Peripheral Arterial Occlusive Disease Atherosclerosis - Risk factors Hypercholesterolemia Diabetes Hypertension Smoking Relative factors - advanced age,

age, male gender, hypertriglyceridemia, hyperhomocysteinemia, sedentary lifestyle, family history Pathophysiology of Atherosclerosis Atheroma porridge; Sclerosis hardening Response to endothelial injury hypothesis Loss of barrier function, antiadhesive properties and antiproliferative influence on underlying SMCs Migration and proliferation of SMCs production of ECM Oxidized lipid accumulation in vessel walls Recruitment of macrophages and lymphocytes Adherence of platelets to dysfunctional endothelium, exposed matrix, and macrophages Diagnostic Modalities Non-invasive ABIs Segmental limb pressures Limb plethysmography Exercise testing Doppler & duplex ultrasound MR angiography Invasive Contrast arteriography CT angiography Ankle-Brachial Index Comparison of ankle pressure to brachial SBP Reproducible, useful for long term surveillance Normal 0.85-1.2 Claudicants 0.5-0.7 Critical ischemia < 0.4 May be falsely elevated in calcified vessels (DM)

PVR Calibrated air plethysmographic wave form recording system Helps localize site of obstruction Placement of cuffs at levels of proximal and distal thigh, calf and ankle

Medical Therapy Risk factor management Lipid-lowering therapy Smoking cessation Exercise regimen Antiplatelet therapy - ASA, ticlodipine, clopidogrel Vasoactive - Cilostazol (Pletal), pentoxyfilline (Trental)

Surgical Interventions Stenosis vs Occlusion Length of segment Vessel Caliber Most Suitable anatomic site ByPass Either Not a factor >2 mm Aortic arch through distal femoral EndArterectomy Stenosis > occlusion Preferably short Preferably > 56mm Carotid bifurcation

Peripheral Arterial Occlusive Disease Third leading cause of death Major modifiable risk factors HTN Smoking Carotid stenosis Cardiac diseases - a-fib, Preferably >4mm endocarditis, MS, recent MI Atherosclerosis = leading cause of Distal abdominal ischemic stroke aorta and illiacs Artery-to-artery emboli Thrombotic occlusion Hypoperfusion from advanced stenosis CAROTID STENOSIS Causes of atherosclerosis at bifurcation Low wall shear stress Flow separation Complex flow reversal along posterior wall of sinus Sequence of events b. Establishment of plaque c. Soft, central necrotic core with overlying fibrous cap d. Disruption of cap - necrotic cellular debris and lipid material become atherogenic emboli e. Empty necrotic core becomes a deep ulcer = thrombogenic thromboembolism Presentation Asymptomatic bruit, * Lateralizing TIA Crescendo TIA * Stroke-in-evolution CVA Amaurosis fugax transient monocular visual disturbance Diagnostic Algorithm PTA Stenting Stenosis > occlusion Preferably short

Indications for CEA * Symptomatic TIA, AF, small stroke Proven Stenosis > 70% Acceptable Stenosis 50-69% Lesser symptoms, failed medical therapy * Asymptomatic Proven Stenosis > 60%, good risk Uncertain High risk patient Surgeon morbidity-mortality >3% Combined carotid coronary operation Non-stenotic ulcerative lesions * Presence of ulceration or contralateral occlusion may lower threshhold for surgery Chronic Occlusive Disease of the Lower Extremities

Signs and symptoms Claudication Extremity pain, discomfort or weakness Consistently produced by the same amount of activity Relieved with rest Rest pain Localized to metatarsal heads and toes Worse with elevation or recumbent position Improved with foot dependency Temperature Hair loss Pallor Nail hypertrophy Ulcer Gangrene Dry - non infected black eschar Wet - tissue maceration and purulence