliac artery (white arrow). A marker pigtail has been used to perform angiography to allow assessment of lesion length. (B) Deployment of a mm Racer bare metal stent (Medtronic, Minneapolis) in the right common iliac lesion (white arrowhead). (C) Post stent digital subtraction angiography demonstrates brisk flow through the stent (black arrow) and patency of the right common iliac artery. (D) Digital subtraction angiography demonstrating a chronic total occlusion of the left common femoral artery (black arrowhead) with well-developed collaterals in the same patient. Cilostazol, a phosphodiesterase type 3 inhibitor, has both vasodilatory and platelet-inhibitory properties and has been shown to improve walking distance by about 50% compared with placebo.1,2,5,6,10 Because other phosphodiesterase inhibitors are associated with an increased mortality in patients with heart failure, care should be taken to avoid cilostazol in patients with left ventricular dysfunction. The efficacy of pentoxifylline remains uncertain.11 Lipid-lowering therapy (statins) for a goal low-density-lipoprotein cholesterol level <100 mg/dl.1,2,5,6 Antihypertensive therapy (angiotensin-converting enzyme [ACE] inhibitor and/or β-blocker) for a goal blood pressure <140/90 mmhg or <130/80 mmhg with diabetes.1,2,5,6 Glucose control with goal hemoglobin A1c <7%.1,2,5,6 Other Nonpharmacologic Therapies Smoking cessation1,2,5,6 Daily foot inspection and proper foot care 14225_ch28_p indd /02/14 9:32 PM

8 General Principles 345 Supervised exercise program: Improvements in functional capacity occur over several months. Trials of 30 minutes of exercise three times per week led to a 150% improvement in maximal walking ability. 1,12 Surgical Management For symptomatic patients with claudication that causes limitations in quality of life or vocational ability and who do not respond adequately to a supervised exercise program and medical management, a revascularization procedure may be considered. Endovascular treatments such as percutaneous transluminal angioplasty (PTA) with or without stenting (Figure 28-4), catheter-based thrombolysis, mechanical thrombectomy, and open surgical procedures are reasonable treatment options based on comorbidities and vascular anatomy. Approximately 5% of patients with intermittent claudication will require a revascularization intervention for severe symptoms or progression to CLI, and only 2% will ultimately require amputation for distal ischemia. In contrast, nearly half of patients with CLI will require revascularization for limb salvage. 1 REFERRAL For rapid disease progression, urgent referral to a vascular specialist is warranted to limit the extent of tissues necrosis and increase the chance of limb salvage. If signs of ALI are present (the six P s), the vascular consult is emergent, and immediate concerns should address anticoagulation to prevent the propagation of thrombus material and initiate plans for urgent or emergent revascularization. MONITORING/FOLLOW-UP Clinically stable patients should be regularly evaluated with history and physical examination as well as noninvasive studies such as ABI. Patients with progressive symptoms may require more intense evaluation including imaging or invasive angiography. All patients with PAD require regular follow-up for continued medical management of both the primary disease and secondary cardiovascular disease. Renal Artery Stenosis GENERAL PRINCIPLES Epidemiology Renovascular hypertension resulting from renal artery stenosis (RAS) is the most common correctable cause of secondary hypertension. In patients undergoing cardiac catheterization, the prevalence of RAS may be as high as 30%, with lesions >50% found in 11% to 18%. 1 Etiology Atherosclerotic disease is the cause of most RAS. Less common causes of RAS are listed in Table Fibromuscular dysplasia (FMD) is the second most common cause of RAS. Although occurring in both genders, the typical presentation of FMD is that of hypertension in a young woman.

9 346 PERIPHERAL ARTERIAL DISEASE TABLE 28-2 CAUSES OF RENAL ARTERY STENOSIS Atherosclerosis Fibromuscular dysplasia Renal artery aneurysms Aortic or renal artery dissection Vasculitis Thrombotic or cholesterol embolization Collagen vascular disease Retroperitoneal fibrosis Trauma Posttransplantation stenosis Postradiation Pathophysiology Renal hypoperfusion leads to activation of the renin angiotensin system. The vasoactive properties of aldosterone and angiotensin II lead to volume expansion and elevated systemic blood pressures. Progression of high-grade RAS can result in loss of renal function, mass, and ultimately ischemic nephropathy. Atherosclerotic RAS tends to involve the ostium of the renal arteries and the aorta. FMD involves the mid- and distal renal artery and may extend into the side branches. The characteristic string of beads appearance (Figure 28-5) and location within the renal artery help to differentiate FMD from atherosclerotic RAS. FMD can also affect other arterial beds, especially the carotid and vertebral arteries. A B C FIGURE Fibromuscular dysplasia of the renal artery in a patient with severe refractory hypertension. (A) Invasive angiography of the right renal artery with classic beads-on-a-string stenotic appearance (white arrow) of the right renal artery. (B) Inflation of a mm Angiosculpt (Angioscore, Freemont) scoring angioplasty balloon (white arrowhead) to treat the stenotic lesion. (C) Final postintervention angiography reveals brisk flow through the right renal artery lesion (black arrow) following further dilatation with a noncompliant angioplasty balloon _ch28_p indd /02/14 9:32 PM

10 Treatment 347 DIAGNOSIS Clinical Presentation RAS may be clinically silent in many individuals. Severe hypertension and fluid retention are the hallmark findings of RAS. Clinical features that should prompt evaluation for RAS include 1 : Onset of hypertension before the age of 30 years Onset of severe hypertension after the age of 55 years Accelerated hypertension (sudden and persistent worsening of previously controlled hypertension) Resistant hypertension (refractory despite three drugs, one of which must be a diuretic) Malignant hypertension (coexistent evidence of acute end-organ damage) Worsening renal function after the administration of an ACE inhibitor or angiotensin receptor blocker (ARB) An unexplained atrophic kidney or >1.5-cm size discrepancy between the two kidneys Sudden unexplained pulmonary edema Diagnostic Testing 1 Duplex ultrasonography with Doppler is recommended as an initial test for the detection of RAS. CT or MRA can define lesion characteristics and is helpful in imaging patients in whom ultrasonography proves difficult. CT uses nephrotoxic contrast, which can be particularly risky in a RAS population. MRA uses gadolinium contrast, traditionally thought to be less nephrotoxic than CT contrast. However, an association with gadolinium and nephrogenic systemic fibrosis has raised concerns in patients with significant renal impairment. If initial tests are inconclusive or considered too risky, catheter angiography could be considered for definitive diagnosis. Owing to the high prevalence of atherosclerotic RAS in patients with lower extremity PAD and CAD, a renal angiogram should be considered in patients with CAD and clinical suspicion for RAS who are already undergoing invasive angiography. 13 Because of the association with cerebral aneurysms, all patients with renal FMD should undergo MRA screening or CT angiography of the head. TREATMENT Medications Medical treatment for atherosclerotic RAS focuses mainly on controlling renovascular hypertension. 1 ACE inhibitors and ARBs should be avoided in bilateral RAS, as these drugs may contribute to worsening the physiologic consequences of RAS. Surgical Management A revascularization strategy may be considered for hemodynamically significant RAS, defined as (1) 50% to 70% diameter stenosis by visual estimation with a peak translesional gradient of >20 mmhg or a mean gradient 10 mmhg with 5-Fr catheter or pressure wire or (2) any stenosis 70% diameter stenosis or (3) 70% diameter stenosis by intravascular ultrasound. 1,5,6 In particular, intervention in the following scenarios may be desired 1,5,6 : Accelerated, refractory, or malignant hypertension Hypertension with an unexplained unilateral small kidney Hypertension with intolerance to medication

11 348 PERIPHERAL ARTERIAL DISEASE Chronic kidney disease with bilateral RAS or a RAS to a solitary functioning kidney Recurrent, sudden unexplained pulmonary edema Recurrent angina in the setting of severe hypertension The type of revascularization strategies for RAS are the subject of ongoing clinical trials. PTA (Figure 28-5) with provisional stenting has resulted in a higher clinical success rate and lower restenosis rate, especially for ostial lesions. Patients with FMD are an exception; in such individuals, balloon angioplasty alone is the therapy of choice. In some situations, specifically macroaneurysmal disease and small, multiple renal arteries, the anatomy is unfavorable for percutaneous therapy and vascular surgical reconstruction may be the treatment of choice. Lifestyle/Risk Modification Cardiovascular risk-factor reduction may aid in treatment of RAS, but is more likely to affect the risks of other cardiovascular diseases. These include: Smoking cessation Blood pressure control (<140/80) Goal serum lipid levels Goal serum glucose control Carotid Artery Stenosis GENERAL PRINCIPLES Stroke is the third leading cause of death in the United States and represents a major cause of long-term disability. The detection of carotid artery stenosis presents an opportunity to identify patients at high risk for stroke and prevent cerebrovascular events and other adverse cardiovascular events. Nearly half of patients with atherosclerotic carotid artery disease have severe CAD. As a result, although recent trials have focused on the role of percutaneous carotid intervention versus carotid endarterectomy in the prevention of stroke, the management of carotid artery disease must be multimodal and include the treatment of modifiable risk factors such as hypertension, dyslipidemia, diabetes, and tobacco abuse. Classification Asymptomatic carotid stenosis is defined as identifiable carotid artery plaque in the absence of neurologic symptoms such as amaurosis fugax, TIA, or CVA. Symptomatic carotid stenosis in contrast is the presence of neurologic symptoms suggestive of embolic or ischemic disease. Transcranial Doppler studies have demonstrated that embolic events may be present in asymptomatic carotid stenosis and is associated with a higher rate of symptomatic events. Epidemiology Carotid stenosis >50% is present in 7% of the men and 5% of the women aged >65 years. Although strokes and TIAs have multiple etiologies, approximately 80% are ischemic in origin. Of the ischemic strokes about 25% are due to a vascular stenosis or occlusion. 14 Modifiable risk factors for stroke include hypertension, tobacco use, dyslipidemia, and diabetes. In general, relative risk of stroke increases as the degree of stenosis progresses and with the development of symptoms.

12 Diagnosis 349 Pathophysiology Carotid artery stenosis is most commonly the result of atherosclerotic plaque formation, although less commonly fibromuscular dysplasia, cystic medial necrosis, or arteritis may play a role. Atherosclerotic carotid artery disease may result in cerebrovascular ischemic events via two mechanisms: Flow limitation: Although collateral circulation via the Circle of Willis may compensate, severe stenosis or acute plaque rupture of the internal carotid can potentially cause ischemia/infarction of the affected hemisphere. Cerebral embolic event: Embolization of thrombus or atheromatous debris from the carotid plaque can result in stroke. DIAGNOSIS Clinical Presentation History Atherosclerotic carotid artery stenosis can present as an asymptomatic carotid bruit, TIA, or stroke. Focal neurologic symptoms suggestive of cerebrovascular ischemia or infarction include, but are not limited to, unilateral weakness, paresthesia, or sensory loss, neglect, abnormal visual-spatial ability, monocular blindness, hemianopsia, aphasia, ataxia, cranial nerve deficits, visual field loss, dizziness, imbalance, and incoordination. Physical Examination Auscultation: Patients presenting to a cardiovascular specialist should undergo auscultation of the carotid arteries. Most bruits detected will be during systole; if the bruit extends into diastole, this indicates a significant gradient in the carotid artery with stenosis of about 80%. Neurologic evaluation: Patients with a carotid bruit should be evaluated for neurologic signs via a brief neurologic examination for strength, sensation, and orientation. Pre-existing neurologic deficits should be examined and documented in patients who have previously had a CVA. Diagnostic Testing Laboratories Routine evaluation of patients with asymptomatic and symptomatic carotid stenosis should include factors important for the medical management of systemic atherosclerosis: Fasting lipid profile Renal function studies Fasting glucose and hemoglobin A1 C Although biomarkers such as C-reactive protein (CRP) and matrix metalloproteinase (MMP) have held promise for prediction of vulnerable carotid plaque, their reliability has not been clearly demonstrated. Imaging Ultrasound with Doppler: Ultrasound has been reported to have a sensitivity of 87% to 99% and specificity of 69% to 96% in the identification of >50% stenosis. 14 Asymptomatic patients should undergo carotid ultrasound if any of the following are true 14 : n Audible carotid bruit n Known or suspected carotid stenosis n Evidence of systemic atherosclerosis (e.g., PAD or CAD)

13 350 PERIPHERAL ARTERIAL DISEASE All symptomatic patients with ischemic focal neurologic symptoms should undergo carotid ultrasound. MRI/MRA: MRI/MRA allows high-resolution imaging of the carotid anatomy as well as the aortic arch vessels up to the Circle of Willis. Contrast MRA improves imaging of high-grade stenosis and slowly flowing blood. Sensitivity of MRA has been reported as 97% to 100% and sensitivity of 82% to 96%, although a weakness of MRA has been the overestimation of degree of stenosis. 14 CT angiography: CT angiography allows imaging of the carotid as well as the arch vessels and cerebral vessels. Multidetector imaging with three-dimensional reconstruction has improved the quality of imaging significantly and now may be near comparable to the resolution of invasive angiography with a sensitivity of 100% and specificity of 63%. 14 Heavily calcified lesions as well as metallic dental or cranial implants can cause significant imaging artifacts. Iodinated contrast is required, which can be nephrotoxic to individuals with pre-existing renal insufficiency. Invasive angiography: Angiography offers excellent resolution of vascular anatomy, though the invasive nature of this technique incurs significant risk, in part dependent on variations in carotid and aortic arch anatomy and potential stroke risk. Outside of a planned catheter-based intervention, the use of routine diagnostic angiography has generally fallen out of favor with the exception of resolving conflicting noninvasive test results. TREATMENT Medications Medical treatment should focus on control of the modifiable risk factors of cerebrovascular events. Antiplatelet medications 14 : If not contraindicated, antiplatelet therapy with aspirin (75 to 325 mg daily) should be administered. Clopidogrel (75 mg daily) may be considered instead of aspirin. Dipyridamole may be considered in conjunction with aspirin in select patients. For patients with a history of TIA or stroke, control of risk factors including hypertension, diabetes, and cholesterol (with a statin medication) should be initiated. Surgical Management Revascularization of the carotid artery continues to be the subject of ongoing clinical investigation. Asymptomatic carotid artery stenosis 14 : Recently published guidelines suggest considering prophylactic carotid endarterectomy in highly selected patients with high-grade asymptomatic carotid stenosis performed by surgeons with <3% morbidity/mortality rates and in patients with a low perioperative risk. Carotid artery stenting may be considered in select asymptomatic patients with >70% stenosis by noninvasive imaging and >60% by invasive imaging. Symptomatic carotid artery stenosis 14 : For patients with a recent (<6 months) TIA or ischemic stroke within the last 6 months with ipsilateral severe (>70% by noninvasive or >50% by invasive imaging)

14 References 351 carotid stenosis, endarterectomy by a surgeon with a perioperative morbidity and mortality of <6% is recommended. Revascularization may be performed earlier (<2 weeks after the index event) if there are no contraindications. Carotid artery stenting may be an alternative in patients with an average or low risk of complications associated with endovascular intervention. The decision for stenting versus endarterectomy should be undertaken on a case-by-case basis factoring in operator experience, patient clinical scenario, vessel anatomy, and lesion complexity. REFERENCES 1. Hirsch AT, Haskal ZJ, Hartzer NR. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic). Circulation 2006;113:e463-e Norgren L, Hiatt WR, Dormandy JA, et al. TASC II Working Group. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg 2007:45:S5-S Hirsch AT, Criqui MH, Treat-Jacobson D, et al. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA 2001;286: White C. Intermittent claudication. N Engl J Med 2007;356: Rooke TW, Hirsch AT, Misra S, et al ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease (updating the 2005 guideline). Circulation 2011;124: Rooke TW, Hirsch AT, Misra S, et al. Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;61: National Institutes of Health. National Heart, Lung, and Blood Institute. National Cholesterol Education Program. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Final Report. NIH Publication No September, Begelman SM, Jaff MR. Noninvasive diagnostic strategies for peripheral arterial disease. Cleve Clin J Med 2006;73:S22-S Robless P, Mikhailidis DP, Stansby GP. Cilostazol for peripheral arterial disease. Cochrane Database Syst Rev 2008;1:CD Salhiyyah K, Senanayake E, Abdel-Hadi M, et al. Pentoxifylline for intermittent claudication. Cochrane Database Syst Rev 2012;1:CD Wong PF, Chong LY, Mikhailidis DP, et al. Antiplatelet agents for intermittent claudication. Cochrane Database Syst Rev 2011;11:CD Watson L, Ellis B, Leng GC. Exercise for intermittent claudication. Cochrane Database Syst Rev 2008;4:CD Weber-Mzell D, Kotanko P, Schumacher M, et al. Coronary anatomy predicts presence or absence of renal artery stenosis. A prospective study in patients undergoing cardiac catheterization for suspended coronary artery disease. Eur Heart J 2002;21: Brott TG, Halperin JL, Abbara S, et al ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/ CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease. Circulation 2011;124:e54-e130.