Evaluation of Peripheral Artery Disease


Arterial Anatomy and Physiology

  1. Structure
    • arterial wall consists of 3 layers: intima, media, and adventitia

    1. Intima
      • selective permeability barrier that has regional variations
      • luminal surface is coated with glycoproteins (heparin sulfate, dermatan sulfate)

      1. Endothelial Cells
        • important modulator of diverse processes such as blood vessel development and remodeling, control of coagulation and platelet activation, thrombolysis, regulation of vascular tone, leukocyte migration, wound healing, immune response and graft rejection, tumor invasion, and atherogenesis
        • secrete numerous biologically active substances
        • under normal conditions, endothelial cells promote the fluidity of blood and enhance blood flow through endogenous anticoagulants, antiplatelet and fibrinolytic factors, and vasodilators
    2. Media
      • composed of smooth muscle cells in an elastin and collagen matrix
      • elastin permits arterial distention and collagen provides tensile strength, limits distention, and prevents disruption
      • the great vessels have a large elastin component that allows for storing of potential energy during systole and then recoil during diastole
      • most arteries are muscular arteries that have dense smooth muscle in the media that is capable of changing luminal size, allowing blood flow to be directed into individual beds

    3. Adventitia
      • merges with the loose connective tissue that surrounds all vessels
      • consists of sparse fibroblasts with layers of collagen and elastin fibers
      • strength layer of the artery

Atherosclerosis

  1. Epidemiology
    • symptomatic peripheral arterial disease (PAD) increases with age, affecting 12 % to 20% of Americans aged 65 or older
    • smoking and diabetes are the two largest risk factors (~4x each)
    • other important risk factors are hypertension, hyperlipidemia, hypercholesterolemia, renal insufficiency, and race (African-American)
    • risk of MI or stroke is four to five times higher in patients with PAD

  2. Pathogenesis
    1. 'Response to Injury’ Hypothesis
      • atheromatous plaques contains lipid, smooth muscle cells, connective tissue, and monocytes/macrophages
      • first detectable change after injury is increased monocyte adhesion to the endothelium
      • monocytes then migrate to the subendothelial area where they localize and accumulate lipids (cholesterol esters), forming ‘foam’ cells
      • accumulation of subintimal foamy macrophages represents the development of the first lesion of atherosclerosis: the fatty streak
      • next comes separation of endothelial cell junctions overlying fatty streaks in areas of turbulent flow (infrarenal aorta, iliac bifurcation)
      • endothelial cell retraction exposes the subintimal connective tissue to the circulation, resulting in platelet adhesion and degranulation
      • growth factors produced by platelets and endothelial cells (platelet-derived growth factor) results in migration of smooth muscle cells from the media to the intima where they proliferate and produce large amounts of connective tissue
      • result is an intimal proliferative lesion consisting of smooth muscle cells, monocytes, and connective tissue: the fibrous plaque

      1. Ischemia as a Result of the Atheromatous Plaque
        • large plaques can cause stenosis of the lumen, resulting in decreased flow
        • unstable plaques can rupture, inducing thrombus formation with total occlusion of the vessel
        • embolization of ruptured plaque contents can result in downstream occlusion

Evaluation of Peripheral Artery Disease

  1. History and Physical Exam
    1. Clinical Presentation
      • most common symptom in lower extremity PAD is pain

      1. Intermittent Claudication
        • signifies mild to moderate extremity PAD
        • burning or aching pain that predictably occurs with ambulation, and is quickly relieved by rest
        • usually involves the calf (superficial femoral artery disease)
        • thighs or buttocks may also be involved (aortoiliac disease)
        • corresponds to an ABI of 0.5 - 0.7
        • serves as a marker for severe atherosclerotic disease

      2. Rest Pain
        • represents critical limb ischemia
        • usually occurs on the dorsum of the foot
        • may awaken the patient from sleep
        • relieved by dangling the foot over the bed

      3. Tissue Loss
        • ulcerations, nonhealing wounds, or gangrene represent end-stage PAD

    2. Past Medical History
      1. Cardiac and Stroke History
        • must obtain a detailed history of any cardiac symptoms
        • all cardiac procedures, including diagnostic procedures (caths, echos, stress tests) must be documented
        • prior stroke or TIA symptoms must be carefully elicited

      2. Past Medical History
        • attention should be paid to atherosclerotic risk factors: diabetes, smoking, hypertension, dyslipidemia

      3. Functional Status
        • detailed information on the patient’s functional status is critical in deciding what the goal of treatment is
        • functional status also helps determine cardiac risk and whether additional cardiac workup is necessary

    3. Physical Exam
      • blood pressure should be taken in both arms
      • heart should be examined for murmurs
      • presence or absence of carotid bruits should be noted
      • abdomen should be examined for aortic pulsations and bruits
      • all peripheral pulses should be palpated and characterized bilaterally
      • if a pulse is not palpable, a Doppler should be used to check for signals
      • dry, shiny skin, hair loss, and nail hypertrophy represent common findings in lower extremity PAD

  2. The Vascular Lab
    • noninvasive testing confirms and localizes disease, documents improvement after interventions, enables long term follow-up, and can detect disease recurrence

    1. ABI Testing
      • usually performed with a manual cuff at the ankle and a continuous wave Doppler probe over the dorsalis pedis or posterior tibial pulse
      • segmental pressures can be measured using multiple cuffs, which is helpful in determining the level of obstruction – a decrease in pressure of 20 to 30 mm Hg between adjacent segments is significant
      • ABI of a limb is calculated using the higher of the two ankle pressures divided by the higher of the two brachial pressures
      • patients with an ABI < 0.90 have a 3x to 6x increased risk of cardiovascular disease
      • a limitation of ABI is that it can be falsely elevated from arterial calcifications, especially in diabetic and ESRD patients

      ABI Chart
      1. Doppler waveforms
        • normal waveform demonstrates triphasic flow: a sharp systolic upstroke, reversal of flow in early diastole from vessel compliance, and low-amplitude forward flow throughout diastole

          • Triphasic Flow
        • mild obstructive disease demonstrates loss of reversal of flow in diastole (multiphasic or biphasic flow)

          • Biphasic Flow
        • severe obstructive disease reveals decreased amplitude and decreased slope of the systolic upstroke
        • end-stage disease reveals increased diastolic flow (monophasic flow)

          • Monophasic Flow
        • a change in waveform, along with a decrease in pressure, is indicative of disease at that level

      2. Postexercise ABI Testing
        • treadmill exercise should be done in symptomatic patients with palpable distal pulses or a normal resting ABI
        • exercise-induced vasodilation will increase the pressure drop across a stenotic lesion
        • patients exercise until symptoms occur
        • a decrease in ankle pressure of 20 mm Hg or a decrease in ABI of 0.20 is considered a positive result
        • failure of ABI to return to pre-exercise baseline within 3 minutes is also considered a positive test

    2. Arterial Duplex Ultrasonography
      • provides Doppler waveform and color flow data for analysis
      • can provide sensitive and specific information about the aorta, visceral, renal, iliac, and distal limb vessels
      • peak systolic and end-diastolic velocities are recorded
      • waveforms are analyzed
      • color flow is useful for distinguishing antegrade flow from retrograde flow
      • color flow can also demonstrate patent vessels in low-flow states
      • a change in waveform from triphasic to monophasic, or an increase in peak systolic velocity followed by a drop in velocity, indicates a hemodynamically significant lesion

  3. Imaging Studies
    • necessary when intervention is planned

    1. Angiography
      • historically, the ‘gold standard’ for delineating the location and nature of the lesion
      • now, angiography is considered a therapeutic tool rather than a diagnostic test
      • endovascular interventions can be performed at the same time as the initial angiogram
      • access is usually obtained through the contralateral femoral artery or the left brachial artery
      • access complications are reduced by ultrasound-guided access and micropuncture techniques
      • contrast nephropathy can be minimized by reducing the contrast load used, using iso-osmolar contrast agents, increasing oral hydration before and after the procedure, and holding diuretics, ACE inhibitors, and metformin before the procedure and for 48 hours after the procedure
      • radiation exposure for both the patient and physician must be routinely monitored

      Angiogram - SFA Stenosis and Occlusion
      Right SFA Stenosis. Left SFA Occlusion

    2. CT Angiography
      • can detect thrombus and calcification; conventional angiography only depicts the lumen of the vessel
      • allows for 3-D reconstructions and multiplanar reformatting
      • complications include contrast nephropathy and accumulation of radiation exposure

      CTA - Brachial Artery Occlusion
      Brachial Artery Occlusion

    3. Magnetic Resonance Angiography
      • requires the use of gadolinium, which is contraindicated in renal disease because of the risk of nephrogenic systemic fibrosis
      • high degree of accuracy for demonstrating the extent of stenosis and lesion length
      • may be superior to angiography in identifying distal target vessels

      MRA - Bilateral Tibioperoneal Disease
      Bilateral Tibioperoneal Disease

Endovascular management

  1. Goal
    • to re-establish straight-line flow to the distal extremity without the morbidity of an open approach
    • a multitude of techniques and devices exist, but there is no consensus as to the best approach

  2. Arterial Access
    1. Retrograde Femoral Access
      • most commonly used technique
      • entry point is 2 – 3 cm below the inguinal ligament
      • once entry is confirmed, a guidewire is placed and advanced under fluoro
      • entry above the inguinal ligament can result in a retroperitoneal hematoma
      • too low an entry can lead to entry into the superficial femoral artery or profunda femoris artery

    2. Antegrade Femoral Access
      • used for difficult infrainguinal lesions

    3. Brachial Artery Access
      • used when femoral access is impossible
      • left brachial artery is used because it avoids the origin of the carotid artery
      • entry site is just proximal to the antecubital crease

  3. Techniques
    1. Balloon Angioplasty
      • requires crossing the lesion transluminally with a guidewire and then inflating a balloon over the lesion
      • success is measured if the residual stenosis is < 30%, or if there is no pressure drop across the treated lesion
      • in the femoropopliteal segments, single tibial vessel runoff was associated with worse long-term patency
      • additional predictors of lower patency include diabetes and ESRD

      Balloon Angioplasty
    2. Stents
      • buttress collapsible vessels and help prevent restenosis
      • eventually a neointima forms over the stent
      • come in two varieties: self-expanding stents and balloon-expanding stents
      • once contraindicated, angioplasty and stenting are finding a role in infrapopliteal disease
      • drug-eluting stents are being developed to help prevent restenosis

      Balloon Expanding Stent Angioplasty
      Balloon Expanding Stent Angioplasty

    3. Stent Grafts
      • combination of a metal stent covered with a cloth fabric (usually PTFE)
      • inner surface is bonded with heparin
      • have the same patency rates as above-knee surgical bypasses

      Stent Graft






References

  1. Sabiston, 20th ed., pgs 1754 – 1764, 1775 – 1777
  2. Schwartz, 10th ed., pgs 828 - 837
  3. Cameron, 13th ed., pgs 999 - 1002
  4. Endovascular Therapy for Critical Limb Ischemia, Arain, Salman and White, Christopher. Vascular Medicine 2008; 13: 267 – 279