Antithrombotic Therapy During Percutaneous Coronary Intervention (PCI)

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Antithrombotic Therapy During Percutaneous
Coronary Intervention (PCI)

• James Lin, DO
• Internal Medicine Resident May 3, 2006.

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Objectives

• To review basic platelet physiology
• To review mechanism of action of different
  Antithrombotic drugs.
• To compare different PCI treatments and PCI vs
  Surgery.
• To review different types of stents.
• To apply the current recommendations of
  Antithrombotic Therapy during PCI. ACCP vs ACC/AHA

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Platelet Physiology

• Platelet is a circulating enucleate disc shaped
  cell, responsible for initiation of hemostatic
  mechanisms which repair injury to the vascular
  endothelium.
• 4 Major platelet functions
• 1. Platelet adherence
• 2. Platelet activation and secretion
• 3. Platelet aggregation
• 4. Interaction with coagulation
  Factors

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Platelet Physiology

• When a break within the integrity of vascular
  lining occurs, platelets are exposed to, and
  interact with collagen fibrils.
• Platelet not only provides a surface for platelet
  adhesion, but also serve as a strong stimulus for
  platelet activation.
• Activated platelets not only secrete thromboxane
  A2 and ADP, but also directly bind to the
  circulating coagulation protein fibrinogen, via
  the abundant platelet integrin, glycoprotein
  (GP)IIb/IIIa (also known as alphaIIb/beta3).

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Platelet Physiology

• In addition to collagen, ADP, and Thromboxane A2,
  other agonist can activate platelets at sites of
  vascular injury.
• Tissue factor, which is expressed on all
  non-vascular cells, is exposed to circulating
  blood upon disruption of the protective
  endothelial layer of the vasculature.
• Tissue factor can interact with Factor VIIa to
  promote local coagulation, and ultimately the
  generation of thrombin, the most potent of the
  platelet agonist.
• Platelets facilitate this process by providing
  procoagulant phospholipids that accelerate
  thrombin generation.
• Platelet activation and fibrin deposition are
  intimately linked, maximizing the growth and
  strength of hemostatic plug.

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Antiplatelet Drugs
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Oral antiplatelet drugs

• Aspirin
• Clopidogrel (Plavix)
• Ticlopidine (Ticlid)
• Aspirin/Dipyridamole (Aggrenox)

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Oral antiplatelet drugs

• Aspirin
• Irreversible inhibitor of cyclooxygenase (COX)
  which prevents formation of the
  platelet-aggregating substance thromboxane A2.
• Monitoring
• Clopidogrel
• Blocks platelet aggregation by inhibition of ADP
  receptor on the platelet membrane.
• Monitoring

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Parenteral antiplatelet drugs

• Glycoprotein IIb/IIIa Inhibitors
• Abciximab (Reopro), eptifibatide (Integrilin),
  tirofiban (Aggrastat)
• Prevent fibrinogen binding to Gly IIb/IIIa
  receptor and block platelet aggregation producing
  profound platelet inhibition.
• Used in conjunction with percutaneous coronary
  interventions (PCI).

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Parenteral antiplatelet drugs

• Often administered with ASA, heparin/LMWH,
  clopidogrel.
• Monitoring
• ACT
• Platelet count

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Antithrombin Drugs

• Vitamin K Antagonists - Warfarin (Coumadin)
• Warfarin interferes with vitamin-K dependent
  carboxylation of several coagulation factors
  including II, VII, IX, and X, as well as
  anticoagulant proteins C and S.
• Full anticoagulant effect is delayed
• Average daily dose 4-5mg.

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Warfarin - monitoring

• International Normalized Ratio (INR)
• The need for frequent testing and dose
  adjustments detracts from warfarins ease of use
  in clinical practice.
• Anticoagulation Clinics
• Coagucheck S

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Unfractionated Heparin

• Complex glycosaminoglycan isolated and purified
  from animal tissues (porcine intestinal mucosa).
  Bovine lung heparin no longer available.
• Binds to endothelial cells and macrophages, as
  well as plasma proteins (platelet factor 4 and
  von Willebrand factor).

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Unfractionated Heparin (UFH)

• Exerts its anticoagulant effect via antithrombin
• Heparin binds to and produces a conformational
  change in antithrombin.
• Anticoagulant effect reversed with protamine.

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Low Molecular Weight Heparin

• Low molecular weight heparins (LMWH) are prepared
  from UFH by enzymatic or chemical hydrolysis.
• Available products
• Fragmin (dalteparin)
• Lovenox (enoxaparin)
• Innohep (tinzaparin

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LMWH

• Binds to antithrombin and inactivates thrombin to
  a lesser extent than UFH because the smaller
  molecule fragments cannot bind thrombin and
  antithrombin simultaneously

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LMWH

• Advantages
• Better bioavailability
• Longer half-life
• Administered subcutaneously either once or twice
  daily
• More predictable dose response
• HIT Type II occurs less often with LMWH
• Disadvantages
• Protamine only partially reverses anticoagulant
  response.

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Direct Thrombin Inhibitors (DTI)

• Available Agents
• Refludan (lepirudin)
• Argatroban
• Angiomax (bivalirudin)
• Exanta (ximelagatran)
• Awaiting FDA approval

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Direct Thrombin Inhibitors

• Thrombin is the central effector of coagulation
  and amplifies its own production, it is a natural
  target for pharmacologic intervention.
• Target sites on the thrombin molecule responsible
  for substrate recognition and/or cleavage.
• By blocking either the active site alone or both
  the active site and exosite I, DTIs specifically
  inhibit thrombin activity.

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Argatroban

• Small molecule that binds reversibly to the
  active site of the thrombin molecule.
• Approved for patients with HIT or HIT with
  thrombosis and patients undergoing percutaneous
  transluminal coronary angioplasty (PTCA) in
  conjunction with aspirin.
• No reversal agent available.

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Argatroban - Monitoring

• normal value is used.
• Argatroban synergistically interferes with the
  INR the PT or INR cannot always be reliably used
  to monitor warfarin therapy in patients receiving
  argatroban. Effect dependent on argatroban dose
  and ISI of thromboplastin used.
• Argatroban alone also interferes with the INR
  and is dependent upon the ISI of the
  thromboplastin used.

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Angiomax (bivalirudin)

• Synthetic molecule designed on the basis of
  structural studies of hirudin formerly known as
  hirulog.
• Undergoes reversible binding may lead to less
  bleeding.
• No antidote available for reversal.

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Angiomax (bivalirudin)

• Therapeutic use
• FDA- approved
• Anticoagulation in patients undergoing
  percutaneous transluminal coronary angioplasty
  (PTCA) in conjunction with aspirin.
• Other
• Treatment of patients with HIT and unstable
  angina.
• Anticoagulation for patients with HIT undergoing
  CABG (on pump or off-pump).

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Angiomax (bivalirudin)

• Monitoring
• ACT for patients undergoing PTCA.
• ACT for patients undergoing CABG.
• aPTT for patients with HIT or unstable angina.

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TYPES OF STENTS

• These can be categorized as
• Balloon-expandable (eg, Palmaz-Schatz, Multilink
  family (currently the Penta), NIR, Bx Velocity)
  vs Self expandable (eg, Wallstent, RADIUS).
• Tublar Vs Coil or Hybrid
• Premounted vs. Unmounted (The latter are not in
  use in the US).
• Bifurcated stents
• Covered Stents, Nonbiodegradable (usually PTFE)
  polymeric or autologous vein graft coverint to
  serve as an impermeable barrier as might be
  sesired to seal a coronary perforation, a passive
  coating to modify platelet adhesion or an active
  coating (heparin coated stents).
• Drug-Eluting stents, which relase
  antiprofliferative agents (eg, Sirolimus,
  paclitaxel) These stents are now used in the
  mjaority of procedures.
• Small vessel stents, which are engineered to
  provide less emtal and smaller strut thickness
  while maintaining optimal scaffolding for vessels
  lt2.5mm in diameter.

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Stents

• Wallstents

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Risks of Stents Bad things can happen

• Acute myocardial infarction (heart attack)
• Arrhythmias (abnormal heart rhythms)
• Death
• Dissection
• Drug reactions to anti-platelet agents
• Emboli (blood clotting)
• Emergent Coronary Artery Bypass Surgery
• Hemorrhage (bleeding)
• Hypotension/Hypertension (low/high blood
  pressure)
• Infection and pain at insertion site

www.guidant.com
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Risks of Stents2 More bad things can happen

• Ischemia (low oxygen state)
• Perforation
• Pseudoaneurysm
• Restenosis
• Spasm
• Stent emobilization
• Stent thrombosis/occlusion
• Stroke/cerebrovascular accident
• Total occlusion of the coronary artery
• www.guidant.com

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Stent vs. Angioplasty

• Bare metal stents, despite leading to a higher
  thrombosis rate, are less risky than balloon
  angioplasty because it results in a lower rate of
  restenosis and lower overall number of adverse
  effects.

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Likeliness of OccurrenceNo, really, will it
happen?

• Very low risk of most complications
• Howeverrestenosis in
• Balloon angioplasty 30-50
• Bare metal stents 20-30
• Drug-eluting stents lt10
• Goal minimize restenosis rate while keeping all
  other risks in check
• (Note Restenosis is defined as gt50 narrowing of
  blood vessel diameter)

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Stents vs. Balloon Angioplasty

• 1991-1996 Restenosis Stent trial (REST) of
  patients with heart disease due to a lesion in a
  coronary artery
• 1/3 patients are high-risk
• 6 month follow-up
• 383 patients assigned to undergo
• Standard balloon angioplasty or
• Stenting with the Palmaz-Shatz stent
• New England Journal of Medicine

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Frequency of Complications
Event Angioplasty Stent
Death 1.7 2.2
Minimal luminal diameter 1.85mm 2.04mm
Myocardial infarction 4.4 8.4
Restenosis 32.0 18.0
Revascularization needed 27.0 10.0
Thrombosis 0.6 3.9
No major adverse event 72.0 84.0
New England Journal of Medicine
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Stent vs. Angioplasty Verdict

• Bare metal stents, despite leading to a higher
  thrombosis rate, are less risky than balloon
  angioplasty because it results in a lower rate of
  restenosis and lower overall number of adverse
  effects.

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Stents vs. Bypass Surgery

• 1997-2001 trial of patients with high-grade
  lesions
• 1/2 patients are high-risk
• 6 month follow-up
• 220 patients assigned to undergo
• Minimally invasive bypass surgery or
• Stenting with a variety of bare metal stents

New England Journal of Medicine
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Frequency of Complications
Event Surgery Stent
Death 2.0 0.0
Minimal luminal diameter 0.38mm 1.70mm
Myocardial infarction 5.0 3.0
Restenosis 18.0 33.0
Revascularization needed 8.0 29.0
Thrombosis ? ?
No major adverse event 85.0 69.0
New England Journal of Medicine
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Stent vs. Surgery Verdict

• Bare metal stents, while giving good short-term
  results, are more risky than minimally invasive
  bypass surgery because the risk of restenosis is
  much higher and so is the need for repeated
  intervention.

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Bare Metal vs. Drug-Eluting Stents

• 2000-2001 RAVEL trial of patients with angina
• 2/5 patients are high-risk
• 6 month follow-up
• 238 patients assigned to undergo
• Stenting with sirolimus-eluting stent or
• Stenting with bare metal Bx Velocity stent

New England Journal of Medicine
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Frequency of Complications
Event Drug-Eluting Stent Bare Metal Stent
Death 1.7 1.7
Minimal luminal diameter 2.42mm 1.64mm
Myocardial infarction 3.3 4.2
Restenosis 0.0 26.6
Revascularization needed 0.0 22.9
Thrombosis 0.0 0.0
No major adverse event 94.1 70.9
New England Journal of Medicine
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Bare Metal vs. Drug-Eluting Stent Verdict

• Drug-eluting stents are a great deal less risky
  than bare metal stents because they almost
  completely prevent restenosis, and similar to the
  surgery case, there is no longer a need for
  repeated intervention.

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Drug-Eluting Stent vs. Bypass Surgery
Complications
Event Drug-Eluting Stent Bypass Surgery
Death 1.7 2.0
Minimal luminal diameter 2.42mm 0.38mm
Myocardial infarction 3.3 5.0
Restenosis 0.0 18.0
Revascularization needed 0.0 8.0
Thrombosis 0.0 ?
No major adverse event 94.1 85.0
New England Journal of Medicine
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Drug-Eluting Stent vs. Bypass Surgery Verdict

• Drug-eluting stents are more effective, safer,
  and pose less risk than bypass surgery because
  they have practically no restenosis or other
  adverse complications.
• REFERENCES
• Coronary Stent System Potential Adverse Effects.
  www.guidant.com.
• De Luna AB, ONeill WW. Drug-coated stents for
  everyone or for selected use in high-risk
  populations. www.cardiosource.com.
• Diegeler A, Thiele H, Falk, V, et al. Comparison
  of stenting with minimally invasive bypass
  surgery for stenosis of the left anterior
  descending coronary artery. N Engl J Med 2002 Aug
  22347561-6.
• Erbel R, Haude M, Hopp HW, et al. Coronary-artery
  stenting compared with balloon angioplasty for
  restenosis after initial balloon angioplasty. N
  Engl J Med 1998 Dec 33391672-8.
• Morice MC, Serruys PW, Sousa JE, et al. A
  randomized comparison of a sirolimus-eluting
  stent with a standard stent for coronary
  revascularization. N Engl J Med 2002 Jun
  63461773-80.

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Grade 1 Recommendations are strong and indicate
  that the benefits do, or do not, outweigh risks,
  burden, and costs.
• Grade 2 suggests that individual patients
  values may lead to different choices.
• CHEST 2004 126179S-187S

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Aspirin
• For pt undergoing PCI, ACCP recommends
  pretreatment with aspirin, 75mg to 325 mg (grade
  1A)
• Mufson et al, total of 495 pts were randomly
  assigned to low-dose (80mg/d) or high-dose (1500
  mg/d) aspirin starting 24 h before balloon
  angioplasty. No differences between the two
  groups respects to occurrence of MI(3.6 vs
  3.9), or need for CABAG (3.6 vs 3.7)
• A longer pretreatment period (up to 24 h) should
  be considered if a lower dose of aspirin (75 to
  100mg) is used because of potential delay in
  bioavailability and attainment of a platelet
  inhibtory effect.
• ACC/AHA 2005 guidelines state the same (level
  Evidence A)
• ACC/AHA recommends pt not already taking daily
  chronic aspirin therapy should be given 300 to
  325 mg of aspirin at least 2 hours and preferably
  24 hours before the PCI Procedure is performed
  (level C evidence)

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Aspirin
• For long-term treatment after PCI, ACCP
  recommends aspirin 75 to 162 mg/d (grade 1A).
• Schwartz et al, 376 pts were randomized to
  treatment with the combination of ASA(990 mg/d)
  and dipyridamole (75mg/d) or with placebo for 6
  months after balloon angioplasty. There was no
  difference in the rate of binary restenosis in
  the two treatment groups (37.7 vs 38.6,
  respectively).
• Taylor et al, 212 pts to 6 months of treatment
  with ASA (100mg/d) vs placebo within 2 weeks of
  successful angioplasty. Angiographic restenosis
  occurred in 25 of aspirin treated pts and in 38
  of those receiving placebo. However, there were
  no significant difference in clinical outcomes
  between the two groups.
• Although these trials suggest that aspirin has
  little or no effect on angiographic or clinical
  re-stenosis, long-term aspirin therapy is useful
  for secondary prevention of cardiovascular events
  (death, MI, or stroke).

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Aspirin
• For long-term treatment after PCI in pts who
  receive antithrombotic agents such as clopidogrel
  or warfarin, we recommend lower-dose aspirin,
  75mg to 100 mg/d (Grade 1 C).
• When aspirin is administered in combination with
  other antiplatelet agents or with anticoagulants,
  it is reasonable to use a daily dose of 75 to 162
  mg, rather than 325 mg, to minimize bleeding
  complications. Concept is supported by CURE
  study.
• CURE Three groups, lt100mg, 101-199mg, gt200mg.
  The combined incidence of major bleeding
  increased as function of the aspirin dose, both
  in patients receiving aspirin plus placebo (1.9,
  2.8, and 3.7 respectively).

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Thienopyridine Derivatives
• Ticlopidine vs Clopidogrel
• Clopidogrel is safer than ticlopidine and easier
  to administer. Clopidogrel does not cause
  neutropenia, thereby obviating the need for blood
  count monitoring. Futhermore, hemolytic uremic
  syndrome and thrombotic thrombocytopentic purpura
  are rare complications of clopidogrel. Finally,
  unlike ticlopidine, which requires BID dosing,
  clopidogrel is Q daily.
• Similar efficacy, clopidogrel fewer side effects.
• For pts who undergo stent placement, ACCP
  recommends the combination of aspirin and a
  thienopyridine over systemic anticoagulation
  therapy.

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• ACCP recommend a loading dose of 300mg of
  clopidogrel at least 6 hrs prior to planned PCI
  (Grade 1B). If clopidogrel is started lt 6 h
  prior to planned PCI, suggest 600 mg loading
  dose of clopidogrel.
• ACC/AHA recommends the same loading dose at least
  6 hours before PCI, and/or GP IIb/IIIa
  antagonists, administered at the time of PCI.
• If ticlopidine is administered, they recommend
  that a loading dose of 500 mg at least 6 h before
  planned PCI. (grade 2c).

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Aspirin intolerant patients
• For PCI pts who cannot tolerate aspirin, ACCP
  recommends that the loading dose of clopidogrel
  (300mg) or ticlopidine (500mg) be adminstered at
  least 24 h prior to planned PCI (Grade 2c).
• Clopidogrel is given at the time of procedure,
  supplementation with GPIIb/IIIa receptor
  antagonists can be beneficial to facilitate
  earlier platelet inhibition than with clopidogrel
  alone.
• When a loading dose of clopidogrel is
  administered, a regimen of greater than 300mg is
  reasonable to achieve higher levels of
  antiplatelet activity more rapidly, but the
  efficacy and safety compare with a 300 mg loading
  dose are less established.

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Duration of thienopyridine therapy after stent
  placement
• After PCI, ACCP recommends, in addition to
  aspirin, clopidogrel (75mg/d) for at least 9 to
  12 months. (Grade 1A)
• If ticlopidine is used in place of clopidogrel
  after PCI, we recommend ticlopidine for 2 weeks
  after placement of a bare metal stent in addition
  to aspirin. (grade 1b)
• In pts with low atherosclerotic risk such as
  those isolated coronary lesions, ACCP recommends
  clopidogrel for at least 2 weeks after placement
  of a bare metal stent (Grade 1A), for 2 to 4
  months after placement of sirolimus-eluting stent
  (grade 1c) and 6 months after placement of
  paclitaxel-eluting stent. (Grade 1C).
• ACC/AHA recommends after the PCI procedure, in
  pts with neither aspirin resistance, allergy, nor
  increased risk of bleeding, aspirin 325 mg daily
  should be given at least 1 month after bare-metal
  stent, 3 months after sirolimus-eluting stent
  implantation, and 6 months after
  paclitaxel-eluting stent implantation, after
  which daily chronic aspirin use should be
  continued indefinitely at a dose of 75mg to 162
  mg.

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Recommendations use of GP IIbIIIa
• For all pts undergoing PCI, particularly those
  undergoing primary PCI, or those with refractory
  UA or other high-risk features, ACCP recommends
  use of a GP IIb-IIIa antagonist (abciximab or
  eptifibatide) grade 1A.
• In pts undergoing PCI for STEMI, ACCP recommends
  abciximab over epifibatide for now.(CADILLAC
  trial) (This is because large randomized trial
  have not yet been performed. However, smaller
  studies shows favorable outcome).
• ACC/AHA recommends that STEMI undergoing PCI, it
  is reasonable to administer abciximab as early as
  possible.

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• ACCP recommends adminsitration of abciximab as a
  0.25 mcg/min (grade 1A) and eptifibatide as a
  double bolus (each of 180mcg/kg adminstered 10
  min apart) followed by an 18-h infusion of 2.0
  mcg/kg/min. (Grade 1A).
• In pts undergoing PCI, ACCP recommends against
  the use of tirofiban as an alternative to
  abciximab (grade 1A)
• RESTORE trial, Major bleeding occurred in 5.8
  of those receiving tirofiban and in 3.7 in
  placebo.

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• For pts with NSTEMI/UA who are designated as
  moderate-to-high risk based on TIMI score, ACCP
  recommends that upstream use of GP IIb-IIIa
  antagonist (either eptifibatide or tirofiban) be
  started as soon as possible prior to PCI (grade
  1A). ACC/AHA especially feels that GP IIb-IIIa
  is especially efficacious when clopidogrel is not
  given.
• In NSTEMI/UA pts who receive upstream treatment
  with tirofiban, ACCP recommends PCI be deferred
  for at least 4 h after initiating the tirofiban
  infusion (grade 2c)
• With planned PCI in NSTEMI/UA pts with an
  elevated troponin level, we recommend that
  abciximab be started within 24 h prior to
  intervention (grade 1A).

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Unfractionated Heparin
• In pts receiving a GP IIb-IIIIa inhibitor, ACCP
  recommends a heparin bolus of 50 to 70 IU/kg to
  achieve a target ACTgt 200s (grade 1C)
• In pts not receiving a GP IIb-IIIa inhibitor,
  ACCP recommends that heparin be administered in
  doses sufficient to produce an ACT of 250 to 350
  s (Grade 1 C). ACC/AHA agrees with this.
• In pts after uncomplicatred PCI, we recommend
  against routine postprocedural infusion of
  heparin (grade 1A).

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• LMWH
• In pts who have received LMWH prior to PCI, ACCP
  recommends that administration of additional
  anticoagulant therapy is dependent on the timing
  of the last dose of LMWH (grade 1 C). If the
  last dose of enxaparin is administered between 8
  hours and 12 hours before PCI, ACCP suggests a
  0.3mcg/kg bolus of IV enoxaparin at the time of
  PCI (grade 2c). If the last enoxaparin dose is
  adminstered gt12 h before PCI, ACCP suggest
  conventional anticoagulation therapy during PCI.
  (0.5mg-1mg/kg).

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Direct thrombin Inhibitors Hirudin,
  bivalirudin, argatroban.
• For pts undergoing PCI who are not treated with a
  GP IIb-IIIa antagonist or heparin, ACCP recommend
  bivalirudin (0.75mg/kg bolus followed by an
  infusion of 1.75 mg/kg/h for the duration of PCI0
  during PCI (Grade 1A).
• In PCI pts who are at low risk for complications,
  ACCP recommend bivalirudin as an alternative to
  heparin as an adjunct to GP IIb-III a antagonists
  (grade 1b). ACC/AHA agrees with this
  recommendation.
• In PCI pts who are at high risk for bleeding,
  ACCP recommends bivalirudin over heparin as an
  adjunct to GP IIb-III a antagonists (Grade 1B).

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Recommendations 2004 Seventh ACCP
Antithrombotic Therapy During PCI

• Warfarin Vitamin K antagonist
• In pt undergoing PCI with no other indication for
  systemic anticoagulation therapy, ACCP recommends
  Against routine use of warfarin after PCI. (grade
  1A).

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CASE

• A 47 year old male presented to MCH ED with c/o
  of chest pain. Pain is described as crushing
  chest pain that radiated to his left arm and neck
  for 1 hour. He has hx of hypertension. Smokes 2
  packs a day for 30 years. The only medication
  that Pt takes is the metoprolol 50mg BID. On
  physical exam, his blood pressure is 130/80, HR
  86 bpm. There is no JVDs and his lungs were
  clear. Initial Troponin I is high at 3 ng/mL.
  ECG

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Question 1

• Decision was made by ER physician to transfer the
  patient down to CIC for immediate PCI. It will
  be another 3 hours before the pt will have PCI.
•  
• 1.        According to the 2004 ACCP guidelines,
  what would be the appropriate antiplatelet drug
  combination that the ER physician could give
  prior to transferring the patient down in
  addition to the unfractionated heparin
• A)        ASA 325 mg, Plavix 75mg
• B)         ASA 650 mg, Plavix 300 mg
• C)        ASA 325mg, Plavix 300mg/ or 600 mg
• D)        ASA 81 mg, Plavix 150mg.

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Answer C.
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Question 2

• Pt arrived at the Heart Center, in the cath. Lab,
  the Cardiologist found that pt had an 75 RCA
  blockage, decision was made to place a
  paclitaxel- stent in patient. According to the
  guidelines, how long should this patient be on
  the plavix?
• A)    At least 3 months
• B)     At least 6 months
• C)    At least 9 months
• D)    indefinite

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Answer C
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Question 3

• According to the guidelines, how long should this
  patient be on ASA, and at what dosage?
• A)        ASA 81 mg for 3 months then 325mg
  chronically
• B)         ASA 325 for at least 9 months, then
  81-160mg chronically
• C)        ASA 160 for at least 6 months, then
  stop
• D)        ASA for 325mg then Stop.

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Answer B.