Peripheral Arterial Disease

Epidemiology
Definition of Peripheral Arterial Disease (PAD)

The presence of a stenosis or occlusion in the aorta or arteries of the limbs
Usually caused by atherosclerosis
Associated with an increased risk of cardiovascular and cerebrovascular events, including death, MI, and stroke
Clinical Manifestations of Atherosclerotic Disease

Carotid artery disease
Transient ischemic attack Stroke
Coronary artery disease

Stable angina pectoris Acute coronary syndromes
Renovascular disease
Hypertension Renal insufficiency
Peripheral arterial disease

Intermittent claudication Critical limb ischemia
Documented Presence of PAD

NHANES1
Age >40
4.3% 11.7% 14.5% 19.1% 19.8%
San Diego2
Mean Age=66
NHANES1
Age 70
When common risk factors were included, the prevalence of PAD was ~1/3 of patients
Rotterdam3
Age >55
Diehm4
Age 65
PARTNERS5
Age >70, or between 50-69 with diabetes or smoking
29%
25% 30% 35%
0%
5%
10%
15%
20%
1. Selvin E, Erlinger TP. NHANES. Circulation. 2004;110:738-743. 2. Criqui MH, et al. Circulation. 1985;71:510-515. 3. Diehm C, et al. Atherosclerosis. 2004;172:95105. 4. Meijer WT, et al. Arterioscler Thromb Vasc Biol. 1998;18:185-192. 5. Hirsch AT, et al. JAMA. 2001;286:1317-1324.
Prevalence of PAD Increases With Age

60
Patients With PAD (%)
50 40 30 20 10 0
Rotterdam Study (ABI<0.9, N=7715) San Diego Study (PAD established with noninvasive test, N=613)
55-59
60-64
65-69
70-74
75-79
80-84
85-89
Age Group (years)

Adapted from Golomb BA, et al. In: Creager MA, ed. Management of Peripheral Arterial Disease: Medical, Surgical and Interventional Aspects; 2000:1-18. Meijer WT, et al. Arterioscler Thromb Vasc Biol. 1998;18:185-192. Criqui MH, et al. Circulation. 1985;71:510-515.
The Aging Population

17% of the population 55-70 years of age has PAD
Population (millions)
25 20 15 10 5 0 10 20 30 40 50 60 70 80 90
1980 1990 2000 2010
N=1592 Age (years)
PAD = peripheral arterial disease

Fowkes FG, et al. Int J Epidemiol. 1991;20:384-392.
PAD in the United States

12 Americans (millions) 10 8 6 4 2 0 PAD PAD with Intermittent Claudication PAD with Cardiovascular Disease
Hirsch AT, et al. JAMA. 2001;286:1317-1324. American Heart Association. Heart Disease and Stroke Statistics - 2005 Update. Dallas, Tex.. American Heart Association; 2004.
Risk Factors
Independent Risk Factors for PAD*

Relative Risk vs the General Population
Reduced Increased
Diabetes
2.55 1.51 1.10
4.05
Smoking
Hypertension
Total cholesterol (10 mg/dL)
* PAD diagnosis based on ABI <0.90.

Newman AB, et al. Circulation. 1993;88:837-845
Diabetes Increases Risk of PAD

25 Prevalence of PAD (%)
22.4*
19.9*
20
15
10
12.5
N=1592
0
Normal Glucose Tolerance
Impaired Glucose Tolerance
Diabetes
IGT = oral glucose tolerance test value 140 mg/dL but <200 mg/dL *P0.05 vs normal glucose tolerance
Lee AJ, et al. Br J Haematol. 1999;105:648-654.
The Metabolic Syndrome

People with the metabolic syndrome are at increased risk of coronary heart disease, stroke, diabetes, and PAD Characterized by a group of metabolic risk factors: Abdominal obesity (waist circumference)
>40 inches men and >35 inches in women
Serum triglycerides 150 mg/dL Serum high-density lipoprotein cholesterol (HDL-C) <40 mg/dL in men and <50 mg/dL in women Blood pressure 130/85 mmHg Fasting blood glucose 110 mg/dL Metabolic syndrome = the presence of at least three of the five traits
Third report of the National Cholesterol Education Program (NCEP) Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Final Report. Circulation. 2002;106:3143-3421.
PAD Risk Factors are Synergistic

Risk of Intermittent Claudication (8-year rate per 1000)
40 Nonsmoker Smoker
36.6
30
20
14.6
10
0.8 2.6 2.5
8.0
0
105 185 150 260 195 335
N=295
Systolic Blood Pressure Total cholesterol Impaired glucose
Adapted from TASC Working Group. J Vasc Surg. 2000;31:S13.
Screening Techniques and Diagnostic Criteria
Clinical Manifestations of PAD

Asymptomatic Intermittent claudication Discomfort, ache, cramping in leg with exerciseresolves with rest Functional impairment Slow walking speed, gait disorder Rest pain Pain or paresthesias in foot or toes, worsened by leg elevation and improved by dependency Ischemic ulceration and gangrene
Clinical Presentation of PAD

Initial PAD Presentation
Asymptomatic PAD 20-50%
Symptomatic PAD
Atypical Leg Pain 40-50%
Intermittent Claudication 10-35%
Critical Limb Ischemia 1-2%
Hirsch AT, Haskal ZJ, Hertzer NR, et al. Available at http://www.acc.org/clinical/guidelines/pad/summary.pdf. Accessed December 13, 2005.
Symptoms of Intermittent Claudication

Aching, pain, tiredness, tightness, cramping in the buttocks, thigh, calf, or foot brought on by exercise and relieved by rest Reproducible with a consistent level of exercise from day to day
Completely resolve within 5 minutes after exercise stops Occur again at the same distance once walking resumes
ABI and Functional Outcomes: 6-Minute Walk

70
Patients Stopping(%)
60
50 40 30 20 10 0
Mean Distance (feet)
1600 1200 800 400 0
ABI
ABI
N=740
McDermott MM, et al. Ann Intern Med. 2002;136:873-883.
Causes of Pseudoclaudication
Spinal canal stenosis Peripheral neuropathy Peripheral nerve pain Herniated disc impinging on sciatic nerve Osteoarthritis of the hip or knee Venous claudication Chronic compartment syndrome Muscle spasms/cramps/restless leg syndrome Cold feet
Does the Patient Have Intermittent Claudication?

Claudication Characteristic of discomfort Location of discomfort Exercise-induced Distance Occurs with standing Action for relief Time to relief Cramping, tightness, aching, fatigue Buttock, hip, thigh, calf, foot Yes Consistent Pseudoclaudication Same, tingling, burning, numbness Same Variable Variable
No
Stand Less than 5 minutes
Yes
Sit, change position Up to 30 minutes
Clinical History
Past medical history Does the patient have a history of atherosclerosis elsewhere? Does the patient have significant comorbidities? Does the patient have risk factors for atherosclerosis? Family history Does the patient have a family history of atherosclerosis or abdominal aortic aneurysm? Review of symptoms Does the patient have symptoms in other vascular beds?
Comprehensive Vascular Examination

Pulse Examination Carotid Radial/ulnar Femoral Popliteal Dorsalis pedis Posterior tibial Physical Examination Bilateral arm blood pressure Cardiac exam Palpation of abdomen for potential aneurysmal disease Auscultation for bruits Examination of legs and feet
Scale 0 = absent 1 = diminished 2 = normal
Screening Techniques
Role of Ankle-Brachial Index
Indications for an ABI

Traditional AHA-ACC ADA
History of classic or suspected claudication History of CLI (rest pain, gangrene, nonhealing wound)
Any diabetic patient >50 years old Any diabetic patient <50 yr old who has risk factors All patients with PAD symptoms
All patients >70 years old All patients >50 years old who smoke or have diabetes
ADA = American Diabetes Association; AHA = American Heart Association; ACC = American College of Cardiology
Hirsch AT, et al. JAMA. 2001;286:1317-1324. American Diabetes Association. Diabetes Care. 2003;26:3333-3341.
ABI Testing: Highly Sensitive and Specific

Effectiveness of ABI vs Other Common Screening Tests Diagnostic Test ABI Pap smear Fecal occult-blood test Mammography
Dormandy JA, et al. Semin Vasc Surg. 1999;12:96-108. Nanda K, et al. Ann Intern Med. 2000;132:810-819. Allison JE, et al. N Engl J Med. 1996;334:155-159. Ferrini R, et al. Am J Prev Med. 1996;12:340-341.
Sensitivity (%) 95 30-87 37-69 75-90
Specificity (%) 99 86-100 87-98 90-95
The Ankle-Brachial Index (ABI)

ABI =
Ankle systolic pressure Brachial systolic pressure
Using the ABI

Right ABI 80/160 = 0.50 Brachial SBP 150 mmHg Left ABI 120/160 = 0.75 Brachial SBP 160 mmHg ABI (normal >0.90) Highest Brachial SBP
PT SBP 40 mmHg DP SBP 80 mmHg
PT SBP 120 mmHg DP SBP 80 mmHg
Highest of PT or DP SBP
PT = posterior tibial; DP = dorsalis pedis; SBP = systolic blood pressure.
Automated Blood Pressure Determination Accurately Measures ABI

201 consecutive subjects underwent standard Doppler and oscillometric measurement of the ABI
1.6 1.4
Doppler Left ABI
1.2
1.0 0.8 0.6
Sensitivity Specificity Positive PV Negative PV
88% 85% 65% 96%
0.4
0.2 0.4 0.6 0.8 1.0
r2 = 0.62
1.2 1.4
Oscillometric Left ABI

Beckman JA, et al. Hypertension. 2006;47:35-38
ABI Limitations
Incompressible arteries (elderly patients, patients with diabetes, renal failure, etc)
Resting ABI may be insensitive for detecting mild aortoiliac occlusive disease Not designed to define degree of functional limitation Normal resting values in symptomatic patients may become abnormal after exercise Does not distinguish between stenosis and occlusion
Diagnostic Tests
Diagnostic Tests
Segmental blood pressure recording
Segmental pulse volume recording Exercise stress testing Continuous wave Doppler and duplex ultrasonography Magnetic resonance angiography (MRA) Computed tomographic angiography (CTA)
Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA Guidelines for the Management of Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic).
Segmental Limb Pressure

150 Brachial 150
150 110
150 146
108 62
100 84
0.54
ABI
0.44
Pulse Volume Recordings
Color Duplex Ultrasonography
Color Duplex Ultrasonography
Magnetic Resonance Angiography (MRA)

MRA has virtually replaced contrast arteriography for PAD diagnosis Excellent arterial picture No ionizing radiation Noniodine-based intravenous contrast medium rarely causes renal insufficiency or allergic reaction ~10% of patients cannot have MRA because of Claustrophobia Pacemaker/implantable cardioverterdefibrillator Obesity
Computed Tomographic Angiography (CTA)
Requires iodinated contrast Requires ionizing radiation
Produces an excellent arterial picture
Differential Diagnosis
PAD: A Full Differential Diagnosis

Atherosclerosis Vasculitis Fibromuscular dysplasia Atheroembolic disease Thrombotic disorders Trauma Radiation Popliteal aneurysm Thromboangiitis obliterans (Buergers disease) Popliteal entrapment Cystic adventitial disease Coarctation of aorta Vascular tumor Iliac syndrome of the cyclist Pseudoxanthoma elasticum Persistent sciatic artery (thrombosed)
PAD: A Full Differential Diagnosis

Popliteal Entrapment Syndrome Popliteal Adventitial Cyst
5%
85%
Atherosclerosis
10%
Popliteal Aneurysm Thromboangiitis Obliterans (Buergers disease) Arteritis Fibromuscular Dysplasia
Pathophysiology of Atherothrombosis
The Normal Artery
Pathophysiology of Atherothrombosis
Adapted from Libby P. Nature. 2002;420:868-874
Platelet Cascade in Thrombus Formation

GP Ib = glycoprotein Ib; ADP = adenosine diphosphate; 5 HT = serotonin; TXA2 = thromboxane A2; GP IIb/IIIa = glycoprotein IIb/IIIa.
von Willebrand Factor/GP lb bind
1 Adhesion
Collagen GP la/lla bind
Lipid core
Platelets
Handin RI. Harrisons Principles of Internal Medicine. vol 1. 14th ed. NY, NY: McGraw-Hill; 1998:339-345. Schafer AI. Am J Med. 1996;101:199-209.

Thrombin ADP 5 HT TXA2
2 Activation
Handin RI. Harrisons Principles of Internal Medicine. Vol 1. 14th ed. NY, NY: McGraw-Hill; 1998:339-345. Schafer AI. Am J Med. 1996;101:199-209.

Fibrinogen
3 Aggregation
Activated GP llb/llla
Handin RI. Harrisons Principles of Internal Medicine. Vol 1. 14th ed. NY, NY: McGraw-Hill; 1998:339-345. Schafer AI. Am J Med. 1996;101:199-209.
Atherothrombosis Pathophysiology:
Endothelial Dysfunction
NO = nitric oxide; PGI2 = prostacyclin; SMC = smooth muscle cell; TxA2 = thromboxane A2; ET-1 = endothelin 1; TF = tissue factor; MMPs = matrix metalloproteinases; solid line = induces; broken line = inhibits.
Viles-Gonzalez JF, et al. Eur Heart J. 2004;25:1197-1207.
PAI-1 = plasminogen activator inhibitor-1; tPA = tissue plasminogen activator; NO = nitric oxide; PGI2 = prostacyclin; SMC = smooth muscle cell; TxA2 = thromboxane A2; ET-1 = endothelin 1; TF = tissue factor; MMPs = matrix metalloproteinases; solid line = induces; broken line = inhibits; open arrow = increases.
Viles-Gonzalez JF, et al. Eur Heart J. 2004;25:1197-1207.
FDP = fibrin degradation product; PAI-1 = plasminogen activator inhibitor-1; tPA = tissue plasminogen activator; NO = nitric oxide; PGI2 = prostacyclin; SMC = smooth muscle cell; TxA2 = thromboxane A2; ET-1 = endothelin 1; TF = tissue factor; VIIa = factor VIIa; Xa = factor Xa; MMPs = matrix metalloproteinases; solid line = induces; broken line = inhibits; downward-pointing open arrow = decreases; upward-pointing open arrow = increases. Viles-Gonzalez JF, et al. Eur Heart J. 2004;25:1197-1207.
Atherosclerosis: Intravascular Ultrasound of a Ruptured Plaque
From Ziada K and Bhatt DL. In Bhatt DL: Essential Concepts in Cardiovascular Intervention, ReMEDICA 2004.
Physiology of Acute Thrombosis

A. Injury

B. Initiation

C. Extension (recruitment)

D. Perpetuation (stabilization)
The Activated Platelet

Platelet Activators Blood Thrombin Thromboxane A2 Adenosine diphosphate Vessel wall Collagen von Willebrand factor
Platelet Inhibitors Nitric oxide Prostacyclin
Ruggeri ZM. Nature Medicine. 2002;8:1227-1234.
Arterial Stenosis Causes Loss of Pressure and Flow

Normal Laminar Flow
An 80% stenosis causes a pressure drop at rest Turbulent flow downstream of stenosis cases a loss of kinetic energy
Turbulent Flow Behind Stenosis
Supply-Demand in PAD
35
Flow (mL/100 mL/min)
30 25 20 15 10 5 0
Control PAD
Rest
Low
Medium
High
Exertion Level
Bauer T, Hiatt WR, In Press.
Natural History of PAD
The Natural History of PAD

Increased risk for cardiovascular ischemic events due to concomitant coronary artery disease and cerebrovascular disease
Cardiovascular events are more frequent than ischemic limb events in any lower extremity PAD cohort, regardless of presentation
Overlap Between PAD, CAD, and CVD
CVD
9.5%
14.2%
CAD
39.4%
PAD
36.9%
Patients with one manifestation often have coexistent disease in other vascular beds.
Bhatt DL, et al. REACH Investigation. Presented at: American College of Cardiology Annual Scientific Session; March 8, 2005; Orlando, FL. Abstract 1127-96.
Natural History of PAD: 5-year Outcomes

Cardiovascular Morbidity and Mortality
Limb Morbidity Morbidity Limb
Stable Claudication 70-80%
Worsening Claudication 10-20%
Nonfatal CV Events 15-30%
Mortality 15-30%
Critical Limb Ischemia 1-2 %
CV Causes 75%
Non-CV Causes 25%
PAD and Relative Risk of Death

10
Relative Risk (95% CI)
8 6 4 2 0
All Causes 3.1 (1.9-4.9)
5.9 (3.0-6.6)
6.6 (2.9-14.9)
Cardiovascular Disease
Coronary Heart Disease
Cause of Death
Criqui MH, et al. N Engl J Med. 1992;326:381-386.
PAD Survival Curve

100 Normal Subjects
Survival (%)
75 50 Asymptomatic PAD Symptomatic PAD Severe Symptomatic PAD
25
10
12
Year
Criqui MH, et al. N Engl J Med. 1992;326:381386.
Cause of Death in IC Patients
Nonvascular 25%
Cardiac 55%
Cerebral 11% Other vascular 9%
Dormandy JA, et al. J Vasc Surg. 2000;31:S1-S296.
CHD Risk Increases With Decreases in Ankle Brachial Index (ABI)

30
Five-Year Incidence of CV Deaths, %*
5-year risk: 21%

20
10
5-year risk: 8%
0 >1.1 1.1-1.01 1.0-0.91 0.9-0.71 <0.7
*Including aneurysm, thromboembolism, stroke, and myocardial infarction.

Leng GC, et al. BMJ. 1996;313:1440-1444.
Association Between ABI and All-Cause Mortality

70
Mortality (%)
60 50 40 30
20
10 0
<0.6 0.7 0.8 0.9 1.0 1.1 1.2 1.3 1.4 1.5 1.5 INC (n=25) (n=21) (n=40) (n=130) (n=195) (n=980) (n=980) (n=954) (n=245) (n=136) (n=89) (n=179)
Baseline ABI
INC=Incompressible
Adapted from Resnick HE. Circulation. 2004;109:733-739.
N=4393
ABI, CRP, and CV Event Risk

ABI
>0.90 0.7-0.9 <0.7
80
Events (%)
60 40 20
N=110
0
>3.0 1.0-3.0 <1.0
CRP (mg/dL)
Beckman JA, et al. Am J Cardiol. 2005;96:1374-1378.
Vascular Laboratory Progression of Disease in Patients with Symptomatic PAD (OHSU Study)
100% ABI progression Carotid stenosis progression ABI or carotid progression
Subjects (%)
75%
50%
25%
0%
0 6 12 18 24 30 36 42 48 54
N=397
60
Months
OHSU = Oregon Health and Science University
Nicoloff AD, et al. J Vasc Surg. 2002; 35:38-47.
Critical Limb Ischemia (CLI)
Peripheral Arterial Disease Complication: Ischemic Ulcer
Amputation
Critical Limb Ischemia (CLI)

Fate of Patients With CLI After Initial Treatment
Summary of 19 studies on 6-month outcomes
Alive With Amputation 35%
Dead 20%
Alive Without Amputation 45%
Early and 2-year Fate of the BelowKnee Amputee

Early
2 Healing 15% Above-knee Amputation 15% Perioperative Death 10% Full Mobility 40%
After 2 Years
Death 30%
1 Healing 60%
Contralateral Amputation 15%
Above-knee Amputation 15%
Treatment of Peripheral Arterial Disease
Two Goals in Treating Patients With PAD

Outcomes in Cardiovascular Morbidity and Mortality
Decrease mortality from MI, stroke, and cardiovascular death Decrease nonfatal MI and stroke
Limb Outcomes
Improve ability to walk Important increase in peak walking distance Improvement in quality of life indicators Prevent progression to critical limb ischemia and amputation
Peripheral Arterial Disease

Management of Cardiovascular Risks
Antiplatelet Therapy
Antiplatelet therapy reduces the risk of MI, stroke, and vascular death in patients with established PAD Aspirin is a well-recognized antiplatelet drug that has been shown to benefit patients with CVD and PAD Clopidogrel is the only antiplatelet agent approved by the FDA to reduce the risk of MI, stroke, or vascular death in patients with established PAD Other antiplatelet drugs used to treat PAD include Dipyridamole Ticlopidine Picotamide Suloctidil Indobufen Sulphinpyrazone
Mechanisms of Action of Oral Antiplatelet Therapies
COX = cyclooxygenase; PDE = phosphdiesterase.

Schafer AI. Am J Med. 1996;101:199-209.
Risk of Occlusive Vascular Events in High-Risk Patients: Antithrombotic Trialists Collaboration

Risk Category (number of trials) Intermittent claudication (N=26) Peripheral grafting (N=12) Patients with Event (%) APT Control 6.4 5.4 2.5 5.8 7.9 6.5 3.6 7.1 0.0
APT=antiplatelet therapy with aspirin, clopidogrel, dipyridamide, or a glycoprotein IIb/IIIa antagonist
Antithrombotic Trialists Collaboration. BMJ. 2002;324:71-86.
Risk versus Control

Reduced Reduced Increased
Peripheral angioplasty (N=4)

All PAD trials (N=42)
N=9706 0.5 1.0 1.5 2.0
Efficacy of Clopidogrel vs Aspirin in MI, Ischemic Stroke, or Vascular Death

Aspirin 16 Aspirin 5.83% 8 5.32% Clopidogrel 4 Clopidogrel 8.7%* Overall Relative Risk Reduction
Cumulative Event Rate (%)
12
0 0 3 6 9 12 15 18 21 24 27 30 33 36
N=19,185
Months of Follow-Up Mean Follow-up = 1.91 years
*ITT analysis.
CAPRIE Steering Committee. Lancet. 1996;348:1329-1339.
Risk Reduction of Clopidogrel vs Aspirin in Patients With Atherosclerotic Vascular Disease

Aspirin Favored Clopidogrel Favored
Stroke
Myocardial Infarction
PAD
All Patients
-40 -30 -20 -10 0 10 20 30
N=19,185
CAPRIE Steering Committee. Lancet. 1996;348:1329-1339.
Peripheral Arterial Disease

Risk Factor Modification
Lifestyle Interventions for PAD

Target Smoking Action Identify smoking as major risk factor Measure weight, body-mass index Measure blood pressure Actively monitor diabetes Therapy Cognitivebehavioral therapy Weight loss to reach ideal body weight DASH diet Exercise Weight loss Exercise
Obesity
Hypertension Type 2 diabetes
DASH = Dietary Approaches to Stop Hypertension
Intensive BP Therapy in Patients With Diabetes: Benefits in the PAD Group

50
Odds of MI, Stroke, or Vascular Death
40 30
Moderate treatment (137/81), n=227 Mean BP 137 mmHg Intensive treatment* (128/75), n=220 Mean BP 128 mmHg P=0.009 *enalapril or nisoldipine
20
P=0.91
10 0 0.0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 1.1 1.2 1.3
Baseline ABI
Odds calculated using moderate treatment and baseline ABI = 1.0 as reference PAD was defined as an ABI <0.9 (n=53) ABCD = Appropriate Blood Pressure Control in Diabetes Study
Reprinted with permission from Mehler PS, et al. Circulation. 2003;107:753-756.
Heart Protection Study: Vascular Event by Prior Disease

Incidence of Events Statin Existing Disease
Previous MI Other CHD No prior CHD or CVD Peripheral arterial disease Diabetes 23.5 18.9
Control
29.4 24.2 23.6 30.5 18.6 25.2
Risk versus Control

Statin Favored Placebo
(n=10,269) (n=10,267)
18.7
24.7 13.8 19.8
24% Reduction (p<0.0001)
All patients
MI - myocardial infarction; CHD - coronary heart disease; CVD - cerebrovascular disease; PAD - peripheral arterial disease; CI - confidence interval; SE - standard error
Heart Protection Study Collaborative Group. Lancet. 2002;360:7-22.
0.4 0.6 0.8 1.0 1.2 1.4
Adult Treatment Panel (ATP III): Updated LDL-C Goals, Treatment Cutpoints
Risk Category
High risk: CHD or CHD risk equivalents* (10-year risk >20%) Moderately high risk: 2 risk factors (10-year risk 10%-20%)
*CHD
Low-density LDL-C Goal <100 mg/dL (optional: <70 mg/dL) <130 mg/dL (optional: <100 mg/dL)
Initiate Therapeutic Consider Lifestyle Change Drug Therapy 100 mg/dL 100 mg/dL (<100 mg/dL: consider drug options) 130 mg/dL (100-129 mg/dL: consider drug options)
130 mg/dL
risk equivalents: clinical manifestations of noncoronary forms of atherosclerotic disease (transient ischemic attacks or stroke of carotid origin >50% obstruction of a carotid artery), diabetes, and 2+ risk factors with 10-year risk >20% for hard CHD. The optional LDL-C goal of <70 mg/dL is favored in those at very high risk (eg, people with diabetes, smokers) as well as those with metabolic syndrome, acute coronary syndrome, high TG, and/or non HDL-C <100 mg/dL. Any person at high or moderately high risk with lifestyle-related risk factors is a candidate for TLC to modify these risk factors regardless of LDL-C level. Grundy SM, et al. Circulation. 2004;110:227-239.
PAD Lipid Recommendations

Reduce CV mortality risk Statin to achieve NCEP guidelines of LDL-C <100 mg/dL 1 mmol/L reduction in LDL-C associated with 20% reduction in major CV outcomes Statin to reduce CRP levels Niacin or fibrate to increase HDL-C, lower TGs
American Heart Association Evidence-Based Guidelines for CVD Prevention: Lifestyle Modification Lifestyle Changes 30 minutes moderate-intensity physical activity daily Smoking cessation Weight maintenance/reduction Heart-healthy low cholesterol diet
Expert Panel/Writing Group. Circulation. 2004;109:672-693.
American Heart Association Evidence-Based Guidelines for CVD Prevention: Treatment Targets
Blood Pressure Baseline BP <120/80 mm Hg: Maintenance with lifestyle approaches Baseline BP 140/90 mm Hg: Treat with thiazide diuretics Lower threshold (<130 mm Hg SBP) for diabetics or patients with target organ damage Diabetes HbA1C <7% using combination of lifestyle changes and antidiabetic drugs Lipid Levels LDL-C <100 mg/dL HDL-C >50 mg/dL Triglycerides <150 mg/dL Non-HDL-C <130 mg/dL Achieve targets with lifestyle modification and, if necessary, pharmacotherapy
NCEP ATP-III LDL-C Goals

LDL-C goal <100 mg/dL for patients with CHD, PAD, or another CHD-risk equivalent CHD risk equivalents have a >20% risk for development of CHD
NCEP Expert Panel. ATP III Guidelines. 2001. NIH publication 01-3670.
HOPE: Primary Endpoints

~42% of Placebo and Ramipril-Treated Patients had PAD
Ramipril Outcome MI, stroke, or CV death CV death Myocardial infarction Stroke N=4645 Placebo N=4652 Relative Risk
Proportion Reaching End-Point
P Value
0.20 Placebo 0.15 P<0.001 0.10 0.05 Ramipril
651 (14%) 282 (6.1%) 459 (9.9%) 156 (3.4%)
826 (17.8%) 377 (8.1%) 570 (12.3%) 326 (4.9%)
0.78 0.74 0.8 0.68 1.03 0.84
<0.001 <0.001 <0.001 <0.001 0.74 0.005
N=9297
0.00
Death -non CV cause

Death from any cause
200 (4.3%)
482 (10.4%)
192 (4.1%)
569 (12.2%)
500 1000 Days of Follow-up
1500
HOPE Study Investigators. N Engl J Med. 2000;342:145-153.
HOPE: Benefits in CV Risk Subgroups

No. of Patients
Relative Risk in Ramipril Group

Reduced Increased
History of CAD No history of CAD

Prior MI No prior MI Cerebrovascular disease No cerebrovascular disease Peripheral vascular disease No peripheral vascular disease Microalbuminuria No microalbuminuria
7477 1820
4892 4405 1013 8284 4051 5246 1956 7341
0.6
HOPE Study Investigators. N Engl J Med. 2000;342:145-153.
0.8
1.0
1.2
HOPE: PAD Outcomes

Incidence of Composite Outcome in Control Group (%)
Relative Risk in Ramipril Group

Reduced Increased
Peripheral arterial disease (n=4046) No peripheral arterial disease (n=5251)
0.5 0.3 0.6 0.8 1.0 1.2
HOPE Study Investigators. N Engl J Med. 2000;342:145-153. Hiatt WR. N Engl J Med. 2001; 344;1608-1621.
Efficacy of ACE-I, Statins, and Antiplatelet Therapy in PAD No. of Patients

in Subgroup
APTC* CAPRIE*
placebo 6.0% 4.9% 3.7% 4.4%
(>9000)
aspirin clopidogrel
placebo
(>6000)
HOPE*
ramipril
3.4%
P < 0.001
6.1% P < 0.001 5 6
(4051)
HPS*
0 1
placebo simvastatin 2 3 4
4.9%
(2701)
7
Event Rate (% per year)

*PAD subgroups only.
APTC Antiplatelet Trialists Collaboration. BMJ. 1994;308:81-106. CAPRIE Steering Committee. Lancet. 1996;348:1329-1339. HOPE Study Investigators. N Engl J Med. 2000;342:145-153. Heart Protection Study Collaborative Group. Lancet. 2002;360:7-22.
PAD Risk-Reduction Therapies

Life Style Modifications 30 minutes moderate-intensity physical activity daily Weight maintenance/reduction Low cholesterol diet Smoking Complete cessation Diabetes mellitus HbA1c <7.0%, treat other risk factors Dyslipidemia LDL <100 mg/dL, modify HDL and TG Hypertension BP <140/90 or <130/80 in diabetes Antiplatelet therapy
Medical Therapy of Claudication

Nonpharmacologic Options
Intermittent Claudication: Exercise Therapy

Frequency: 3-5 supervised sessions/week Duration: 35 to 50 minutes of exercise/session Type of exercise: treadmill or track walking to near-maximal claudication pain Length: 6 months or more Results: 100%-150% improvement in maximal walking distance Improvement in quality of life
Stewart KJ, et al. N Eng J Med. 2002;347:1941-1951.
Efficacy of Exercise Training as a Therapeutic Intervention for Claudication

300 250
Controlled trials Uncontrolled trials
% Improvement
200 150 100 50 0

Pain-Free Peak
134 % 96 %
Treadmill Walking Time

Gardner AW, Poehlman ET. JAMA. 1995;274:975-980.
Effects of Exercise Training on Claudication

Meta-analysis of 21 Studies
200
180
Exercise Training Control
Walking Distance (%)
Change in Treadmill
160 140 120
100
80 60 40
20
0 Onset of Claudication Pain Maximal Claudication Pain
Gardner AW, Poehlman ET. JAMA. 1995;274:975-980.
Medical Therapy of Claudication

Pharmacologic Options
Cilostazol vs. Pentoxifylline: Increased Walking Distance in Claudication

Percent Change From Baseline MWD (mean) 50 40 30 20 10 0
* P<0.001
Cilostazol 100 mg 2x/day (n=227) Pentoxifylline 400 mg 3x/day (n=232) Placebo (n=239)
vs pentoxifylline
12
16
20
24
Weeks of Treatment
MWD = maximal walking distance
Dawson DL, et al. Am J Med. 2000;109:523-530.
Effect of Pentoxifylline on Pain-Free Walking Distance in Patients with IC

Study Di Perri and Guerrini, 1983 Donaldson et al, 1984 Gillings et al, 1987 Lindgarde et al, 1989 Rudofsky et al, 1992 Treatment Control (n) (n) 24 40 67 76 75 24 40 61 74 79
Ernst et al, 1992

Meta-analysis
20
302
20
298
-300 -200 -100 0 100 200 300 Pain-Free Walking Distance (m)
Girolami B, et al. Arch Intern Med.1999;159:337-345.
Effect of Cilostazol on Walking Distance in Patients With Claudication

Meta-analysis of 4 randomized, placebo-controlled trials Compound, dose N
Placebo Treatment Favored
Pentoxifylline, 1200 mg/day 698 Cilostazol, 200 mg/day Cilostazol, 200 mg/day Cilostazol, 100 mg/day Cilostazol, 200 mg/day Cilostazol, 200 mg/day 516 239 81
0.6 0.8 1.0 1.2 1.4 1.6 1.8 Relative Increase in Maximum Walking Distance (ratio of
change in exercise performance versus placebo)
Hiatt WR. N Engl J Med. 2001; 344;1608-1621.
Contraindications to Cilostazol Use

Cilostazol and several of its metabolites are inhibitors of phosphodiesterase III. Several drugs with this pharmacologic effect have caused decreased survival compared to placebo in patients with class III-IV congestive heart failure. PLETAL is contraindicated in patients with congestive heart failure of any severity.
CHF of any severity Any known or suspected hypersensitivity to any of its components
PLETAL Package Insert, 1999.
Therapy of Intermittent Claudication: Magnitude of Functional Improvement
Pentoxifylline
Cilostazol
Supervised Exercise
50
100
150
200
Improvement Over Baseline After 90 to 180 Days (%)

Gardner AW, Poehlman ET. JAMA. 1995;274:975-980; Girolami B, et al. Arch Intern Med. 1999;159:337-345. Hiatt WR. N Engl J Med. 2001; 344;1608-1621.
Revascularization
Surgical and Endovascular Options
Indications for Intervention

Persistent, lifestyle limiting claudication despite maximal medical therapy Rest pain Nonhealing ulcer Gangrene
Options in Revascularization
Endovascular Reconstruction Options Percutaneous transluminal angioplasty (PTA) Stents Surgical Reconstruction Options Aortoiliac/aortofemoral reconstruction Femoropopliteal bypass (above-knee and below-knee) Femorotibial bypass
Aortoiliac Occlusive Disease
Aortoiliac Occlusive Disease

Angioplasty + Stenting
High procedural success rates (90%) Excellent long-term patency (up to 70% at 5 years) No clear benefit of primary stenting vs angioplasty and selective stent placement Factors associated with a poor outcome Long segment occlusion Multifocal stenoses Eccentric calcification Poor runoff
Aortoiliac Occlusive Disease (contd)

Aortobiiliac/Aortobifemoral Bypass
Excellent long-term patency rate 85%-90% at 5 years Requires general anesthesia Can be done via laparotomy or retroperitoneal exposure
Aortoiliac Occlusive Disease (contd)

Axillobifemoral bypass
Patency rate lower than that of aortobifemoral bypass 30%-70% at 5 years Avoids laparotomy Useful in patients who have History of aortoiliac surgery Severe aortic calcification Hostile abdomen Can be done in the debilitated patient after induction of local anesthesia
Femoropopliteal Occlusive Disease
Femoropopliteal Disease
Endovascular Options
Excellent procedural success Low complication rates (3%-6%) Reported patency varies widely 30%-80% at one year Nitinol stents may have better patency than stainless steel No clear benefit of primary stenting vs angioplasty alone
Femoropopliteal Disease
Endovascular Options
Limited by recurrent stenosis Numerous adjuncts to minimize effect of restenosis Drug-eluting stents Atherectomy catheter Cryoplasty balloon Laser atherectomy Brachytherapy
Infrainguinal Bypass for Limb Salvage: Ideal Results

Uncomplicated operation Prompt wound healing Rapid return to premorbid functional status Long-term symptom relief Cure of ischemia No recurrence of ischemic ulcer No need for repeated surgery
Femoropopliteal Occlusive Disease: Surgical Bypass

Bypass of choice for superior femoral artery or above-knee popliteal occlusion Choice of conduitvein vs poly-tetrafluoroethylene Have similar above-knee patency rate Vein has better below-knee patency rate Limb salvage rates are 70% at 5 yrs
Tibial Occlusive Disease
Tibial Occlusive Disease

Angioplasty + Stenting
Small case series Feasible, safe Little long-term data Provides another therapeutic alternative in this complex patient population
Dorsalis Pedis (DP) Bypass

1032 DP bypasses in 865 patients between January 1990 and January 2000 DP bypasses were 28% of all infrainguinal procedures done 5-year patency: Primary = 57% Secondary = 63% Limb salvage at 5 years = 78%
Pomposelli FB, et al. J Vasc Surg 2003;37:307-315.
Durability of Endovascular Procedures

Primary Patency (%, 95% CI)
0 20 40 60 80 100
Iliac PTA
Iliac Stent
Femoropopliteal PTA
Femoropopliteal Stent Infrapopliteal PTA

Mean 1-year data 2-year data 3-year data 4-year data 5-year data
Durability of Surgical Interventions for Inflow Improvement

Operative Mortality (%) 3.3 1-2 0 6 6 4.9 Expected Patency Rate at Follow-up (%) 87.5 85-90 79-90 71 49-80 63-67.7
Inflow Procedure Aortobifemoral bypass Aortoiliac or aortofemoral bypass Iliac endarterectomy Femorofemoral bypass Axillofemoral bypass Axillofemoral-femoral bypass
Follow-up 5 years 5 years 5 years 5 years 3 years 5 years
Durability of Surgical Interventions for Outflow Improvement

Outflow Procedure
Femoral - popliteal V ein, above the knee P rosthetic , above then knee Vein , below the knee P rosthetic , below the knee 1.3-6.3 1.3-6.3 1.3-6.3 1.3-6.3 66 47 66 33 5 years 5 years 5 years 5 years Operative Mortality (%) Expected Patency Rate At Follow-up (%)
Follow-up
Femoral -tibial
Vein P rosthetic B lind segment bypass Com posite sequential byp ass Profundaplasty 1.3-6.3 1.3-6.3 2.7-3.2 0-4 0-3 74-80 25 64-67 28-40 49-50 5 years 3 years 2 years 5 years 3 years
Limb Salvage and Overall Survival

VA National Surgical Quality Improvement Program
1.0 0.9 0.8 0.7 0.6 0.5 0.4 20 40 60 80 Follow-up in Months
Feinglass J, et al. J Vasc Surg. 2001;34:283-290.
Kaplan-Meier (Probability)
Major amputation after femoropopliteal bypass Major amputation after tibial bypass
Survival 100
N=4288
Outcomes in Patients Following Limb Salvage Procedure

100
80
Patients (%)
60 40
20
0
Mortality Primary Patency Limb Salvage
Conte MS, et al. Presented at: Society for Vascular Surgery; June 16, 2005; Chicago, IL.
PREVENT III Trial: QoL

6 5.11.4*
Global QoL Scores
5 4 3 2 1 2.81.1
4.71.4*
N=1404 (patients with CLI after lower extremity vein bypass)

*P<0.0001
0 Baseline 3 Months 12 Months
Moneta GL, et al. Presented at: Western Vascular Society; September 27, 2005; Park City, UT.
Postoperative Mortality and Cardiac Morbidity

6565 vascular operations in 5126 patients between January 1990 and May 2000 4052 lower extremity revascularization 1679 carotid 834 aortic Outcomes Mortality: 1.14% MI: 1.59% CHF: 1.13%
Hamdan AD, et al. Arch Surg. 2002;137:417-421.
CARP Trial: Effect of Prior Coronary Revascularization on Mortality after Vascular Surgery
100 2.7-Year Mortality (%) 80 60 40
22%
23%
N=510
20 0 After Revascularization No Revascularization
McFalls EO, et al. N Engl J Med. 2004;351:2795-2804.
Management of Leg Symptoms in Patients With PAD

PAD
Claudication: Assess severity Treadmill ACD/ICD Questionnaires SF-36/WIQ Claudication therapy: Supervised exercise Cilostazol
Critical Leg Ischemia
Symptoms improve
Continue
Symptoms deteriorate Localize the lesion: Hemodynamic localization Duplex ultrasound imaging Magnetic resonance angiography Conventional angiography
Revascularization: Angioplasty Bypass surgery
Hiatt WR. N Engl J Med. 2001;344:1608-1621.
Future Therapies
Medical Therapies Under Investigation for PAD

Cilostazol analogs Nitric acidderivative of aspirin Immune modulation therapy Liposome-encapsulated form of prostaglandin E-1 Angiogenic growth factors Hypoxia inducible factor1 Hepatocyte growth factor Vascular endothelial growth factor-2 Endothelial progenitor cells
Investigational Devices for PAD

Cryo-balloon Enhanced external counterpulsation (EECP) Paclitaxel-eluting stent SilverHawk plaque excision system
2005 ACC/AHA Guidelines for the Management of Peripheral Arterial Disease

Introduction to the Guidelines
Why a PAD Guideline?

Aid in the recognition, diagnosis, and treatment of PAD of the aorta and lower extremities Address the prevalence, impact on quality of life, cardiovascular ischemic risk, and risk of critical limb ischemia
Classification of Recommendations
Class I: Evidence and/or general agreement that procedure or treatment is beneficial, useful, and effective
Class II: Conflicting evidence and/or divergence of opinion about usefulness or efficacy of a procedure or treatment Class IIa: Weight of evidence or opinion favors usefulness or efficacy Class IIb: Usefulness or efficacy is less well established by evidence or opinion Class III: Evidence and/or general agreement that procedure is not useful or effective and in some cases may be harmful
Levels of Evidence
Level of Evidence A: Data derived from multiple randomized clinical trials or meta-analyses
Level of Evidence B: Data derived from a single randomized trial or nonrandomized studies Level of Evidence C: Only consensus opinion of experts, case studies, or standard of care
Supporting Vascular Societies

Collaborative reported from American Association for Vascular Surgery/Society for Vascular Surgery Society for Cardiovascular Angiography and Interventions Society of Interventional Radiology Society for Vascular Medicine and Biology ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease
Endorsed by American Association of Cardiovascular and Pulmonary Rehabilitation National Heart, Lung, and Blood Institute Society for Vascular Nursing TransAtlantic Inter-Society Consensus Vascular Disease Foundation
Definition of PAD
Vascular diseases caused primarily by atherosclerosis and thromboembolic pathophysiological processes Encompasses stenotic, occlusive, and aneurysmal disease Affects the normal structure and function of the aorta, its visceral arterial branches, and the arteries of the lower extremities Exclusive of the coronary arteries
The Natural History of PAD

Increased risk for cardiovascular ischemic events due to concomitant coronary artery disease and cerebrovascular disease Cardiovascular events are more frequent than ischemic limb events in any lower extremity PAD cohort, regardless of presentation

Diagnosis
Diagnosis of PAD: The Ankle-Brachial Index

Use resting ABI to establish lower extremity PAD diagnosis
Use ABI to establish baseline in all new patients with PAD, regardless of severity Use toe-brachial index in patients with noncompressible vessels

Risk Factor Management
Risk Factor Management: Lipid-lowering Drugs

All patients with PAD: Statin treatment to achieve LDL level <100 mg/dL
Patients with very high risk of ischemic events: Consider LDL target of <70 mg/dL Fibric acid derivatives useful in patients with low HDL, normal LDL, and elevated trigylcerides
Risk Factor Management: Antihypertensive Drugs

Target blood pressure <140/90 mm Hg to reduce cardiovascular/cerebrovascular risk If comorbid diabetes or chronic renal disease, target blood pressure <130/80 mm Hg -blockers are effective and not contraindicated Consider ACE inhibitors For patients with symptomatic PAD For patients with asymptomatic PAD
Risk Factor Management: Diabetes Therapies

Encourage proper foot care
Appropriate footwear, chiropody/podiatric medicine, daily foot inspection, skin cleansing, and topical moisturizing creams Urgently address skin lesions and ulcerations Target HbA1C<7% to reduce microvascular complications and potentially improve cardiovascular outcomes
Risk Factor Management: Smoking Cessation

Patient should discontinue use of cigarettes or other forms of tobacco
Offer comprehensive smoking cessation interventions Behavior modification therapy, nicotine replacement therapy, and/or bupropion
Risk Factor Management: Homocysteine-lowering Drugs

Value of folic acid and B12 vitamin supplements for homocysteine levels >14 M is not well established
Risk Factor Management: Antiplatelet and Antithrombotic Treatments

Antiplatelet therapy can reduce the risk of MI, stroke, or vascular death
Aspirin 75-325 mg per day is safe and effective
Clopidogrel 75 mg per day is an effective alternative to aspirin

Warfarin is not indicated

Treatment for Claudication
Claudication Treatment: Exercise

Supervised exercise training should be the initial treatment 30-45 minute sessions 3 or more times per week At least 12 weeks Value of unsupervised exercise programs is not well established
Claudication Treatment: Cilostazol and Pentoxifylline

Cilostazol 100 mg PO BID Can improve symptoms Can increase walking distance Indicated for all patients with lifestyle-limiting claudication Contraindicated in patients with heart failure Pentoxifylline 400 mg TID Consider as an alternative to cilostazol Effectiveness of pentoxifylline is marginal and not well established
Claudication Treatment: Other Medical Therapies

Value of L-arginine, propionyl-L-carnitine, and ginkgo biloba unknown
Oral prostaglandins do not improve walking distance Vitamin E is not recommended Chelation therapies are not indicated and may have harmful effects
Claudication Treatment: Endovascular Therapies

Only indicated for patients with Vocational or lifestyle-limiting disability; Reasonable likelihood of symptomatic improvement; Prior failure of exercise therapy or pharmacological therapy; and, Favorable risk-benefit ratio Not indicated as a prophylactic treatment for asymptomatic patients Preferred method for revascularization of Transatlantic Inter-society Consensus type A iliac and femoropopliteal arterial lesions
Claudication Treatment: Stenting

Evaluate iliac artery stenoses with translesional pressure gradients Endovascular intervention not indicated in the absence of significant pressure gradient across a stenosis despite flow augmentation with vasodilators Provisional stent placement is indicated as a salvage therapy for iliac arteries after suboptimal or failed balloon dilation Stenting is effective for Common iliac artery stenoses External iliac artery stenoses
Claudication Treatment: Stenting and Adjunctive Techniques

Primary stent placement is not recommended in the femoral, popliteal, or tibial arteries Stents and other adjunctive techniques can be useful In femoral, popliteal, and tibial arteries As salvage therapies for suboptimal or failed balloon dilation Value of stents, atherectomy, cutting balloons, thermal devices, and lasers for femoral-popliteal arterial lesions is not well established except as salvage therapies after balloon dilation Value of uncoated/uncovered stents, atherectomy, cutting balloons, thermal devices, and lasers for infrapopliteal lesions is not well established except as a salvage therapy after balloon dilation
Claudication Treatment: Surgical Revascularization

Indicated for patients
With significant functional disability from symptoms Who are unresponsive to exercise or pharmacotherapy
Who have a reasonable likelihood of symptomatic improvement

Value of surgical intervention in patients <50 with atherosclerotic disease is unclear Surgical intervention is not indicated to prevent progression to limb-threatening ischemia

Treatment for Critical Limb Ischemia
Medical Treatment of Critical Limb Ischemia

Parenteral pentoxifylline is not useful Parenteral prostaglandin E-1 or iloprost for 7-28 days May reduce ischemic pain May facilitate ulcer healing Is effective in only a small fraction of patients Oral iloprost does not reduce the risk of amputation or death Value of angiogenic growth factors not well established
Endovascular Treatment of Critical Limb Ischemia

For combined inflow and outflow disease
Inflow lesions should be addressed first Perform outflow revascularization if symptoms or infection persist after inflow revascularization Assess inflow disease with intra-arterial pressure measures across suprainguinal lesions before and after administration of a vasodilator
Thrombolytic Treatment of Critical Limb Ischemia

Catheter-based thrombolysis is effective and beneficial for patients with Rutherford category IIIa acute limb ischemia of less than 14 days duration Mechanical thrombectomy can be used as an adjunctive therapy for acute limb ischemia
Catheter-based thrombolysis or thrombectomy may be considered for Rutherford category IIb acute limb ischemia of more than 14 days duration
Surgical Treatment of Critical Limb Ischemia

For combined inflow and outflow disease Address inflow lesions first Perform outflow revascularization if symptoms or infection persists after inflow revascularization Consider primary amputation for patients with Significant necrosis of weight-bearing portions of the foot An uncorrectable flexion contracture Paresis Refractory ischemic rest pain Sepsis Very limited life expectancy due to comorbid conditions Surgical or endovascular intervention is not indicated For patients with severe decrements in limb perfusion (eg, ABI <0.4) In the absence of clinical symptoms

Peripheral Arterial Disease

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Peripheral Arterial Disease

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Epidemiology

Definition of Peripheral Arterial Disease (PAD)

Clinical Manifestations of Atherosclerotic Disease

Coronary artery disease

Peripheral arterial disease

Documented Presence of PAD

4.3% 11.7% 14.5% 19.1% 19.8%

Prevalence of PAD Increases With Age

Patients With PAD (%)

Age Group (years)

The Aging Population

1980 1990 2000 2010

N=1592 Age (years)

PAD = peripheral arterial disease

PAD in the United States

Independent Risk Factors for PAD*

* PAD diagnosis based on ABI <0.90.

Diabetes Increases Risk of PAD

Normal Glucose Tolerance

Impaired Glucose Tolerance

The Metabolic Syndrome

PAD Risk Factors are Synergistic

Systolic Blood Pressure Total cholesterol Impaired glucose

Adapted from TASC Working Group. J Vasc Surg. 2000;31:S13.

Screening Techniques and Diagnostic Criteria

Clinical Manifestations of PAD

Clinical Presentation of PAD

Asymptomatic PAD 20-50%

Atypical Leg Pain 40-50%

Intermittent Claudication 10-35%

Critical Limb Ischemia 1-2%

Symptoms of Intermittent Claudication

ABI and Functional Outcomes: 6-Minute Walk

Mean Distance (feet)

1600 1200 800 400 0

McDermott MM, et al. Ann Intern Med. 2002;136:873-883.

Does the Patient Have Intermittent Claudication?

Comprehensive Vascular Examination

Scale 0 = absent 1 = diminished 2 = normal

Indications for an ABI

ABI Testing: Highly Sensitive and Specific

Sensitivity (%) 95 30-87 37-69 75-90

Specificity (%) 99 86-100 87-98 90-95

The Ankle-Brachial Index (ABI)

Using the ABI

PT SBP 40 mmHg DP SBP 80 mmHg

PT SBP 120 mmHg DP SBP 80 mmHg

PT = posterior tibial; DP = dorsalis pedis; SBP = systolic blood pressure.

Automated Blood Pressure Determination Accurately Measures ABI

Doppler Left ABI

Sensitivity Specificity Positive PV Negative PV

88% 85% 65% 96%

Oscillometric Left ABI

Segmental Limb Pressure

Pulse Volume Recordings

Color Duplex Ultrasonography

Color Duplex Ultrasonography

Magnetic Resonance Angiography (MRA)

Computed Tomographic Angiography (CTA)

Requires iodinated contrast Requires ionizing radiation

Produces an excellent arterial picture

PAD: A Full Differential Diagnosis

PAD: A Full Differential Diagnosis