Medication Summary
Daily aspirin is recommended for overall cardiovascular care. In addition, the following agents have shown promise in the management of peripheral arterial occlusive disease (PAOD) and may be considered:
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Pentoxifylline
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Clopidogrel
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Enoxaparin
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Cilostazol
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Simvastatin
Antiplatelet Agents
Class Summary
Antiplatelet agents decrease the overall risk of cardiovascular disease from myocardial infarction (MI) and stroke. They also improve walking distance by enhancing circulation.
Aspirin (Ascriptin, Bayer aspirin, Aspirtab, Ecotrin, Halfprin)
Aspirin inhibits prostaglandin synthesis, thereby preventing formation of platelet-aggregating thromboxane A2.
Clopidogrel (Plavix)
Clopidogrel selectively inhibits binding of adenosine diphosphate (ADP) to platelet receptors and subsequent ADP-mediated activation of glycoprotein IIb/IIIa complex, thereby inhibiting platelet aggregation. It is indicated for reduction of atherosclerotic events.
Cilostazol (Pletal)
The mechanism by which cilostazol affects symptoms of intermittent claudication is not fully understood. Cilostazol and several of its metabolites are phosphodiesterase (PDE) subtype 3 (PDE3) inhibitors, inhibiting PDE activity and suppressing degradation of cyclic adenosine monophosphate (cAMP); the resultant increase in cAMP in platelets and blood vessels leads to inhibition of platelet aggregation and vasodilation, respectively.
Cilostazol reversibly inhibits platelet aggregation induced by various stimuli, including thrombin, ADP, collagen, arachidonic acid, epinephrine, and shear stress.
Pentoxifylline
Pentoxifylline is indicated for treatment of patients with intermittent claudication due to atherosclerosis or other obstructive arteriopathies. It improves blood flow by increasing red blood cell deformability, thereby decreasing blood viscosity.
Antilipemic Agents
Class Summary
Antilipemic agents are beneficial in lowering blood cholesterol profiles, thereby possibly reducing the rate of first major vascular events.
Simvastatin (Zocor)
Simvastatin reduces cardiovascular heart disease mortality and morbidity (eg, nonfatal MI or stroke and revascularization procedures) in high-risk patients (ie, those with existing coronary heart disease, diabetes, peripheral vessel disease, or a history of stroke or other cerebrovascular disease). Simvastatin competitively inhibits HMG-CoA, which catalyzes the rate-limiting step in cholesterol synthesis. Patients should be placed on a cholesterol-lowering diet; the diet should be continued indefinitely.
Pravastatin (Pravachol)
Pravastatin is a lipid-lowering HMG-CoA reductase inhibitor. This agent reduces cholesterol biosynthesis and is orally administered in its active form. Pravastatin is rapidly absorbed (peak plasma 1-1.5 h), with a therapeutic response usually seen in 1 week. This agent is highly effective in reducing total cholesterol, LDL cholesterol, and triglyceride levels in patients with heterozygous familial hypercholesterolemia, presumed familiar forms of primary hypercholesterolemia, and mixed dyslipidemia.
Lovastatin (Mevacor, Altoprev)
Lovastatin is a cholesterol-lowering agent that is isolated from a strain of Aspergillus terreus. This HMG-CoA reductase inhibitor catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate-limiting step in the biosynthesis of cholesterol. Lovastatin is available in immediate-release (Mevacor) and sustained-release (Altocor) dosage forms.
Rosuvastatin (Crestor)
Rosuvastatin is also an HMG-CoA reductase inhibitor that decreases cholesterol synthesis and increases cholesterol metabolism. This agent reduces total cholesterol, LDL cholesterol, and triglyceride levels but increases HDL cholesterol levels. Rosuvastatin is used adjunctively with diet and exercise to treat hypercholesterolemia.
Atorvastatin (Lipitor)
Atorvastatin competitively inhibits HMG-CoA reductase, which is responsible for the rate-limiting step in cholesterol synthesis. Before initiating therapy, place patients on a cholesterol-lowering diet for 3-6 months, and continue the diet indefinitely. Dosing usually starts with 10 mg/day orally once daily; titrate to a maximum of 80 mg/day as necessary.
Fluvastatin (Lescol)
Fluvastatin competitively inhibits HMG-CoA reductase, which is responsible for the rate-limiting step in cholesterol synthesis. Before initiating therapy, place patients on a cholesterol-lowering diet for 3-6 months, and continue the diet indefinitely. Immediate-release capsules (Lescol) and extended-release tablets (Lescol XL) are available. Dose at 20-80 mg/day orally once daily or divided twice daily.
Anticoagulants, Hematologic
Class Summary
Anticoagulants decrease microthrombus formation. Reversible elevation of hepatic transaminase levels occurs occasionally. Heparin-associated thrombocytopenia has been observed with low-molecular-weight heparin (LMWH).
Enoxaparin (Lovenox)
Enoxaparin enhances the inhibition of factor Xa and thrombin by increasing antithrombin III activity. It also slightly affects thrombin and clotting time and preferentially increases the inhibition of factor Xa.
This agent has a wide therapeutic window; the prophylactic dose is not adjusted based on the patient's weight. Enoxaparin is safer and more effective than unfractionated heparin for prophylaxis of venous thromboembolism. The average duration of treatment is 7-14 days.
Dalteparin (Fragmin)
Dalteparin is an LMWH with antithrombotic properties. It enhances the inhibition of factor Xa and thrombin by increasing antithrombin. It has a minimal effect on activated partial thromboplastin time (aPTT).
Tinzaparin
Tinzaparin is an LMWH with antithrombotic properties. It enhances the inhibition of factor Xa and thrombin by increasing antithrombin. It has a minimal effect on aPTT.
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Peripheral arterial occlusive disease. Measuring segmental pressures.
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Peripheral arterial occlusive disease. Angiogram shows superficial femoral artery occlusion on one side (with reconstitution of suprageniculate popliteal artery) and superficial femoral artery stenosis on other side. This is most common area for peripheral vascular disease.
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Peripheral arterial occlusive disease. Procedures performed during acute admission for peripheral arterial disease in US from 1996 to 2005. Reprinted from Journal of Vascular Surgery, Vol 49(4), Rowe VL et al, Patterns of treatment for peripheral arterial disease in the United States: 1996-2005, Pages 910-7, Apr 2009, with permission from Elsevier.
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- DFA Guidelines on Management of Peripheral Arterial Disease in Diabetes-Related Foot Disease
- CCS Guidelines on Management of Peripheral Arterial Disease
- SVS/ESVS/WFVS Guidelines on Chronic Limb-Threatening Ischemia
- ESC/ESVS Guidelines on Lower-Extremity Arterial Disease
- AHA/ACC Guideline on Lower-Extremity Peripheral Arterial Disease
- SVS Guidelines on Atherosclerotic Occlusive Disease of Lower Extremities
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