1. PERIPHERAL ARTERIAL DISEASE (PAD)
Dr. Riko Prima Putra, Sp.JP

2. Peripheral Arterial Disease
= Peripheral Vascular Disease
Vascular disease caused primarily by atherosclerosis & thromboembolic pathophysiological processes that alter the normal structure and function of the aorta, its visceral arterial branches, and the arteries of the lower extremities

3. Peripheral Arterial Disease
Stenotic
Occlusive
Aneurysma

4. Prevalence of PAD Extremely common Increasingly common with age
20% of people over age 70 have PAD
5% of people over age 40 have PAD
Prevalence of PAD: 11 Million, compared to stroke: 4.4 Million, and MI: 7 Million

5. PAD and mortality

6. Morbidity & mortality
Only 5% of PAD patients will need treatment for limb related sequelae.
23% will die within 5 years from cardiac, cerebral, or other vascular events (Aronow, 1994).

7. Risk factors Older age (> 40 years) Male gender Smoking
Diabetes mellitus
Hyperlipidemia
Hypertension
Hyperhomocysteinemia
When risk factors coexist, the risk increases several-fold

8. Clinical presentation
Asymptomatic
Claudication
Critical limb ischemia
Acute limb ischemia
Prior limb arterial revascularization

9. A recent review in The New England Journal of Medicine noted that more than 50% of patients with peripheral arterial disease (PAD) do not have “typical” claudication or leg ischemia at rest, but instead have leg pain on exertion associated with reduced ambulatory activity and quality of life.[1] Less than 5% to 10% of patients with PAD have critical leg ischemia (defined as ischemic pain in the distal foot, ischemic ulceration, or gangrene), and approximately one-third present with typical claudication.
Hiatt WR. Medical treatment of peripheral arterial disease and claudication. N Engl J Med. 2001;344:

11. 21/04/2017

12. Note: Plavix® (clopidogrel bisulfate) is not indicated for all the conditions listed on this slide.
Vascular disease is the common underlying disease process for MI, ischemia and vascular death.
Acute coronary syndrome (ACS) is a classic example of the progression of vascular disease to an ischemic event.
ACS (in common with ischemic stroke and critical leg ischemia) is typically caused by rupture or erosion of an atherosclerotic plaque followed by formation of a platelet-rich thrombus.
Atherosclerosis is an ongoing process affecting mainly large and medium-sized arteries, which can begin in childhood and progress throughout a person’s lifetime.
Stable atherosclerotic plaques may encroach on the lumen of the artery and cause chronic ischemia, resulting in (stable) angina pectoris or intermittent claudication, depending on the vascular bed affected.
Unstable atherosclerotic plaques may rupture, leading to the formation of a platelet-rich thrombus that partially or completely occludes the artery and causes acute ischemic symptoms.

13. Atherosclerosis results from an extensive inflammatory and fibroproliferative response to insults within the vasculature leading to disruption of normal homeostasis of the endothelium. The dysfunctional endothelium leads to an increase in adhesiveness and procoagulant properties of platelets. Atherosclerotic lesions form and through progression of the disease eventually become atherosclerotic plaques. Activated platelets can amplify the inflammatory response and are an important component leading to vasoconstriction. Rupture of the atherosclerotic plaque occurs in advanced stages of the disease and results in the formation of a thrombus and arterial occlusion. Atherosclerotic plaque, thrombosis, and vasoconstriction of the arteries all lead to decreased blood flow in the periphery. Ischemia may lead to painful symptoms that can be worsened as the demand of oxygen increases in response to activity such as walking. Painful symptoms at rest are signs of progressive disease. Ischemia may lead to cell death and tissue destruction. Progression of limb pain and destruction of tissue eventually leads to physical impairment.
Ross R. Atherosclerosis—an inflammatory disease. N Engl J Med. 1999;340:

14. PRIMARY SITES OF INVOLVEMENT
Femoral & Popliteal arteries: 80-90%
Tibial & Peroneal arteries: 40-50%
Aorta & Iliac arteries: 30%
Harrison’s Principles of Int Med

15. Differential diagnosis
CALF
Venous occlusion
Tight bursting pain / dull ache that worsens on standing and resolves with leg elevation
Positional pain relief
Chronic compartment syndrome
Tight bursting pain
Nerve root compression
Baker’s cyst
HIP/THIGH/BUTTOCK
Arthritis
Persistent pain, brought on by variable amounts of exercise
Associated symptoms in other joints
Spinal cord compression
History of back pain
Symptoms while standing
Positional pain relief
FOOT
Arthritis
Buerger disease (thromboangitis obliterans)
Am J Cardiol 2001; 87 (suppl): 3D-13D

16. Diagnosis
Symptoms
Diagnostic studies
Laboratory

17. Symptoms
Leg pain, particularly when walking or exercising, which disappears after a few minutes of rest
Numbness, tingling, or coldness in the lower leg or feet
Sores or infection on feet or legs that heal slowly

18. Fontaine Classification
Claudication
Critical limb ischemia
Fontaine Ⅰ,Ⅱ　　　　　 Ⅲ,Ⅳ
Pentecost MJ, Circulation 89:51, 1994

19. Rutherford Classification
Stage
Stage Clinical
Claudication
Critical limb ischemia
Asymptomatic
Mild claudication
Moderate claudication
Severe claudication
Ischemic rest pain
Minor tissue loss
Major tissue loss
Rutherford RB, et al, J Vasc Surg 1986;4:80-94

21. Rutherford 4
Ischemic rest pain
Rutherford 5
Minor tissue loss
Rutherford 6
Major tissue loss

22. Critical Limb Ischemia
Resting ischemic pain
PAD with skin breakdown
Nonhealing ulcers
Gangrene

23. Spectrum of Peripheral Arterial Disease
As the topic title would suggest, this represents a very wide spectrum of potential disease presentations, the use of a wide of variety of diagnostic tools, and a diversity of both endovascular and surgical modalities. An adequate discussion of this important topic is clearly of the realm of a 20 min talk, and therefore I have decided that rather than discuss superficially many topics, I would like to discuss in-depth two ot three core issues regarding treating patients with PVD.
Worsening flow limitation

24. Vascular diagnostic technique
Ankle-brachial index (ABI)
Toe-brachial index
Segmental pressure measurement
Pulse volume recording

25. Vascular diagnostic technique
Continuous-wave doppler ultrasound
Duplex ultasound
Treadmill exercise testing with & without ABI assessments, 6-minute walk test

26. Vascular Echo and ABI for PAD

27. Ankle-brachial index (ABI)

28. Ankle-Brachial Index Values and Clinical Classification
Clinical Presentation Ankle-Brachial Index
Normal > 0.90
Claudication
Rest pain
Tissue loss < 0.20
Values >1.25 falsely elevated; commonly seen in diabetics
Am J Cardiol 2001; 87 (suppl): 3D-13D
NEJM 2001; 344:

29. McDermott and colleagues evaluated the relationship between the ankle brachial index (ABI) and leg function in 740 patients (460 with peripheral arterial disease [PAD]).[1] They demonstrated that ABI is more closely related with leg function than intermittent claudication or other leg symptoms. Lower ABI scores were consistently associated with shorter distance walked in 6 minutes, lower accelerometer-measured activity over 7 days, poorer standing balance, slower walking velocity at usual and fast pace, and lower overall summary performance scores.
McDermott MM, Greenland P, Liu K, et al. The ankle brachial index is associated with leg function and physical activity: the walking and leg circulation study. Ann Intern Med. 2002;136:

30. Duplex in SFA Disease

31. Doppler at Popliteal Artery
Systolic +　Diaslic flow
Triphasic
Systolic flow
Biphasic

32. Multi-level of Stenosis Findings by Doppler
CFA
POP AT

33. Echo Assessment of Infrapopliteal arteryAT PT AT TP PT TP Pe Pe PT

34. How many tests do we need to evaluate PVD ?
TCD
Duplex
Duplex
MRA
CTA
ABI
DSA
Segmental pressure
Treadmill ABI
ABI
Pulse volume
Toe pressure
tPO2

35. Vascular diagnostic technique
Magneting resonance angiography (MRA)
Computed tomographic angiography (CTA)
Contrast angiography

36. In the past, invasive vascular testing was considered the gold standard for vascular imaging and planning of revascularization procedures.[1] Images obtained using this procedure provide information about the level and severity of vascular disease. However, the utility of invasive imaging in all patients has been challenged, as duplex ultrasonography may provide adequate information for planning revascularization procedures in some patients.
Collins KA, Sumpio BE. Vascular assessment. Clin Podiatr Med Surg. 2000;17:

37. The history and physical examination (pulse evaluation and careful examination of the leg) are usually sufficient to establish the diagnosis

38. Laboratory Hemoglobin Serum creatinine Lipid profile
Hypercoagulability screen
Homocysteine level
Lp(a) lipoprotein

39. Goals of treatment
To relieve exertional symptoms and improve walking capacity
To improve quality of life
To reduce total mortality as well as cardiac and cerebrovascular morbidity and mortality

40. Management Risk factor modification Exercise therapy
Antiplatelet therapy
Medical therapy targeted at symptoms
Revascularisation procedures

42. Cardiovascular risk reduction
Lipid lowering drugs
Antihypertensive drugs
Diabetes therapies
Smoking cessation
Homocysteine lowering drugs
Antiplatelet and antihtrombotic drugs

43. Cardiovascular risk reduction
Diabetes control (FBG mg/dl, PPG < 180 mg/dl, HbA1c < 7%)
Dyslipidemia management (LDL < 100 mg/dl, TG < 150 mg/dl): Statins (RR 38%; 4S)
Hypertension control (BP < 130/85 mmHg)

44. Claudication Exercise and lower extremity PAD rehabilitation
Exercise program :
Improves walking ability
Requires motivation & personalised supervision
Benefits lost if not maintained on regular basis
Overall effectiveness limited

45. Claudication Medical and pharmacological treatment Cilostazol
Pentoxifylline
Other proposed medical therapies (?)
L-arginine
Propionil-L-carnitine
Ginkgo biloba

46. Claudication
Endovascular treatment
Surgery

47. Revascularisation procedures
Incapacitating claudication
Limb-threatening ischemia (pain at rest, non-healing ulcers and/or infections or gangrene)
If symptoms persist despite medical therapy
AHA guidelines 1996

48. Revascularisation procedures
Angioplasty (balloon angioplasty)
PTA (percutaneous transluminal angioplasty)
Artery bypass graft

49. PTA & stenting

50. Screening for PAD

51. Low-tech, low cost and few people involved
Angioplasty for PAD
Low-tech, low cost and few people involved

52. Iliac Artery Intervention

56. TASC D lesions of the Pelvic Artery: Is there still a role for Aorta-Femoral bypass ?

57. SFA Intervention

58. 71 y/o Male
CAD, HTN, DM
Rutherford 5

59. 71 y/o Male
CAD, HTN, DM
Rutherford 5

60. Pre
71 y/o Male
CAD, HTN, DM
Rutherford 5
2 weeks
2 mo

61. Infrapopliteal Intervention for CLI

62. Pre
3mo

63. Thank you for your attention