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Zontivity

Generic Name: Vorapaxar Sulfate
Class: Platelet-aggregation Inhibitors
ATC Class: B01AC04
Chemical Name: [(1R,3aR,4aR,6R,8aR,9S,9aS) - 9 - [(1E) - 2 - [5 - (3 - Fluorophenyl) - 2 - pyridinyl]ethenyl]dodecahydro - 1 - methyl - 3 - oxonaphtho[2,3 - c]furan - 6 - yl] - carbamic acid, ethyl ester
Molecular Formula: C29H33FN2O4
CAS Number: 618385-01-6

Warning(s)

  • Bleeding
  • Risk of bleeding, including intracranial hemorrhage and fatal bleeding.1 (See Bleeding under Cautions.)

  • Avoid use in patients with active pathological bleeding or history of stroke/TIA or intracranial hemorrhage.1 (See Contraindications under Cautions.)

Introduction

Platelet-aggregation inhibitor; protease-activated receptor-1 (PAR-1) antagonist.1 6 18 19 27 34

Uses for Zontivity

Cardiovascular Risk Reduction in Established Atherosclerotic Disease

Reduction of the risk of thrombotic cardiovascular events (e.g., cardiovascular death, MI, stroke, urgent coronary revascularization) in patients with a history of MI or with peripheral arterial disease (PAD).1 3 4 5 6 10 33 34

Use in conjunction with aspirin and/or clopidogrel; data lacking on use of vorapaxar in combination with other antiplatelet agents (e.g., prasugrel, ticagrelor) or as monotherapy.1 3 4 5 8 12 17

Efficacy and safety established in patients with stable atherosclerotic disease; favorable benefit versus risk not established in the setting of acute coronary syndrome (ACS).1 3 6 8 11 17 20 (See Acute Coronary Syndrome under Uses.)

The American Heart Association (AHA), American College of Cardiology Foundation (ACCF), American College of Chest Physicians (ACCP), and other experts recommend long-term antiplatelet therapy (e.g., aspirin and/or clopidogrel) in patients with established coronary artery disease.6 990 992 1010 Long-term antiplatelet therapy (e.g., clopidogrel, aspirin) also recommended in patients with symptomatic PAD, including those with intermittent claudication, critical limb ischemia, or prior revascularization or amputation of the lower extremity.992 1011 1012 When added to aspirin and/or clopidogrel therapy, vorapaxar reduces cardiovascular events (e.g., composite outcome of cardiovascular death, MI, stroke, and urgent coronary revascularization) but increases risk of bleeding, including intracranial hemorrhage.1 3 4 5 8 12 14 17

Balance incremental benefits against risk of bleeding; certain patients (e.g., those with a history of MI who are at high risk of recurrence but low risk of bleeding and who have not had a previous stroke or TIA) may have greater potential for net clinical benefits.3 4 5 11 12 13 14 15 16 19 31 Overall risk-benefit of vorapaxar in routine clinical practice remains to be fully elucidated.12 13 14 15

Acute Coronary Syndrome

Has been used in patients with ACS; however, current evidence suggests that the addition of vorapaxar to standard antiplatelet therapy in such patients does not substantially reduce rate of ischemic events but substantially increases risk of clinically important bleeding.6 8 17 20 21 22

Many clinicians currently advise against use of vorapaxar in patients with ACS.1 12 17 31

Zontivity Dosage and Administration

Administration

Oral Administration

Administer orally without regard to food.1

Dosage

Available as vorapaxar sulfate; dosage expressed in terms of vorapaxar.1

Adults

Cardiovascular Risk Reduction in Established Atherosclerotic Disease
Patients with Previous MI or with PAD
Oral

2.08 mg once daily in conjunction with aspirin and/or clopidogrel therapy.1 3 4 6 990 992 1010

Managing Antiplatelet Therapy During Invasive Procedures
Oral

ACCP recommends individualizing decision to interrupt antiplatelet therapy prior to surgery or other invasive procedure based on risks of thromboembolism and perioperative bleeding.1004 In principal efficacy study of vorapaxar, investigators were encouraged not to discontinue study drug prior to surgery (e.g., coronary artery bypass grafting [CABG]).1 7 8 11

Manufacturer recommends use of clinical judgment and consideration of patient-specific information such as type of procedure, risk and potential consequences of bleeding, and pharmacologic properties of the drug.17

Special Populations

Hepatic Impairment

No dosage adjustment necessary in patients with mild or moderate hepatic impairment; use not recommended in patients with severe hepatic impairment.1 23 (See Hepatic Impairment under Cautions.)

Renal Impairment

No dosage adjustment necessary in patients with renal impairment, including those with end-stage renal disease.1 24 (See Renal Impairment under Cautions.)

Geriatric Patients

No dosage adjustment necessary.1

Other Special Populations

No dosage adjustments necessary based on age, race, gender, or weight.1 25

Cautions for Zontivity

Contraindications

  • History of stroke, TIA, or intracranial hemorrhage.1

  • Active pathological bleeding (e.g., intracranial hemorrhage, peptic ulcer).1

Warnings/Precautions

Warnings

Bleeding

Moderate to severe bleeding, including intracranial hemorrhage and fatal bleeding, reported.1 3 4 5 6 9 11 12 20 (See Boxed Warning.)

Prior history of stroke associated with substantially greater risk of intracranial hemorrhage; do not use in patients with previous stroke or TIA.1 3 (See Contraindications under Cautions.)

Because bleeding risk with vorapaxar increases in proportion to underlying risk, evaluate baseline bleeding risk prior to initiating therapy.1 Risk factors for bleeding generally include advanced age, low body weight (e.g., <60 kg), renal or hepatic impairment, history of bleeding disorders, and concomitant use of certain drugs (e.g., anticoagulants, fibrinolytics, NSAIAs, SSRIs, SNRIs).1 4 8 11 (See Interactions.)

Suspect bleeding in any patient who is hypotensive and has recently undergone coronary angiography, PCI, CABG, or other surgical procedure.1 If bleeding occurs during therapy, initiate standard treatment measures.8 Withholding dose for a brief period unlikely to resolve an acute bleeding episode because of the drug’s prolonged half-life and inhibitory effects on platelet function.1 No known reversal agent for drug's antiplatelet effects; drug not expected to be dialyzable.1 24

Other Warnings and Precautions

Concomitant Use of Potent CYP3A Inhibitors or Inducers

Avoid concomitant use of potent CYP3A inhibitors and inducers.1 (See Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes under Interactions.)

Specific Populations

Pregnancy

Category B.1

Animal studies suggest low risk of adverse fetal effects and maternal toxicity; however, no adequate and well-controlled studies in pregnant women.1 17 Use during pregnancy only if potential benefits justify potential risks to fetus.1

Lactation

Distributed into milk in rats; not known whether distributed into human milk.1 Discontinue nursing or the drug.1

Pediatric Use

Safety and efficacy not established in pediatric patients.1

Geriatric Use

No overall differences in safety and efficacy relative to younger adults.1 However, consider that older patients generally are at higher risk of bleeding.1

Hepatic Impairment

Pharmacokinetics of vorapaxar and its main active metabolite not substantially altered in patients with hepatic impairment (mild, moderate, or severe).1 23

Use not recommended in patients with severe hepatic impairment because of inherent increased bleeding risk in such patients.1

Renal Impairment

Pharmacokinetics and inhibition of platelet aggregation not substantially altered in patients with renal impairment, including those with end-stage renal impairment.1 24

Common Adverse Effects

Bleeding.1 3 20

Interactions for Zontivity

Metabolized by CYP3A4 and 2J2.1 29 Does not appear to inhibit or induce major CYP isoenzymes.1 30

Weak inhibitor of P-glycoprotein (P-gp).1 Does not inhibit organic anion-transporting polypeptides (OATP) 1B1 and 1B3, organic anion transporters (OAT) 1 and 3, organic cation transporter (OCT) 2, and the breast cancer resistance protein (BCRP).1

Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes

Potent CYP3A inhibitors or inducers: Possible increased or decreased vorapaxar concentrations, respectively.1 29 Avoid concomitant use.1 29 (See Specific Drugs under Interactions.)

Weak to moderate CYP3A inhibitors: Clinically important pharmacokinetic interactions unlikely; may be administered concomitantly without the need for dosage adjustment.1

CYP2C8/9 substrates: Clinically important pharmacokinetic interactions unlikely.1 30

Drugs Affected by Efflux Transport Systems

P-gp substrates: Possible increased plasma concentrations of the substrate.1

Drugs Affecting Hemostasis

Possible increased risk of bleeding.1 (See Specific Drugs under Interactions.)

Specific Drugs

Drug

Interaction

Comments

Antacids (aluminum- and magnesium-containing)

Peak plasma concentrations and systemic exposure of vorapaxar slightly decreased1

Dosage adjustment not necessary1

Anticoagulants (e.g., warfarin)

Possible increased risk of bleeding1

Warfarin: Clinically important pharmacokinetic and pharmacodynamic interactions unlikely1 30

Avoid concomitant use1 17

Anticonvulsants (carbamazepine, phenytoin)

Potential for decreased vorapaxar concentrations via CYP3A induction1

Avoid concomitant use1

Antifungals, azole (itraconazole, ketoconazole, posaconazole)

Potential for increased vorapaxar concentrations via CYP3A inhibition1

Ketoconazole: Substantially (approximately twofold) increased peak plasma concentrations and systemic exposure of vorapaxar29

Avoid concomitant use1

Antiplatelet agents (e.g., aspirin, clopidogrel, prasugrel)

Aspirin, clopidogrel: Used concomitantly as part of dual or triple antiplatelet therapy in clinical studies evaluating efficacy and safety of vorapaxar1 3 20

Clopidogrel: Specific pharmacokinetic interaction studies not conducted1

Prasugrel: Pharmacokinetics of prasugrel or vorapaxar not substantially altered; however, very limited clinical experience with concomitant use1 17

Consider possibility that risk of bleeding may be increased with concomitant antiplatelet therapy19

Clarithromycin

Potential for increased vorapaxar concentrations via CYP3A inhibition1

Avoid concomitant use1

Conivaptan

Potential for increased vorapaxar concentrations via CYP3A inhibition1

Avoid concomitant use1

Digoxin

Peak plasma concentrations of digoxin (P-gp substrate) increased, but systemic exposure not affected1

Dosage adjustment not necessary1

Fibrinolytics

Potentially increased risk of hemorrhage1

HCV protease inhibitors (boceprevir, telaprevir)

Potential for increased vorapaxar concentrations via CYP3A inhibition1

Avoid concomitant use1

HIV protease inhibitors (ritonavir, saquinavir, nelfinavir, indinavir)

Potential for increased vorapaxar concentrations via CYP3A inhibition1

Avoid concomitant use1

Nefazodone

Potential for increased vorapaxar concentrations via CYP3A inhibition1

Avoid concomitant use1

NSAIAs

Potentially increased risk of hemorrhage1

Proton-pump inhibitors

Pantoprazole: Peak plasma concentrations and systemic exposure of vorapaxar not substantially affected1

Dosage adjustment not necessary1

Rifampin

Peak plasma concentrations and systemic exposure of vorapaxar reduced by approximately 50%29

Avoid concomitant use1

Rosiglitazone

Pharmacokinetics of rosiglitazone not substantially altered1 30

Dosage adjustment not necessary1

SNRIs

Potentially increased risk of hemorrhage1

SSRIs

Potentially increased risk of hemorrhage1

St. John's wort (Hypericum perforatum)

Potential for decreased vorapaxar concentrations via CYP3A induction 1

Avoid concomitant use1

Telithromycin

Potential for increased vorapaxar concentrations via CYP3A inhibition1

Avoid concomitant use1

Zontivity Pharmacokinetics

Absorption

Bioavailability

Rapidly absorbed after oral administration; peak plasma concentrations occur within approximately 60 minutes (range 1–2 hours).1 19 23 26 29 30

Mean absolute bioavailability approximately 100%.1

Onset

Following oral administration of recommended dose, complete inhibition (≥80%) of thrombin receptor agonist peptide (TRAP)-induced platelet aggregation observed within 1 week.1

Duration

Dose- and concentration-dependent; following discontinuance of recommended dosage, platelet-inhibitory effects expected to persist at a level of 50% inhibition for about 4 weeks.1 17 18 25 26

Food

Administration with a high-fat meal moderately decreased peak plasma concentrations and delayed time to peak concentrations, but did not substantially alter systemic exposure.1 25

Distribution

Plasma Protein Binding

Both drug and active M20 metabolite extensively (>99%) bound to human plasma proteins.1

Extent

Does not preferentially distribute into RBCs.1

Not known whether vorapaxar is distributed into human milk.1

Elimination

Metabolism

Extensively metabolized by CYP3A4 and CYP2J2.1 The major circulating metabolite (M20) is pharmacologically active and accounts for approximately 20% of total drug exposure.1 23

Elimination Route

Eliminated principally by hepatobiliary excretion; following administration of radiolabeled drug, approximately 84% of dose was recovered (58% in feces and 25% in urine).1 24

Eliminated principally as metabolites.1

Half-life

Effective half-life 3–4 days; apparent terminal half-life of drug and active metabolite approximately 8 days (range 5–13 days).1 17 23 26

Stability

Storage

Oral

Tablets

20–25°C (may be exposed to 15–30°C).1 Store in original package.1

Actions

  • Platelet-aggregation inhibitor.1 6 18 19 27 Binds selectively and reversibly to PAR-1, the primary thrombin receptor expressed on human platelets, resulting in potent inhibition of thrombin-induced platelet aggregation.1 6 8 18 19 27

  • Produces rapid and prolonged dose-dependent inhibition of thrombin- and TRAP-induced platelet aggregation.1 18 26 27

  • Although binding of vorapaxar to PAR-1 is reversible, antiplatelet effects are essentially irreversible because of drug's prolonged half-life.1 18

  • Does not inhibit platelet activation induced by adenosine diphosphate (ADP), collagen, or arachidonic acid; also does not affect standard coagulation tests (PT, aPTT, thrombin time [TT], activated clotting time [ACT], and ecarin clotting time [ECT]).1 25 26

  • No effect on QT interval corrected for rate (QTc) at usual dosages.1

Advice to Patients

  • Importance of advising patients to read the manufacturer's patient information (medication guide).1 2

  • Importance of counseling patients about the potential risks versus benefits of vorapaxar.1

  • Importance of taking vorapaxar exactly as prescribed and not discontinuing therapy without first consulting the prescribing clinician.1 2

  • Importance of informing patients that they may bruise and/or bleed more easily when taking vorapaxar; such effects may last for 4 weeks after drug discontinued.1 2 Patients should be advised to report to their clinician any unexpected, prolonged, or excessive bleeding.1 2

  • Importance of informing clinicians (e.g., physicians, dentists) about vorapaxar therapy before any invasive procedure or surgery is scheduled.1 Clinicians performing invasive procedures should consult with prescribing clinician before discontinuing vorapaxar.1

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription drugs, dietary supplements, and OTC drugs, particularly drugs that affect bleeding risk (e.g., warfarin, NSAIAs).1

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.1

  • Importance of informing patients of other important precautionary information.1 (See Cautions.)

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

Vorapaxar Sulfate

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Tablets

2.08 mg (of vorapaxar)

Zontivity

Merck

AHFS DI Essentials. © Copyright, 2016, American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814. Review Date: September 06, 2016.

References

1. Merck. Zontivity (vorapaxar sulfate) tablets prescribing information. Whitehouse Station, NJ; 2015 April.

2. Merck. Zontivity (vorapaxar sulfate) tablets medication guide. Whitehouse Station, NJ; 2014 May.

3. Morrow DA, Braunwald E, Bonaca MP et al. Vorapaxar in the secondary prevention of atherothrombotic events. N Engl J Med. 2012; 366:1404-13. [PubMed 22443427]

4. Scirica BM, Bonaca MP, Braunwald E et al. Vorapaxar for secondary prevention of thrombotic events for patients with previous myocardial infarction: a prespecified subgroup analysis of the TRA 2°P-TIMI 50 trial. Lancet. 2012; 380:1317-24. [PubMed 22932716]

5. Bonaca MP, Scirica BM, Creager MA et al. Vorapaxar in patients with peripheral artery disease: results from TRA2{degrees}P-TIMI 50. Circulation. 2013; 127:1522-9, 1529e1-6. [PubMed 23501976]

6. . Vorapaxar (Zontivity) for prevention of thrombotic cardiovascular events. Med Lett Drugs Ther. 2014; 56:85-6. [PubMed 25211301]

7. Food and Drug Administration. Summary Review: NDA 204886000. From FDA website.

8. Baker NC, Lipinski MJ, Lhermusier T et al. Overview of the 2014 Food and Drug Administration Cardiovascular and Renal Drugs Advisory Committee meeting about vorapaxar. Circulation. 2014; 130:1287-94. [PubMed 25287768]

9. Morrow DA, Alberts MJ, Mohr JP et al. Efficacy and safety of vorapaxar in patients with prior ischemic stroke. Stroke. 2013; 44:691-8. [PubMed 23396280]

10. Bonaca MP, Scirica BM, Braunwald E et al. New ischemic stroke and outcomes with vorapaxar versus placebo: results from the TRA 2 °P-TIMI 50 trial. J Am Coll Cardiol. 2014; 64:2318-26. [PubMed 25465417]

11. Cheng JW, Colucci V, Howard PA et al. Vorapaxar in atherosclerotic disease management. Ann Pharmacother. 2015; 49:599-606. [PubMed 25680760]

12. Krantz MJ, Kaul S. Secondary prevention of cardiovascular disease with vorapaxar: a new era of 3-drug antiplatelet therapy?. JAMA Intern Med. 2015; 175:9-10. [PubMed 25365757]

13. Ben-Yehuda O. Vorapaxar in patients undergoing coronary artery bypass grafting: insights from a subgroup analysis. J Am Coll Cardiol. 2014; 63:1058-60. [PubMed 24269365]

14. Hart RG, Halperin JL, Weitz JI. Vorapaxar, combination antiplatelet therapy, and stroke. J Am Coll Cardiol. 2014; 64:2327-9. [PubMed 25465418]

15. Goto S, Goto S. Selection of a Suitable Patient Population for New Antiplatelet Therapy From the Large Clinical Trial Database of the Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events-Thrombolysis in Myocardial Infarction 50 (TRA-2P-TIMI50) Trial. Circulation. 2015; 131:1041-3. [PubMed 25681465]

16. Cavender MA, Scirica BM, Bonaca MP et al. Vorapaxar in Patients With Diabetes Mellitus and Previous Myocardial Infarction: Findings From the Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events-TIMI 50 Trial. Circulation. 2015; 131:1047-53. [PubMed 25681464]

17. Merck, North Wales, PA: Personal communication.

18. Poole RM, Elkinson S. Vorapaxar: first global approval. Drugs. 2014; 74:1153-63. [PubMed 24962425]

19. French SL, Arthur JF, Tran HA et al. Approval of the first protease-activated receptor antagonist: Rationale, development, significance, and considerations of a novel anti-platelet agent. Blood Rev. 2014; :. [PubMed 25467961]

20. Tricoci P, Huang Z, Held C et al. Thrombin-receptor antagonist vorapaxar in acute coronary syndromes. N Engl J Med. 2012; 366:20-33. [PubMed 22077816]

21. Jones WS, Tricoci P, Huang Z et al. Vorapaxar in patients with peripheral artery disease and acute coronary syndrome: insights from Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome (TRACER). Am Heart J. 2014; 168:588-96. [PubMed 25262270]

22. Valgimigli M, Tricoci P, Huang Z et al. Usefulness and safety of vorapaxar in patients with non-ST-segment elevation acute coronary syndrome undergoing percutaneous coronary intervention (from the TRACER Trial). Am J Cardiol. 2014; 114:665-73. [PubMed 25129064]

23. Statkevich P, Kosoglou T, Preston RA et al. Pharmacokinetics of the novel PAR-1 antagonist vorapaxar in patients with hepatic impairment. Eur J Clin Pharmacol. 2012; 68:1501-8. [PubMed 22527342]

24. Kosoglou T, Kraft WK, Kumar B et al. Pharmacokinetics and pharmacodynamics of the novel PAR-1 antagonist vorapaxar in patients with end-stage renal disease. Eur J Clin Pharmacol. 2012; 68:1049-56. [PubMed 22315147]

25. Kosoglou T, Reyderman L, Kasserra C et al. No differences in the pharmacodynamics and pharmacokinetics of the thrombin receptor antagonist vorapaxar between healthy Japanese and Caucasian subjects. Eur J Clin Pharmacol. 2012; 68:291-300. [PubMed 21969227]

26. Kosoglou T, Reyderman L, Tiessen RG et al. Pharmacodynamics and pharmacokinetics of the novel PAR-1 antagonist vorapaxar (formerly SCH 530348) in healthy subjects. Eur J Clin Pharmacol. 2012; 68:249-58. [PubMed 21935705]

27. Storey RF, Kotha J, Smyth SS et al. Effects of vorapaxar on platelet reactivity and biomarker expression in non-ST-elevation acute coronary syndromes. The TRACER Pharmacodynamic Substudy. Thromb Haemost. 2014; 111:883-91. [PubMed 24402559]

29. Kosoglou T, Statkevich P, Kumar B et al. The effect of multiple doses of ketoconazole or rifampin on the single- and multiple-dose pharmacokinetics of vorapaxar. J Clin Pharmacol. 2013; 53:540-9. [PubMed 23426761]

30. Kosoglou T, Zhu Y, Xuan F et al. Vorapaxar, an oral PAR-1 receptor antagonist, does not affect the pharmacokinetics and pharmacodynamics of warfarin. Eur J Clin Pharmacol. 2012; 68:1509-16. [PubMed 22476387]

31. Reviewers' comments (personal observations).

32. Magnani G, Bonaca MP, Braunwald E et al. Efficacy and safety of vorapaxar as approved for clinical use in the United States. J Am Heart Assoc. 2015; 4:e001505. [PubMed 25792124]

33. Roffi M, Patrono C, Collet JP et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2016; 37:267-315. [PubMed 26320110]

34. Magnani G, Bonaca MP, Braunwald E et al. Efficacy and safety of vorapaxar as approved for clinical use in the United States. J Am Heart Assoc. 2015; 4:e001505. [PubMed 25792124]

990. American Diabetes Association. Standards of medical care in diabetes--2014. Diabetes Care. 2014; 37 Suppl 1:S14-80. [PubMed 24357209]

992. Smith SC, Benjamin EJ, Bonow RO et al. AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients with Coronary and other Atherosclerotic Vascular Disease: 2011 update: a guideline from the American Heart Association and American College of Cardiology Foundation. Circulation. 2011; 124:2458-73. [PubMed 22052934]

1004. Douketis JD, Spyropoulos AC, Spencer FA et al. Perioperative management of antithrombotic therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012; 141(2 Suppl):e326S-50S. [PubMed 22315266]

1010. Vandvik PO, Lincoff AM, Gore JM et al. Primary and secondary prevention of cardiovascular disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012; 141(2 Suppl):e637S-68S.

1011. Alonso-Coello P, Bellmunt S, McGorrian C et al. Antithrombotic therapy in peripheral artery disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012; 141(2 Suppl):e669S-90S. [PubMed 22315275]

1012. 2011 WRITING GROUP MEMBERS, 2005 WRITING COMMITTEE MEMBERS, ACCF/AHA TASK FORCE MEMBERS. 2011 ACCF/AHA Focused Update of the Guideline for the Management of patients with peripheral artery disease (Updating the 2005 Guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2011; 124:2020-45. [PubMed 21959305]

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