medical education continuing peripheral arterial · the dorsalis pedis artery. the doppler device...

Peripheral ArterialDisease: Diagnostic

Evaluation andCurrent Therapeutic

OptionsNew treatments offer an improved

prognosis for PAD.

Peripheral ArterialDisease: Diagnostic

Evaluation andCurrent Therapeutic

OptionsNew treatments offer an improved

prognosis for PAD.

AUGUST 2004 • PODIATRY MANAGEMENTwww.podiatrym.com 181

grene. Prompt recognition of thisdisorder is critical to avoid progres-sive deterioration in physical func-tion, limb loss, and premature deathfrom myocardial infarction or stroke.The podiatrist plays an importantrole in this process, and must under-stand the prevalence and natural his-tory, presenting symptoms andsigns, objective diagnostic tests, im-portance of risk factor intervention,and therapeutic alternatives.

Epidemiology The prevalence of PAD depends

on how one defines the disease.

Given the inaccuracy of physical ex-amination, using pulse examinationas the sole criterion will grossly over-estimate the true prevalence. In con-trast, an historical query for the pres-ence of intermittent claudication un-derestimates the prevalence of PAD.Epidemiological studies have wide-ranging prevalence rates from 1.6%to 12%, while other studies using ob-jective disease detection with non-in-vasive tests have prevalence rates var-ing from 3.8% to 33%.(1) Non-inva-sive methods for disease definition inepidemiological surveys have usually

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Following this article, an answer sheet and full set of instructions are provided (p. 190).—Editor

Goals and ObjectivesAfter reading this article, the pod-

iatrist should be able to:

1) Verbalize a definition of periph-eral arterial disease

2) Understand the risk factors asso-ciated with peripheral arterial disease

3) Identify the objective methodsused to confirm the diagnosis of pe-ripheral arterial disease

4) Appreciate the importance ofrisk factor intervention as primarytherapy of peripheral arterial disease

5) Develop a strategy for treat-ment of peripheral arterial diseaseusing medical, endovascular, andsurgical modalities.

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Peripheral arterial disease (PAD)is defined as occlusive arterialdisease of the lower extremities

that reduces arterial flow during ex-ercise or, in advanced stages, at rest.The presentation of PAD is varied,and may appear as asymptomatic ar-terial disease with abnormal non-in-vasive tests; symptomatic diseasepresenting as either classic or atypi-cal intermittent claudication (IC);and critical limb ischemia (CLI),manifesting as ischemic rest pain,non-healing ischemic ulcers, or gan-

C L I N I C A L P O D I A T R YC L I N I C A L P O D I A T R Y

By Michael R. Jaff, DO

The first objective test whichmust be performed in patients eitherat risk for PAD, or with symptomsand physical findings of PAD is theankle-brachial index (ABI). The ABI isa safe, simple, highly accurate, andreproducible method of determining* The presence and severity of PAD *The cardiovascular risk of myocardialinfarction, stroke, and vascular death.

This test is easily performed in thepodiatric specialist’s office. It requires

* Routine sphygmomanometer * Hand held, continuous wave

Doppler * Acoustic Gel.In patients with symptoms sug-

gestive of PAD, physical findings in-creasing the likelihood of PAD, or inpatients at high risk for PAD, the ABIis the ideal office-based objectiveevaluation.

A sphygmomanometer is placedon the upper arm, and the systolic

pressure is measured using a hand-held Doppler device. This process isrepeated on the contralateral upperarm. The higher of the two pressuresis used as the denominator of theABI calculation. Following this, thesphygmomanometer is placed onthe lower leg, just above the ankle.Again utilizing the hand-heldDoppler, an arterial Doppler signal isobtained in the dorsalis pedis artery,the cuff inflated until the arterialDoppler signal disappears, and thenthe cuff is gradually deflated. Whenthe arterial Doppler signal returns,this represents the arterial pressure inthe dorsalis pedis artery. TheDoppler device is then positionedposterior to the medial malleolus,and the arterial Doppler signal of theposterior tibial artery is obtained.Using the identical method as de-scribed for the dorsalis pedis artery,the pressure is then determined inthe posterior tibial artery.

The higher of the two ankle pres-sures (either the dorsalis pedis orposterior tibial artery) is used as thenumerator of the ABI calculation.

The process is repeated on thecontralateral limb.

A normal ABI is defined as a rest-ing measurement > 0.90. Any value <0.90 represents the presence of PAD.Obviously, the lower the ABI, themore severe the PAD. Patients withABI values > 0.70 may be asymp-tomatic, or have very mild symptomsof intermittent claudication. ABI val-ues between 0.40 and 0.70 representpatients with mild to moderate inter-mittent claudication. Values < 0.40suggest the most advanced stages ofPAD, with ischemic rest pain, non-healing ulcerations, and gangrene oc-curring with frequency.

The ABI provides informationabout the presence or absence ofPAD, along with the severity and risk

of co-morbid atheroscleroticevents. If the clinician, however,desires more detailed informationconcerning the location of arterialocclusive disease, whether diseaseis represented by stenoses or oc-clusions, the length of atheroscle-rotic disease, and the status of the‘run-off’ arteries, other diagnostictests such as segmental limb pres-sures, pulse volume recordings,Doppler segmental waveforms,and arterial duplex ultrasonogra-phy should be considered.The ABI is a highly accurate

method of determining the presenceof PAD and its severity. However, ifthe ankle vessel is calcified, com-monly seen in patients with diabetesmellitus or end-stage renal disease,an accurate ankle pressure cannot beobtained. The pressure in these calci-fied arteries is often > 200-250mmHg. If not recognized as artifac-tually high, the physician may false-ly conclude that arterial circulationis adequate, or even normal, in thesepatients. In this scenario, other testsavailable in the vascular diagnosticlaboratory are necessary, includingphotoplethysmography, digital pres-sures, arterial duplex ultrasonogra-phy, and even assessments of woundhealing potential utilizing transcuta-neous oximetry (TcP02).

Patients with classic historicalsymptoms of PAD may have a normalphysical examination and ABI. In this


182 www.podiatrym.comPODIATRY MANAGEMENT • AUGUST 2004

PAD...

included statistically validatedclaudication questionnaires. The

Edinburgh Claudication Question-naire (a modification of the WorldHealth Organization/Rose claudica-tion questionnaire), when comparedwith the independent assessment bytwo physicians of 300 patients overage 55, demonstrated a sensitivity of91% and specificity of 99% for the di-agnosis of intermittent claudication.1

The ankle-brachial index (ABI),which is a comparison of the systolicblood pressure in the dorsalis pedisand posterior tibial arteries of thelimb to the brachial artery of the armusing a hand-held Doppler, has beenvalidated against angiographicallyconfirmed PAD and found to be 95%sensitive and almost 100% specific.2

In clinical practice, this is the mostsimple, inexpensive, reliable and re-producible method of identifyingpatients with PAD.

The age-adjusted prevalenceof PAD, as defined by an ankle-brachial index < 0.9 is 12%1. PADprevalence rates defined by non-invasive testing are reported to be2.5% at age 40 to 59 years, 8.3%at age 60 to 69 years, and 18.8%at age 70 to 79 years.3

Diagnosis of PeripheralArterial Disease

Classic (“Rose”) intermittentclaudication, the most commonsymptom of PAD, is characterized byexertional discomfort in a majormuscle group in a limb, which devel-ops with exercise and is promptly re-lieved with rest. A significant propor-tion of patients with symptomaticPAD will not describe classic symp-toms, making the diagnosis moredifficult. More than 50 percent of pa-tients with PAD are either asymp-tomatic or have atypical symptoms,one-third have classic symptoms ofintermittent claudication, and 10percent of patients develop criticallimb ischemia.4 The spectrum of PADis not a continuum. Patients com-monly present with CLI withouthaving experienced prior symptoms(the classic example is the patientwith diabetes mellitus who sustainsminor trauma to a foot after wearingill-fitting shoes and develops gan-grene, never having experiencedclaudication in the past).

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require a highly trained technologist,as well as a physician who under-stands the subtleties of waveform in-terpretation.

Segmental arterial Doppler wave-forms may also be performed, andare easier to interpret. Using a bidi-rectional Doppler probe, Dopplerwaveforms are obtained at each arte-rial level. Normal Doppler wave-forms are triphasic. Mild to moderatePAD are represented by biphasicDoppler waveforms. Severe PAD re-sults in monophasic and ultimately,flat waveforms. Segmental Dopplerwaveforms are easy to perform, andrequire little training to interpret. In

the scenario of non-compressible ar-teries, however, Doppler waveformslose accuracy.

Arterial duplex ultrasonogra-phy is a highly accurate examina-tion, which may be performed fromthe aortic bifurcation to the ankles.Utilizing currently available Duplexultrasound scanners, arteries are vi-sualized, often with color imaging,and Doppler velocities are obtained.A doubling in the peak systolic ve-locity suggests a 50-99% stenosis. Ar-terial duplex ultrasonography re-quires a highly skilled technologist.In addition, a complete examinationof both lower extremities is time-consuming. In patients who are in

scenario, the astute clinician mustpursue an exercise physiologic studyperformed in the vascular diagnosticlaboratory. Patients have resting pres-sures measured, and are then placedon a treadmill at a constant speed andconstant grade of incline. The patientis asked to report initial symptoms oflimb discomfort, and then terminatethe exercise when the discomfort islimiting. After exercise, pressures areagain measured. A significant de-crease in post-exercise pressures con-firms the diagnosis of PAD, and alsocharacterizes the functional limita-tion of the symptoms.

With the use of sequentiallimb blood pressure cuffs andcommercially available equip-ment, segmental limb arterialblood pressures may be obtained.Each pressure measurement iscompared to its proximal cuff,and to the cuff on the contralat-eral limb. For example, the pres-sure obtained in the proximalthigh cuff is normally > 30mmHg higher than the brachialpressure. If this is not found, thiswould suggest the presence of in-flow aorto-iliac artery disease.Each cuff pressure should be nolower than 20 mmHg than thepressure cuff proximal to thatlevel. Disease localization occursone segment proximal to the cuffwith the lower pressure. There-fore, if the pressure in the lowerthigh cuff is 40 mmHg lowerthan the high thigh cuff, thiswould suggest superficial femoralartery occlusive disease.

Pulse volume recordings(PVR’s) are plethysmographic testswhich provide qualitative informa-tion. Simply put, a blood pressurecuff is inflated to a level that doesnot interrupt arterial flow (usually ~60-65 mmHg). As each arterial pulsepasses through the segment of arterybeneath the cuff, the volume ofblood causes distention of the artery.This is sensed by the cuff, whichthen transmits the volume change toa recorder, providing a waveform. Inthe normal setting, this waveform issimilar in appearance to an intra-ar-terial pressure waveform. As the arte-rial circulation worsens, the PVRlooses the dicrotic notch, lowers inamplitude, and widens. These tests

PAD... need of revascularization,this examination is as accu-rate as arteriography in predict-ing the optimal revascularizationmethod.

In patients who are beingconsidered for revascularization, du-plex ultrasound scanning, magneticresonance angiogram (MRA), andmore recently computer tomograph-ic angiography (CTA) are valuable inlocalizing arterial disease. Duplex ul-trasonography can be used for directvisualization of arteries and is espe-cially useful after revascularization(surgical bypass grafts or stent place-ment). MRA is considered one of the

most significant advances in di-agnostic techniques in the past10 years, as blood flow imaging ispossible without the administra-tion of radiocontrast media. Stud-ies have demonstrated the MRAtechnique is accurate and compa-rable to angiography. Both ofthese tests are noninvasive andthus pose no significant risk foranaphylaxis or nephrotoxicity.CTA is emerging as a very usefultest to plan revascularizationstrategies. This technique requiresthe administration of intra-venous contrast. Angiographyshould be reserved for those pa-tients in whom revascularizationis mandatory.

Risk factors for theDevelopment of PAD

The risk of developing PADcan be predicted by age and well-defined atherosclerotic risk fac-tors, including tobacco use, dia-betes mellitus, hypercholes-terolemia and hypertension. The

Framingham Heart Study data hasdefined age, sex, serum cholesterollevel, hypertension, tobacco use, dia-betes mellitus, and coronary heartdisease as factors associated with anincreased risk for PAD and intermit-tent claudication.5 This “risk factorprofile” is useful in determining pop-ulations and patients at risk.

AgeThe prevalence of PAD increases

sharply with age, from 3% in pa-tients < 60 years of age to 20% in pa-tient >75 years of age.4 Data fromsubjects in the Framingham study re-vealed that the prevalence of PAD


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long-term risk of complications, in-cluding progression of PAD, myocar-dial infarction and mortality. In astudy by Jonason et al., the rate of de-velopment of rest pain in intermittentclaudication patients was 0% in non-smokers and 16% in smokers, while10 year rates of myocardial infarctionwere 11% and 53%, 10 year cumula-tive rates of cardiac death were 6%and 43% and 10-year survival rates82% and 46% among non-smokersand smokers respectively.15 From thelimb standpoint, tobacco cessation isassociated with improved post-opera-tive graft patency rates.16

Diabetes Mellitus PAD is prevalent in patients with

diabetes mellitus. A survey of pa-tients with diabetes 50 years of ageor older demonstrated a prevalenceof PAD of 29%.17 In the Rotterdamstudy, diabetes was present in 11.9%and 16% of male and female patientsrespectively, with abnormal ABI, ver-sus 6.7% and 6.3% for those withoutPAD.18 In the Cardiovascular HealthStudy, diabetes was associated with a3.8-fold increased prevalence of PADin patients over age 65.19 In a Veter-ans Administration patient popula-tion with intermittent claudication,diabetes was the major independentpredictor of death.20

HyperlipidemiaThe Lipid Research Clinics (LRC)

Prevalence Study confirmed the asso-ciation of dyslipoproteinemia(specifically low HDL-cholesterol andelevated LDL-cholesterol) withsymptoms and signs of PAD.21 In theNational Cholesterol Education Pro-gram Adult Treatment Panel III re-port on detection, evaluation andtreatment of high blood cholesterolin adults, PAD (regardless of diagnos-tic methods) is considered a coro-nary artery risk equivalent.22 Lipid-lowering agents, most commonlyHMG-CoA reductase inhibitors(“statins”) are thought to benefitPAD patients by decreasing risk forcoronary events and by potentiallyreversing atherosclerotic lesions.Data from the Scandinavian Simvas-tatin Survival Study (4S) of 4,444 pa-tients with known cardiovasculardisease revealed that use of simvas-tatin reduced episodes of new orworsening IC by 38%.23 In familialhypercholesterolemic patients treat-

ed with simvastatin for 2 years, theintima-media thickness in thefemoral artery decreased by a meanof 0.283 mm. This suggestsatherosclerotic disease reversal withstatin treatment in high-risk hyperc-holesterolemic patients.24

HyperhomocyteinemiaMultiple prospective and case

controlled studies have suggestedthat an elevated plasma homocys-teine concentration is an indepen-dent risk factor for atherothromboticvascular disease in the coronary,cerebral, and peripheral vasculature.In a meta-analysis of 27 studies, amodest increase in homocysteinewas independently associated withan increased risk of CAD, cerebrovas-cular disease and PAD.25 In a prospec-tive study of patients with symp-tomatic PAD, for each 1.0 mol/L in-crease in the plasma homocysteinelevel, there was a 3.6% increase inthe risk of all-cause mortality at threeyears and a 5.6% increase in the riskof cardiovascular-related death.

C-Reactive Protein C-reactive protein (CRP) has re-

cently emerged as a novel risk factorassociated with risk of systemicatherosclerosis. CRP together withthe total cholesterol-HDL-C ratiowere the strongest independent pre-dictors of development of symp-tomatic PAD in a study by RidkerPM, et al. CRP in the same study pro-vided additive prognostic informa-tion over standard lipid measures.26

Natural History of PeripheralArterial Disease

The impact of peripheral arterialdisease on limb and life is quite differ-ent, and has implications on manage-ment strategies. Weitz, et al., definedthe 5-year outcomes (on both limband life) of PAD on patients over age55 with IC. The majority of patientshave no progression of limb symp-toms over the subsequent five yearsafter initial presentation. Of the re-maining, 27% demonstrate progres-sion of symptoms, while the need forrevascularization or limb loss occursin a minority (<10%) of patients.1

Despite the relatively stable prog-nosis for the affected limb, there is amarked risk of cardiovascular mor-bidity and mortality over 5-years



PAD...

increased 10-fold from menaged 30-44 to men aged 65-74

and almost 20-fold in women fromthe younger to older age-groups.6 Inthe Rotterdam and San Diego epi-demiological studies, prevalencerates increased with advancing ageboth for IC and for PAD definedwith the use of objective tests.7,8

HypertensionThe role of hypertension as a

major risk factor for the develop-ment and progression of PAD is welldemonstrated in the FraminghamOffspring Study and the GermanEpidemiological Trial on AnkleBrachial Index (GET ABI study).9,10 Nostudies are available, however, toevaluate whether antihypertensivetherapy directly alters the progres-sion of symptomatic PAD. The Ap-propriate Blood Pressure Control inDiabetes (ABCD) Study demonstrat-ed a marked reduction in cardiovas-cular events in normotensive PADpatients with diabetes when treatedwith an intensive blood pressure-lowering strategy as compared tostandard antihypertensive therapy.11

In the most recent guidelines fromthe Joint National Committee on theDetection, Evaluation, and Treat-ment of hypertension, PAD is con-sidered equivalent in risk to ischemicheart disease, therefore supportingaggressive blood pressure control.12

Tobacco UseThe single most important modifi-

able risk factor for the development ofatherosclerotic disease is tobacco use.The amount and duration of tobaccouse correlate directly with the devel-opment and progression of PAD.Smoking increased the risk of inter-mittent claudication by 8 to 10-fold inthe Reykjavik Study and cessation oftobacco use resulted in a 50% reduc-tion in rates of intermittent claudica-tion over a 20-year period among Ice-landic men.13 The best evidence for acausal role of tobacco use inatherosclerotic PAD is an improve-ment in outcome with tobacco cessa-tion. Tobacco cessation results in im-proved ankle pressure and exercise tol-erance in patients with intermittentclaudication as early as 10 monthsafter tobacco cessation.14 Tobacco ces-sation also has a major impact on the

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prevent limb loss, and improve func-tional status of patients with inter-mittent claudication. Patients withPAD must be approached with thesame intensity for secondary cardio-vascular disease prevention and riskfactor modification as recommendedfor patients with coronary artery orcarotid artery disease. In 2001, amultidisciplinary task force of theAmerican College of Cardiology andAmerican Heart Association pub-lished recommendations for risk fac-tor modification in patients withatherosclerotic cardiovascular dis-ease.32 In these guidelines, all pa-tients diagnosed with PAD must re-ceive aggressive therapy to preventsubsequent atherosclerotic diseaseand clinical events. Secondary pre-

vention strategies include: 1. Tobacco cessation 2. Physical activity 3. Dietary modification 4. Weight maintenance/ reduc-

tion with target BMI 18.5-24.9kg/m2 and waist circumference <35in women and <42 inches for men.

5. Blood pressure control 6. Modification of elevated total

and LDL-cholesterol levels 7. Anti-platelet therapy. 8. ACE inhibitor therapy 9. Glycemic control in patients

with diabetes mellitus Modificationof risk factors requires knowledge,patience, and perseverance by theclinician, as most patients find thisaspect of their care very challengingwith limited short-term rewards.

Anti-platelet TherapyAnti-platelet agents are recom-

mended to prevent associated car-

after diagnosis of intermittent claudi-cation. The rate of nonfatal cardio-vascular events (myocardial infarc-tion and stroke) is 20%, with 5-yearmortality rates of 30 %.27 At the timeof diagnosis of IC, at least 10% of pa-tients with PAD have concomitantcerebrovascular disease, and 28%have coronary heart disease.

The overall mortality rate in pa-tients with intermittent claudicationis 30% at 5 years, 50% at 10 years,and 70% at 15 years. The mortalityof patients with intermittent claudi-cation is approximately 2.5-fold thatof an age-matched general popula-tion.34 The majority of these deathsare caused by coronary artery dis-ease, cerebrovascular disease, andother vascular diseases (i.e. abdomi-nal aortic aneurysm, mesenteric is-chemia).28 Subjects with asymp-tomatic PAD appear to have thesame risk of cardiovascular eventsand death seen in patients with in-termittent claudication.

For patients with critical limb is-chemia, the outcomes are signifi-cantly worse. In addition to themarked increase in rates of limb loss,20% of these patients die within 6months. The annual mortality ratein patients with CLI is 25%. Virtuallyall patients who present with gan-grene and/or ischemic rest pain aredead within 10 years. 34, 29

Severity of PAD can be definedbased on ABI values. An abnormalABI is a potent predictor of cardio-vascular events and premature mor-tality. In the Heart Outcomes Pre-vention Evaluation (HOPE) study, anabnormal ABI was a strong predictorof cardiovascular morbidity andmortality during 4.5 years of follow-up, even in patients without symp-toms suggestive of PAD.30

These findings have promptedthe American Diabetes Associationto recommend screening ABI in alldiabetic patients over age 50, and indiabetic patients < 50 with otherPAD risk factors (e.g., smoking, hy-pertension, hyperlipidemia, or dura-tion of diabetes >10 years).31

The Management of PADThe goals of therapy for patients

with PAD are to prevent systemicatherosclerotic disease progressionand clinical cardiovascular events,

PAD... diovascular morbidityand mortality. Platelet acti-vation is increased in patientswith PAD, suggesting an under-lying prothrombotic state.33 Untilrecently, however, the use of aspirinin patients with PAD was not basedon direct evidence, but only onanalogous data in coronary andcerebral atherosclerosis, where anti-platelet therapy has documentedclear efficacy.

A meta-analysis of anti-platelettreatment in patients after peripheralarterial bypass surgery, albeit demon-strating a non-significant effect oncardiovascular outcomes and sur-vival, revealed a mildly positive ef-fect on the patency of peripheral ar-terial bypass grafts.34

The Antithrombotic Trialists’Collaboration summarized the re-sults from 287 studies involving135,000 patients randomized to anti-platelet therapy or placebo. Thismeta-analysis also evaluated 77,000patients treated with different anti-latelet regimens. In the subset of pa-tients treated with anti-platelet ther-apy for PAD (N=9214), anti-platelettherapy demonstrated a 23% reduc-tion in serious vascular events, withsimilar benefits among patients withintermittent claudication and thosepatients undergoing lower extremityrevascularization.35

Ticlopidine, a thienopyridinederivative which blocks the activa-tion of platelets by adenosinediphosphate (ADP), has demonstrat-ed significant benefit in patientswith PAD. Enthusiasm for this drughas been tempered, however, by thesubstantial risk of thrombocytope-nia, neutropenia (which occurs in2.3 % of treated patients), andthrombotic thrombocytopenic pur-pura (which occurs in 1 in 2000-4000 patients).36 We do not recom-mend the routine use of ticlopidinein patients with PAD.

Clopidogrel (Plavix), a secondthienopyridine derivative, has an ac-tion similar to ticlopidine withoutthe serious hematological side ef-fects. The Clopidogrel Versus Aspirinin Patients at Risk of Ischemic Events(CAPRIE) Study, a multicenter,multinational, prospective random-ized trial, evaluated aspirin versusclopidogrel in over 19,000 patientswith recent stroke, MI, or symp-


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Regular aerobic exercise reduces

cardiovascular risk (by lowering cholesterol,

blood pressure, and improving glycemiccontrol) and produces

symptomaticimprovement

in patients with PAD.

duces symptomatic improvement inpatients with PAD. The beneficialeffects of exercise may be explainedby several mechanisms, includingimprovements in endothelial va-sodilator function, skeletal musclemetabolism, blood viscosity and in-flammatory responses. Exercisetraining also improves oxygen ex-traction and walking efficiency bydecreasing oxygen consumption forthe same workload.40

In a meta-analysis of randomizedtrials of exercise in patients with in-termittent claudication, exercisetherapy significantly improved pain-free walking time by 180% and max-imal walking time by 150% over 6months. When compared to percuta-neous revascularization, supervisedexercise produced significant im-

provements in walking time at sixmonths, and did not differ signifi-cantly from surgical treatment.41

We recommend a supervised ex-ercise program which encompassesspecific factors. Supervised exercisetherapy is the most effective symp-tomatic therapy for patients withIC. Supervised exercise therapy in-cludes 6-month programs, with ses-sions three times per week, walkingas the main form of exercise, andsessions lasting 60 minutes. Themain factors limiting success of ex-ercise therapy include lack of pa-tient motivation and compliance,and the economic obstacles for re-imbursement in the United States.Available data analyzing the imple-mentation of supervised exercise inpatients with PAD are pessimistic.In the United Kingdom, regularwalking exercise was not followedby almost 50% of patients with in-

termittent claudication.42

Pharmacologic Treatment ofPeripheral Arterial Disease

Pentoxifylline (Trental®), amethylxanthine derivative, improvesred cell deformability, lowers fibrino-gen levels, and retards platelet aggre-gation. It is the first medication ap-proved by the FDA (in 1984) for thetreatment of patients with IC.1 A re-cent review of all available trials con-cluded that the actual improvementin walking distance attributable topentoxifylline is unpredictable, maynot be clinically important com-pared with the effects of placebo,and does not justify the added ex-pense for most patients.43 Based oncurrent evidence we do not recom-mend the routine use of pentoxi-fylline in patients with PAD.

Cilostazol, a phosphodiesteraseIII inhibitor, was the second oralagent approved for the treatment ofmild to moderate intermittent clau-dication in 1999. In addition to itsantiplatelet properties, cilostazol pro-motes vasodilatation, increases plas-ma HDL and decreases plasmatriglycerides, and potentially inhibitssmooth muscle cell accumulationafter percutaneous coronary inter-vention.1 The true mechanismwhereby cilostazol improves pain-free walking distance is unknown.

Cilostazol increases pain-freeand maximal walking distances by40-70% and 65-83% respectivelyafter 12-24 weeks when used at therecommended dose of 100 mg oral-ly twice daily. Treatment withcilostazol is also associated with im-provements in health-related quali-ty of life.44

In the pivotal prospective, multi-center, 24-week randomized trialcomparing cilostazol to pentoxi-fylline and placebo in 698 patientswith intermittent claudication, theimprovement seen with cilostazol (amean percent increase of 54% frombaseline) was significantly greaterthan that seen with either pentoxi-fylline (a 30% mean percent in-crease) or placebo. Side effects, suchas headache, palpitations, and diar-rhea, were more common in thecilostazol group, but discontinuationrates were similar between cilostazoland pentoxifylline (16% vs. 19%).45

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PAD...

tomatic PAD. Clopidogrel wasassociated with a modest yet sig-

nificant reduction in the primarycomposite endpoint of MI, ischemicstroke, and vascular death whencompared with aspirin. In a sub-group analysis of 6,452 patients en-rolled in CAPRIE due to PAD, clopi-dogrel offered a relative risk reduc-tion of 24% over aspirin.

Clopidogrel is well-tolerated,with no increase in adverse events ordiscontinuation when compared toaspirin. Clopidogrel has been associ-ated with a low risk of adverse hema-tologic effects. The estimated risk ofthrombotic thrombocytopenic pur-pura is 4 per million patients, a levelthat does not warrant routine hema-tologic monitoring.37 Clopidogrel isthe only anti-platelet agent approvedby the United States Food and DrugAdministration (FDA) specifically forthe reduction of cardiovascularevents in patients with PAD.38

The combined effect of aspirinplus clopidogrel has been demon-strated in patients with acute coro-nary syndromes.39 Currently en-rolling trials will address combina-tion therapy in PAD; however, thisrecommendation cannot be made atpresent.

We recommend anti-platelettherapy in every eligible patient withPAD. If the economic issues of long-term clopidogrel are manageable,this agent is superior to aspirin in re-ducing the risk of major cardiovascu-lar events and vascular death.

Exercise Therapy Patients with intermittent claudi-

cation have marked impairment inexercise performance and overallfunctional capacity. Reduced walk-ing capacity is associated with im-pairment in the performance of ac-tivities of daily living and in generalquality of life. Their peak oxygenconsumption measured during grad-ed treadmill exercise is 50 % of age-matched subjects with normal pe-ripheral arterial circulation, indicat-ing a level of impairment similar topatients with debilitating congestiveheart failure.23

Regular aerobic exercise reducescardiovascular risk (by loweringcholesterol, blood pressure, and im-proving glycemic control) and pro-

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Revascularizationattempts are warranted

in patients withsymptom-limiting

intermittent claudicationor in those patients

who progress to ischemic rest pain withor without ulceration.


therapy, first proposed more than 35years ago by Dotter and Judkins51 forthe treatment of diseased coronaryarteries, revolutionized the manage-ment of certain patients with periph-eral arterial disease (PAD). This ap-proach, however, with its reliance ontechniques such as angioplasty,stents, stent-grafts, and various me-chanical devices, was not viewed bythe practicing interventionist as a vi-able option for individuals with PADuntil the 1980’s. Since then, interesthas rapidly grown and endovasculartherapy has now become a primaryoption in the treatment of PAD.52

While the technology and de-vices available for endovascular ther-apy in PAD have become increasing-ly more sophisticated and reliable, areview of the data reveals that en-dovascular therapy is not risk-free.Early experience with angioplasty forPAD in 352 patients (453 angioplas-ties) resulted in 59 complications in53 patients53 The advent of endovas-cular stents led to improved patency,but not a significant reduction in ad-verse events, including access sitecomplications. In a series of patientswith iliac artery atherosclerosis forwhom 147 iliac artery stents in 98limbs were deployed, there were 29(19.4%) complications.54

Vascular surgical procedures areclassically reserved for patients withcritical limb ischemia (ischemic restpain, non-healing ischemic ulcers,gangrene). These patients have mul-tilevel arterial disease, and requirebypass procedures to targets belowthe knee. The autogenous saphenousvein is the ideal conduit to use forsuch procedures, and if performed byskilled and experienced surgeons,limb salvage and patency rates arequite acceptable.55

References:1 Leng GC, Fowkes FGE. The Edinburgh

Claudication Questionnaire: an improved ver-sion of the WHO/Rose Questionnaire for usein epidemiological surveys. J Clin Epidemiol.1992; 45:1101-1109.

2 Bernstein EF, Fronek A: Current status ofnon-invasive tests in the diagnosis of peripher-al arterial disease. Surg Clin North Am 1982;62:473-487.

3 Criqui MH, Denenberg JO, Langer RD,Fronek A. The epidemiology of peripheral arte-rial disease: importance of identifying the pop-ulation at risk. Vasc Med. 1997; 2(3): 221-6.

4 Hiatt WR. Medical treatment of periph-eral arterial disease and claudication. N Engl J

esterase III inhibitors in patientswith congestive heart failure hasbeen associated with an increase inmortality due to a proarrhythmic ef-fect. Therefore, cilostazol must notbe prescribed to patients with inter-mittent claudication who have con-gestive heart failure.46 The safety datafrom eight phase 3 clinical trials in-volving 2,702 patients and frompostmarketing surveillance in theUnited States representing 70,430patient-years of exposure did not re-veal increased cardiovascular mor-bidity or mortality risk in patients re-ceiving cilostazol.47

Cilostazol should be taken one-half hour before or two hours afterfood, as high-fat meals markedly in-crease its absorption. Diltiazem, grape-fruit juice or omeprazole can increaseserum concentration of cilostazol ifthey are taken concurrently. Cilostazolcan be safely administered with as-pirin or clopidogrel without any fur-ther increase in bleeding time.48 Werecommend the use of cilostazol asinitial therapy for patients with mildto moderate intermittent claudication.

Revascularization forPeripheral Arterial Disease

Revascularization for peripheralarterial disease cannot occur on thebasis of angiographic or non-inva-sive physiologic test results alone.The finding of a stenosis or shortsegment occlusion of these vesselsdoes not indicate the need for revas-cularization. It is the clinical symp-tomatology of the patient, coupledwith the presence of atheroscleroticrisk factors, other co-morbid medicalconditions, and the results of non-invasive tests that allows for appro-priate decisions concerning the needfor revascularization. It is unlikelythat a patient presenting with mildsymptoms will require revasculariza-tion. Risk factor modification, enroll-ment in a supervised exercise pro-gram49 or an experimental trial ofpharmacotherapy for intermittentclaudication50 seems more appropri-ate.

Revascularization attempts arewarranted in patients with symp-tom-limiting intermittent claudica-tion or in those patients whoprogress to ischemic rest pain withor without ulceration. Endovascular

PAD... Med. 2001 May 24; 344(21):1608-21.

5 Murabito JM, D’Agostino RB, Sil-bershatz H, Wilson WF. Intermittent clau-dication. A risk profile from The Framing-ham Heart Study Circulation. 1997 Jul 1; 96(1):44-9.

6 Kannel W, Skinner JJ, Schwartz M et al.Intermittent claudication; incidence in theFramingham study. Circulation 1970; 41: 875-83.

7 Criqui M, Fronek A, Barrett-Connor E etal. The prevalence of peripheral arterial diseasein a defined population. Circulation 1985; 71:510-5.

8 Meijer WT, Hoes AW, Rutgers D et al. Pe-ripheral arterial disease in the elderly: the Rot-terdam Study. Arterioscler Thromb Vasc Biol1998; 18: 185-92.

9 Murabito JM, Evans JC, Nieto K, LarsonMG, Levy D, Wilson PW. Prevalence and clini-cal correlates of peripheral arterial disease inthe Framingham Offspring Study Am Heart J.2002 Jun; 143(6): 961-5.

10 Diehm C, Schuster A, Allenberg JR, Dar-ius H, Haberl R, Lange S, Pittrow D, vonStritzky B, Tepohl G, Trampisch HJ Highprevalence of peripheral arterial disease and co-morbidity in 6880 primary care patients: cross-sectional study Atherosclerosis. 2004 Jan;172(1): 95-105.

11 Mehler PS, Coll JR, Estacio R, Esler A,Schrier RW, Hiatt WR Intensive blood pressurecontrol reduces the risk of cardiovascularevents in patients with peripheral arterial dis-ease and type 2 diabetes. Circulation. 2003 Feb11; 107(5): 753-6.

12 Chobanian AV, Bakris GL, Black HR,Cushman WC, Green LA, Izzo JL, Jones DW,Materson BJ, Oparil S, Wright JT, Roccella EJ.The seventh Report of the Joint National Com-mittee on prevention, detection, evaluation,and treatment of high blood pressure. JAMA2003; 289:2560-2572.

13 Ingolfsson IO, Sigurdsson G, Sigvalda-son H, Thorgeirsson G, Sigfusson N. Markeddecline in the prevalence and incidence of in-termittent claudication in Icelandic men 1968-1986: a strong relationship to smoking andserum cholesterol—the Reykjavik Study. J ClinEpidemiol. 1994 Nov; 47(11):1237-43.

14 Quick CR, Cotton LT The measured ef-fect of stopping smoking on intermittent clau-dication. Br J Surg. 1982 Jun; 69 Suppl: S24-6.

15 Jonason T, Bergstrom R. Cessation ofsmoking in patients with intermittent claudi-cation. Effects on the risk of peripheral vascularcomplications, myocardial infarction and mor-tality. Acta Med Scand. 1987; 221(3):253-60

16 Ameli FM, Stein M, Provan JL, Prosser R.The effect of postoperative smoking onfemoropopliteal bypass grafts Ann Vasc Surg.1989 Jan; 3(1):20-5.

17 Hirsch AT, Criqui MH, Treat-JaconsonD, Regensteiner JG et al.. Peripheral ArterialDisease detection, awareness and treatment inprimary care. JAMA 2001;286:1317-1324.

18 Meijer WT, Grobbee DE, Hunink MG,


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peripheral arterial disease. Eur Heart J. 2004Jan; 25(1): 17-24.

31 American Diabetes Association Peripher-al arterial disease in people with diabetes. Dia-betes Care. 2003 Dec; 26(12): 3333-41.

32 Smith SC Jr, Blair SN, Bonow RO, BrassLM, Cerqueira MD, Dracup K, Fuster V, GottoA, Grundy SM, Miller NH, Jacobs A, Jones D,Krauss RM, Mosca L, Ockene I, Pasternak RC,Pearson T, Pfeffer MA, Starke RD, Taubert KA.AHA/ACC Guidelines for Preventing Heart At-tack and Death in Patients with AtheroscleroticCardiovascular Disease: 2001 update. A state-ment for healthcare professionals from theAmerican Heart Association and the AmericanCollege of Cardiology.

33 Brittenden J Platelet activation is in-creased in peripheral arterial disease. J VascSurg. 2003 Jul; 38(1):99-103.

34 Dorffler-Melly J, Koopman MM, AdamDJ, Buller HR, Prins MH. Antiplatelet agents forpreventing thrombosis after peripheral arterialbypass surgery Cochrane Database Syst Rev.2003 ;( 3): CD000535.

35 Antithrombotic Trialists’ Collaboration.Collaborative meta-analysis of randomised tri-als of antiplatelet therapy for prevention ofdeath, myocardial infarction, and stroke inhigh risk patients. BMJ. 2002 January 12; 324(7329): 71-86.

36 Bennett CL, Weinberg PD, Rozenberg-Ben-Dror K, Yarnold PR, Kwaan HC, Green D.Thrombotic thrombocytopenic purpura asso-ciated with ticlopidine. A review of 60 casesAnn Intern Med. 1998 Apr 1; 128(7):541-4.

37 Bennett CL, Connors JM, Carwile JM, etal. Thrombotic thrombocytopenic purpura as-sociated with clopidogrel. N Engl J Med 2000;342:1773-1777.

38 CAPRIE Steering Committee: A ran-domized, blinded, trial of clopidogrel versus as-pirin in patients at risk of ischemic events (CA-PRIE). 1996 Lancet 348:1329-1339 1996.

39 Yusuf S, Zhao F, Mehta SR, ChrolaviciusS, Tognoni G, Fox KK; Clopidogrel in UnstableAngina to Prevent Recurrent Events Trial In-vestigators Effects of clopidogrel in addition toaspirin in patients with acute coronary syn-dromes without ST-segment elevation. N EnglJ Med. 2001 Aug 16; 345(7):494-502

40 Stewart KJ, Hiatt WR, Regensteiner JG,Hirsch AT. Exercise training for claudication. NEngl J Med. 2002 Dec 12; 347(24): 1941-51.

41 Gardner AW, Poehlman ET. Exercise re-habilitation programs for the treatment ofclaudication pain. A meta-analysis. JAMA.1995 Sep 27; 274(12): 975-80.

42 Bartelink ML, Stoffers HE, Biesheuvel CJ,Hoes AW Walking exercise in patients with in-termittent claudication. Experience in routineclinical practice. Br J Gen Pract. 2004 Mar;54(500): 196-200.

43 Radack K, Wyderski RJ. Conservativemanagement of intermittent claudication.Ann Intern Med.. 1990; 113:135-146.

44 Thompson PD, Zimet R, Forbes WP,Zhang P. Meta-analysis of results from eightrandomized, placebo-controlled trials on theeffect of cilostazol on patients with intermit-

tent claudication. Am J Cardiol. 2002 Dec 15;90(12): 1314-9.

45 Dawson DL, Cutler BS, Hiatt WR, Hob-son RW 2nd, Martin JD, Bortey EB, Forbes WP,Strandness DE Jr. A comparison of cilostazoland pentoxifylline for treating intermittentclaudication Am J Med. 2000 Nov; 109(7):523-30.

46 Evaluation of the effect of phosphodi-esterase inhibitors on mortality in chronicheart failure patients. A meta-analysis Eur JClin Pharmacol. 1994; 46(3): 191-6.

47 Pratt CM. Analysis of the cilostazol safe-ty database Am J Cardiol. 2001 Jun 28;87(12A):28D-33D.

48 Medical Letter 2003:45:46.49 Patterson RB, Pinto B, Marcus B, et. al.

Value of a supervised exercise program for thetherapy of arterial claudication. J Vasc Surg1997;25:312-9.

50 Diehm C, Balzer K, Bisler H, et. al. Effica-cy of a new prostaglandin E1 regimen in out-patients with severe intermittent claudication:results of a multicenter placebo-controlleddouble-blind trial. J Vasc Surg 1997;25:537-44.

51 Dotter CT, Judkins MP: Transluminaltreatment of arteriosclerotic obstruction: de-scription of a new technic and a preliminaryreport of its applications. Circulation 30:654-670, 1964.

52 Isner JM, Rosenfield K: Redefining thetreatment of peripheral artery disease. Role ofpercutaneous revascularization. Circulation88:1534-1557, 1993.

53 Gardiner GA Jr, Meyerovitz MF, StokesKR, et al: Complications of transluminal angio-plasty. Radiology 159:201-208, 1986.

54 Ballard JL, Sparks SR, Taylor FC, et al:Complications of iliac artery stent deploy-ment. J Vasc Surg 24:545-555, 1996.

55 Kalra M, Gloviczki P, Bower TC, et al.Limb salvage after successful pedal bypassgrafting is associated with improved long-termsurvival. J Vasc Surg 2001;33:6-16.


PAD...

Hofman A, Hoes AW. Determinants ofperipheral arterial disease in the elderly: the

Rotterdam study. Arch Intern Med. 2000 Oct23; 160(19): 2934-8.

19 Newman AB, Siscovick DS, Manolio TAet al. Ankl-arm index as a marker of atheroscle-rosis in the Cardiovascular Health Study. Car-diovascular Heart Study (CHS) collaborativeResearch Group. Circulation 193;88(3):837-45.

20 Muluk SC, Muluk VS, Kelley ME, Whit-tle JC, Tierney JA, Webster MW, MakarounMS. Outcome events in patients with claudica-tion: a 15-year study in 2777 patients. J VascSurg. 2001 Feb;33(2):251-7.

21 Pomrehn P, Duncan B, Weissfeld L,Wallace RB, Barnes R, Heiss G, Ekelund LG,Criqui MH, Johnson N, Chambless LE. The as-sociation of dyslipoproteinemia with symp-toms and signs of peripheral arterial disease.The Lipid Research Clinics Program PrevalenceStudy Circulation. 1986 Jan; 73(1 Pt 2):I100-7.

22 Third report of the National CholesterolEducation Program (NCEP) Expert Panel ondetection, evaluation, and treatment of highblood cholesterol in adults (Adult TreatmentPanel III). Circulation 2002;106:3143.

23 Pedersen TR, Kjekshus J, Pyorala K, Ols-son AG, Cook TJ, Musliner TA, Tobert JA,Haghfelt T. Effect of simvastatin on ischemicsigns and symptoms in the Scandinavian sim-vastatin survival study (4S). Am J Cardiol. 1998Feb 1; 81(3):333-5.

24 Nolting PR, de Groot E, ZwindermanAH, Buirma RJ, Trip MD, Kastelein JJ. Regres-sion of carotid and femoral artery intima-media thickness in familial hypercholes-terolemia: treatment with simvastatin Arch In-tern Med. 2003 Aug 11-25; 163(15):1837-41.

25 Boushey CJ, Beresford SA, Omenn GS,Motulsky AG. A quantitative assessment ofplasma homocysteine as a risk factor for vascu-lar disease. Probable benefits of increasing folicacid intakes JAMA. 1995 Oct 4; 274(13): 1049-57.

26 Ridker PM, Stampfer MJ, Rifai N Novelrisk factors for systemic atherosclerosis: a com-parison of C-reactive protein, fibrinogen, ho-mocysteine, lipoprotein(a), and standardcholesterol screening as predictors of peripher-al arterial disease JAMA. 2001 May16;285(19):2481-5.

27 Weitz JI, Byrne J, Clagett GP, FarkouhME, Porter JM, Sackett DL, Strandness DE Jr,Taylor LM. Diagnosis and treatment of chronicarterial insufficiency of the lower extremities: acritical review. Circulation 1996; 94:3026-3049.

28 Duprez D. Natural history and evolutionof peripheral obstructive arterial disease. IntAngiol. 1992 Jul-Sep; 11(3): 165-8.

29 Dormandy JA, Heeck L, Vig S. The fateof patients with critical leg ischemia. SeminVasc Surg1999; 12:142-147.

30 Ostergren J, Sleight P, Dagenais G,Danisa K, Bosch J, Qilong Y, Yusuf S; HOPEstudy investigators. Impact of ramipril in pa-tients with evidence of clinical or subclinical

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Dr. Jaff. is cur-rently the Direc-tor of VascularMedicine andthe Vascular Di-agnostic Labora-tory and Associ-ate Program Di-rector in Inter-nal Medicine atLenox Hill Hospi-tal in New York City. He is president ofthe Society for Vascular Medicine andBiology, and serves as a member of theBoard of Directors for the IntersocietalCommission for the Accreditation ofVascular Laboratories. He is a memberof the editorial board of several journalsincluding Vascular Medicine, Angiology,Catheterization and Cardiovascular In-terventions, the Journal of Vascular Sur-gery, Annals of Internal Medicine, andthe Journal of Endovascular Therapy.


program for intermittentclaudication?

A) Six month durationB) Supervision by an exercisephysiologist/physical therapistC) Each session lasts 10 minutesD) 3 sessions per week.

6) Clopidogrel has demonstrated asignificant reduction in myocardialinfarction, stroke, and vascular deathin patients with intermittentclaudication and peripheral arterialdisease when compared to similarpatients treated with aspirin.Cilostazol has demonstrated

A) Antiplatelet effects whichexceed that of aspirin andclopidogrelB) A reduction in stroke whencompared to aspirin therapyC) An improvement in pain-freewalking distance to a statisticallysignificant degree over placeboand pentoxifylline.D) Similar impact on pain-freewalking distance whencompared to clopidogrel.

7) A patient presents with a painlessulcer on the plantar aspect of theleft foot. The patient is unsure as tohow the ulcer formed, and does notknow the duration of the ulcer. Thepatient has no history of exercise-induced limb discomfort, and hasnever been told of peripheralarterial disease in the past. The ulceris located on the plantar aspect ofleft second metatarsal head. Thebase of the ulcer has extensiveyellow exudate, and there is a largeamount of surrounding callusformation. The patient has nopinprick or light touch sensation,proprioception, or vibratorysensation of the feet. The first stepin the management of this patient is

A) Schedule the patient for anarteriogramB) Perform an ankle-brachialindex at the bedsideC) Debride the ulcerD) Order transcutaneousoximetry

8) When performing an ankle-brachial index, if a systolic Dopplerpressure exceeds 250 mmHg, onecan presume that

A) The patient’s circulation isabnormal

1) The most common symptomaticmanifestation of peripheral arterialdisease is

A) Ischemic ulcerationB) Classic “Rose” intermittentclaudicationC) Atypical exertional limbsymptomsD) Gangrene

2) Peripheral arterial disease affectswhat percent of adults over age 60in the United States?

A) 1%B) 8%C) 15%D) 50%

3) The ankle-brachial indexA) Has a 15% risk of invokingsignificant limb pain during theexamination.B) Carries sensitivity andspecificity rates of ~80%.C) Requires an advanced degree inphysiology to accurately performD) Requires a sphygmomanometer,acoustic gel, and Doppler.

4) A 57 y.o. female presents withbilateral buttocks numbness withwalking 50 yards. These symptomshave been noticeable for the past 3years, and have progressivelyworsened over the past 6 months.When the patient stops and stands,the numbness resolves within 5minutes. She does not experiencesimilar symptoms at rest, or withstanding. Her right arm bloodpressure is 170 mmHg; left armblood pressure 200 mmHg. Thepressure via hand-held continuouswave Doppler of the right dorsalispedis artery is 140 mmHg, posteriortibial artery 130 mmHg; left dorsalispedis artery 110 mmHg, posteriortibial artery 90 mmHg. Which of thefollowing is a true statement:

A) Based on the history andDoppler pressures, thesymptoms are clearly non-vascular in nature.B) The right leg ankle-brachialindex is 0.65.C) The left leg ankle-brachialindex is 0.65.D) The patient has rightsubclavian artery disease.

5) Which of the following is not acomponent of an effective exercise

B) The Doppler is malfunctioningC) You are performing the testincorrectlyD) The patient’s circulation isnormal.

9) A patient with hypertension andhyperlipidemia describes a historyclassic for intermittent claudicationof the right lower extremity. Thereare no rest symptoms or ulcerations.Both pedal pulses are easilypalpable. The ankle-brachial index isnormal. Your next step is

A) Prescribe custom orthoticdevices for plantar fasciitisB) Either refer the patient for atreadmill challenge test orperform toe raises in your officefollowed by repeat ABIdetermination.C) Order an MRI of thelumbosacral spine looking forlumbar canal stenosisD) Order an MRA of the lowerextremity arteries.

10) Which of the followingdiagnostic tests will not help planrevascularization in a patient withischemic rest pain of the foot?

A) Magnetic resonancearteriographyB) Arterial duplexultrasonographyC) Transcutaneous oximetryD) Computed TomographicAngiography

11) The most important modifiablerisk factor for the development ofperipheral arterial disease is

A) Male sexB) HypertensionC) AgeD) Tobacco Use

12) In the Cardiovascular HealthStudy, diabetes was associated witha ___-fold increased prevalence ofPAD in patients over age 65.

A) 2.0B) 3.8C) 5.0D) 7.0

13) Patients with asymptomatic PADhave mortality rates which are_______________ to those patientswith intermittent claudication?

A) Similar

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B) Lower thanC) Higher thanD) Unknown

14) Secondary prevention strategies in patients withPAD include all of the following EXCEPT

A) Tobacco CessationB) Weight lossC) Use of wool socksD) Reduction in LDL-cholesterol

15) The CAPRIE study demonstrated superiority ofwhat agent over aspirin in preventing recurrent heartattacks, strokes, or dying from vascular disease?

A) PersantineB) InderalC) TrentalD) Clopidogrel (Plavix)

16) Cilostazol is a phosphodiesterase III inhibitorwhose mechanism of action includes all of thefollowing EXCEPT

A) Increased dilation of arteriesB) Promotes platelet aggregation and adhesionC) Reduction in triglycerides and elevation ofHDL-cholesterolD) Inhibition of smooth muscle cells in coronaryarteries after angioplasty

17) Which of the following instructions for use ofcilostazol is correct?

A) Take immediately after eatingB) Avoid spicy foodsC) Avoid diltiazem or omeprazoleD) Take each dose with grapefruit juice

18) Indications for revascularization in patients withPAD include all of the following EXCEPT

A) Limb discomfort after walking 1.0 milesB) Rest pain that awakens a patient from sleepC) GangreneD) Non-healing ulceration on the toe

19) Which of the following treatment strategies ismost appropriate?

A) Surgical bypass in a patient with 10 blockintermittent claudicationB) Percutaneous transluminal angioplasty in apatient with 10 block intermittent claudicationC) Risk factor modification, antiplatelet therapy,exercise in a patient with 10 block intermittentclaudicationD) Pentoxifylline in a patient with 10 blockintermittent claudication

20) Complication rates of patients who undergo iliacartery intervention occur in what % of cases?

A) 0.5B) 10C) 20D) 50

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EXAM #7/04Peripheral Arterial Disease

(Jaff)

1. A B C D

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