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Treatment Guidelines
from The Medical Letter®
Published by The Medical Letter, Inc. • 1000 Main Street, New Rochelle, NY 10801 • A Nonprofit Publication
Volume 6 (Issue 69) May 2008
www.medicalletter.org
Antiplatelet and Anticoagulant Drugs
Arterial and venous thrombosis are major causes of
morbidity and mortality. Arterial thrombi consist of
platelet aggregates held together by small amounts of
fibrin. Antiplatelet drugs are the drugs of choice for
prevention and treatment of arterial thrombosis, but
anticoagulants are also effective, and their effects can
add to those of antiplatelet drugs. Venous thrombi are
composed mainly of fibrin and trapped red blood cells,
with relatively few platelets. Anticoagulants are the
agents of choice for prevention and treatment of
venous thromboembolism and for prevention of car-
dioembolic events in patients with atrial fibrillation.
ANTIPLATELET DRUGS
ASPIRIN — Aspirin acetylates cyclooxygenase-1,
blocking thromboxane synthesis and inhibiting platelet
activation and aggregation for 5-7 days. Its use slightly
increases the risk of major bleeding. In addition, like
other nonsteroidal anti-inflammatory drugs, aspirin
can cause asthma and other hypersensitivity symptoms
in aspirin-intolerant patients.
DIPYRIDAMOLE — A pyrimidopyrimidine deriva-
tive, dipyridamole inhibits platelet uptake of adenosine
and blocks adenosine diphosphate (ADP)-induced
platelet aggregation. Although the antiplatelet effect of
dipyridamole, which was first marketed as a vasodila-
tor (Persantine), has been known for decades, the drug
was not widely used for this indication until it was
marketed in an extended-release formulation in combi-
nation with aspirin (Aggrenox).1 Dipyridamole causes
severe headache and diarrhea, which tend to disappear
with continued use. It should be used with caution in
patients with severe or recent coronary artery disease.
THIENOPYRIDINES — The thienopyridines clopi-
dogrel (Plavix) and ticlopidine (Ticlid, and others) irre-
versibly inhibit P2Y12, a major ADP receptor on the
Federal copyright law prohibits unauthorized reproduction by any means and imposes severe fines.
Tables
1. Antiplatelet and Anticoagulant Drugs Page 30
2. Drugs for PCI Page 32
3. Drugs for Treatment of VTE Page 33
4. Drugs for Prevention of VTE Page 34
5. Antiplatelet and Anticoagulant Drugs Page 35
of Choice
platelet surface. Some patients do not respond to these
agents and their delayed onset of action (they are pro-
drugs that must be metabolized before becoming
active) can be problematic in patients who require a
rapid antithrombotic effect.2 Like aspirin, they are irre-
versible platelet inhibitors, increasing the risk of bleed-
ing for 5-7 days after drug cessation. Ticlopidine is
used less commonly because it can cause skin reac-
tions and thrombotic thrombocytopenic purpura; it has
largely been supplanted by clopidogrel.
GLYCOPROTEIN IIb/IIIa (GPIIb/IIIa) RECEP-
TOR ANTAGONISTS — The GPIIb/IIIa receptor
antagonists, which are administered intravenously, pre-
vent platelet aggregation by competing with fibrino-
gen and von Willebrand factor for occupancy of
platelet receptors. Abciximab (ReoPro) is the Fab frag-
ment of a chimeric monoclonal antibody to the
GPIIb/IIIa receptor that binds to both activated and
non-activated platelets. While the plasma half-life of
abciximab is only 30 minutes, a strong platelet affinity
results in measurable platelet inhibition after 24-48
hours, with low levels still detectable after 15 days.
Eptifibatide (Integrilin) and tirofiban (Aggrastat) bind
to the GPIIb/IIIa receptor of activated platelets.
Bleeding at arterial access sites is the most common
complication of these drugs. GPIIb/IIIa inhibitors, par-
ticularly abciximab, can also cause profound acute
thrombocytopenia.
ANTICOAGULANTS
HEPARIN — Heparins act by combining with plasma
antithrombin III to form a complex that is more active
in neutralizing thrombin and factor Xa. Unfractionated
heparin (UFH) has numerous disadvantages compared
to low-molecular-weight heparin (LMWH). UFH is
more likely to cause heparin-induced thrombocytope-
nia.3,4 It also has a more variable anticoagulant
29
Antiplatelet and Anticoagulant Drugs

Table 1. Antiplatelet and Anticoagulant Drugs

Drug Some Available Formulations Usual Dosage Cost1
Antiplatelet Drugs
Aspirin – generic 81 mg chew tab; 81, 162, 325, 81-325 mg PO daily $1.20
500, 650, 975 mg tab;
800 mg ER tab
Dipyridamole – 25, 50, 75 mg tabs 75-100 mg PO qid 121.20
Persantine (Boehringer Ingelheim) 182.40
Dipyridamole/aspirin
Aggrenox (Boehringer Ingelheim) 200/25 mg caps 1 cap PO bid (morning and 157.20
evening)
Clopidogrel –
Plavix (Sanofi Aventis) 75, 300 mg tabs 300-600 mg PO loading dose; 149.70
75 mg PO daily
Ticlopidine – generic 250 mg tabs 250 mg PO bid 94.20
Ticlid (Roche) 153.00

GPIIB/IIIA Inhibitors
Abciximab – Reopro (Centocor/Lilly)
Eptifibatide – Integrilin2(Schering-
Plough)
Tirofiban – Aggrastat (Medicure)
Anticoagulants, Parenteral
Unfractionated Heparin – generic
Low-Molecular-Weight Heparin2
Enoxaparin – Lovenox
(Sanofi-Aventis)
Dalteparin – Fragmin (Pfizer)
Tinzaparin – Innohep (Pharmion)
10 mg/5 mL vial1 0.25 mg/kg IV bolus, then 693.16
10 mcg/min IV x 12-24 hrs
20 mg/10 mL1; 75, 180 mcg/kg IV bolus 1-2x, 107.21
200 mg/100 mL vials (10 min apart), then
2 mcg/kg/min IV x 18-24 hrs
12.5 mg/50 mL vial; 0.4 mcg/kg/min IV x 30 min, then 253.62
5 mg/100 mL,1 12.5 mg/250 mL 0.1 mcg/kg/min IV
premixed container
1000,1 5000, 10,000, 20,000 60-100 units/kg IV bolus, then 1.10
units/mL injection; 1000 12-18 units/kg/hr IV; or
(500 mL), 2000 (1000 mL), 5000 units SC q8-12h
10,000 (100 mL), 12,500 (250 mL)
20,000 (500 mL), 25,000 (250,
500 mL), units IV
30 mg/0.3 mL, 40 mg/0.4 mL,1 1 mg/kg bid or 1.5 mg/kg SC daily; 32.50
100 mg/1 mL, 120 mg/0.8 mL, 30 mg bid or 40 mg SC daily
150 mg/1 mL syringe; 300 mg/3 mL vial
syringe: 2500, 5000 IU/0.2 mL1; 5000-10,000 IU SC daily or 32.55
7500/0.3 mL; 10,000 IU/0.4 mL; q12h
10,000 IU/1 mL
vial: 95,000 IU/3.8 mL, 95,000 IU/9.5 mL
40,000 IU/2 mL vial1 175 IU/kg SC daily 173.66

Direct Thrombin Inhibitors

Argatroban – Argatroban3 250 mg/2.5 mL vial 2-40 mcg/kg/min IV4 1,197.01
(GlaxoSmithKline)
Lepirudin – Refludan3 (Bayer) 50 mg vial 0.2-0.4 mg/kg IV bolus, then 191.04
0.1-0.15 mg/kg/hr IV
Bivalirudin – Angiomax 250 mg/vial 0.1-0.75 + 0.3 mg/kg IV bolus, 571.40
(The Medicines Co.) then 0.2-1.75 mg/kg/h IV
Others
Fondaparinux – Arixtra2 2.5 mg/0.5 mL,1 5 mg/0.4 mL, 2.5-10 mg SC daily 50.41
(GlaxoSmithKline) 7.5 mg/0.6 mL, 10 mg/0.8 mL syringe
Anticoagulants, Oral
Warfarin – generic 1, 2, 2.5, 3, 4, 5, 6, 7.5, 10 mg tabs; 2-5 mg PO daily 15.90
Coumadin (Bristol Myers Squibb) 5 mg/2.5 mL vial (Coumadin only) 28.50
1. For oral drugs, cost is for a 30-day supply at the lowest usual dosage. For parenteral drugs, cost is for one unit of the underlined formulation. Cost is based on
the most recent data (February 29, 2008) from retail pharmacies nationwide available from Wolters Kluwer Health, or based on AWP listings in Drug Topics
Red Book 2007 and April 2008 Update.
2. Dosing adjustments may be necessary for renal insufficiency.
3. For patients with heparin-induced thrombocytopenia.
4. Patients undergoing PCI receive a loading dose of 350 mcg/kg by IV injection over 3-5 minutes.

30 Treatment Guidelines from The Medical Letter • Vol. 6 ( Issue 69) • May 2008

response that requires monitoring. But UFH has advan-
tages over LMWH that have kept it from becoming
obsolete: its anticoagulant effect can be rapidly neu-
tralized by protamine; it is not cleared by the kidneys
and therefore may be safer in patients with renal insuf-
ficiency; and it directly inhibits the contact activation
pathway (important in the genesis of thrombi in stents,
filters and catheter tips), possibly preventing coagula-
tion initiated by contact activation more than LMWH
or fondaparinux.4
LMWH — LMWHs, produced by cleaving UFH into
shorter chains, inhibit factor Xa more than they inhibit
thrombin. Their excretion is primarily renal, with an
elimination half-life of 3-4 hours. Compared to UFH,
LMWHs have longer half-lives that permit fewer doses
per day, and their greater bioavailability leads to a more
predictable anticoagulant response. Meta-analyses of
clinical trials comparing them with UFH indicate that
generally they are at least as effective and safe.
Three LMWHs, enoxaparin (Lovenox), dalteparin
(Fragmin) and tinzaparin (Innohep), have been
approved by the FDA; they generally appear to be
similar, but in clinical trials in patients with unstable
angina/non-ST segment elevation myocardial infarc-
tion (UA/NSTEMI), enoxaparin has been associated
with better outcomes, mainly because of a lower inci-
dence of non-fatal myocardial infarction (MI).5
Enoxaparin has been at least as safe as UFH in
patients undergoing elective percutaneous coronary
intervention (PCI).6
FONDAPARINUX — Fondaparinux (Arixtra), a
synthetic analog of the pentasaccharide binding
sequence of heparin, inhibits factor Xa without neu-
tralizing thrombin. Factor Xa inhibitors have no activ-
ity against thrombin that is already formed.
Fondaparinux appears to be as effective and at least as
safe as UFH or LMWH for prophylaxis and treatment
of venous thromboembolism (VTE).7-9 It may also be
used as an alternative to UFH or LMWH in
UA/NSTEMI. 5 The drug has a long half-life and
requires injection only once daily. One limitation of
fondaparinux is that it accumulates in patients with
renal insufficiency, which can be problematic in the
elderly, and is contraindicated in patients with a CrCl
<30 mL/min.
DIRECT THROMBIN INHIBITORS — Unlike
heparins and fondaparinux, direct thrombin inhibitors
inhibit clot-bound as well as circulating thrombin.
Bivalirudin (Angiomax), which is given IV and has a
short half-life, can be used instead of heparin in
patients undergoing coronary angioplasty.10 Whether
it is safer or more effective than UFH, LMWH or fon-
Treatment Guidelines from The Medical Letter • Vol. 6 ( Issue 69) • May 2008
Antiplatelet and Anticoagulant Drugs
daparinux is unclear. The other two approved par-
enteral thrombin inhibitors, lepirudin (Refludan) and
argatroban (Argatroban), are indicated for use in
patients with heparin-induced thrombocytopenia.11
ORAL ANTICOAGULANTS — For long-term anti-
coagulation, oral agents are preferred over parenteral
drugs. Vitamin K antagonists such as warfarin
(Coumadin, and others), which require monitoring,
have long been the only oral anticoagulants available.
The orally active, direct thrombin inhibitor ximelaga-
tran, which never received FDA approval and was
withdrawn by the manufacturer because of hepatotox-
icity, did not require monitoring, and was at least as
effective as warfarin.12,13 Ongoing clinical trials with
other orally active direct thrombin inhibitors will
determine whether hepatotoxicity is a class effect.
Pharmacogenetic tests that have recently become
available may make warfarin dosing more precise in
the future.
CLINICAL USE
The antiplatelet and anticoagulant drugs of choice for
various indications are discussed below and summa-
rized in Tables 2 to 5.
PREVENTION — Aspirin prophlyaxis reduces the
incidence of MI and/or death by 15-20% in patients
with UA/NSTEMI, acute MI or cerebrovascular dis-
ease, and in those undergoing angioplasty or a coro-
nary artery bypass graft (CABG). Aspirin can also
prevent MIs in asymptomatic men and ischemic
stroke in asymptomatic women, but the risk-benefit
ratio is less favorable because of the small increased
risk of hemorrhagic stroke.14
A randomized controlled trial in 2739 patients who
had a transient ischemic attack (TIA) or minor stroke
in the previous 6 months found that a combination of
extended-release dipyridamole (200 mg bid) and
low-dose aspirin (30-325 mg per day) was more
effective than aspirin alone in preventing a composite
of vascular death, stroke, MI or major bleeding (173
vs. 216 events). However, many more patients dis-
continued the combination (470 vs. 184), mainly
because of headache.15
The CAPRIE study in patients with recent MI,
ischemic stroke or peripheral vascular disease found a
significantly lower annual incidence of vascular events
with clopidogrel than with aspirin (5.32% vs. 5.83%).
Occurrence of severe bleeding was similar (1.38% of
patients taking clopidogrel and 1.55% of those taking
aspirin).16 In the MATCH trial, taking clopidogrel and
aspirin together offered no advantage over clopidogrel
31
Antiplatelet and Anticoagulant Drugs

Table 2. Drugs for Percutaneous Coronary Intervention (PCI)

Initiation Duration of
Drug Dose Relative to PCI Therapy
Unfractionated Heparin 60-100 units/kg IV bolus, titrate Immediately prior to PCI No additional heparin
to ACT 250-300 sec1 (50-70 post-PCI
units/kg IV if GP IIb/IIIa used,
titrate to ACT 200-250 sec)

Enoxaparin 1 mg/kg SC, with an additional 2-12 hours prior to PCI No additional enoxaparin
0.3 mg/kg IV if 8-12 hrs post-PCI
since last dose2

Bivalirudin 0.75 mg/kg IV bolus, then Immediately prior to PCI Until end of PCI
1.75 mg/kg/h IV2

Aspirin 162-325 mg PO >30 minutes prior to PCI Lifelong

Clopidogrel 300-600 mg PO load, then 6-15 hours prior to PCI >12 months for drug-
75 mg PO daily eluting stents
1-3 months for bare
metal stents

Abciximab 0.25 mg/kg IV bolus, then 10-60 min prior to PCI 12 hours
0.125 mcg/kg/min IV
(max 10 mcg/min)3

Eptifibatide 180 mcg/kg IV bolus x2, Immediately prior to PCI 12-24 hours
10 min apart, then
2 mcg/kg/min IV2

Tirofiban 0.4 mcg/kg/min IV for 30 min, Prior to PCI (for ACS) 12-24 hours post-PCI
then 0.1 mcg/kg/min IV2

ACT = Activated coagulation time; ACS = acute coronary syndrome

1. With Hemotec device and 300-350 sec with the Hemochron device.
2. Dosing adjustments may be necessary for renal insufficiency.
3. For patients with unstable angina and planned PCI: 0.25 mg/kg bolus IV followed by 18-24 hrs IV infusion of 10 mcg/min, concluding 1 hr after PCI.

alone in prevention of vascular events in patients with
recent ischemic stroke or transient ischemic stroke
(TIA) and substantially increased the risk of serious
bleeding.17
The CHARISMA study compared addition of clopi-
dogrel to aspirin with aspirin alone in patients with
cardiovascular (CV) risk factors (e.g., diabetes, hyper-
tension) or established coronary, cerebrovascular or
peripheral arterial disease. MI, stroke or CV death
occurred in 6.8% of patients treated with both drugs
and 7.3% of those who took aspirin alone, which was
not statistically significant. There was no difference
in the rate of severe bleeding; moderate bleeding
occurred in 2.1% of patients taking clopidogrel with
aspirin and 1.3% of those taking aspirin alone, which
was statistically significant. A subgroup analysis
found that patients with only risk factors (primary pre-
vention) had a higher risk of death from CV causes
with both drugs than with aspirin alone, and those
with established CV disease (secondary prevention)
had a lower risk.18
UA/NSTEMI — The American College of
Cardiology and American Heart Association have
updated recommendations for the management of
patients with UA/NSTEMI, some of whom go on to
PCI. 5 They recommend that patients with
UA/NSTEMI be treated with aspirin, clopidogrel and
an anticoagulant, usually UFH or enoxaparin.
The CURE trial in patients with UA or NSTEMI
found that those treated with clopidogrel in addition to
aspirin had significantly lower rates of CV death, MI
or stroke (9.3% vs. 11.4%) but a significantly higher
risk of major bleeding (3.7% vs. 2.7%) than those
treated with aspirin alone.19 In patients who went on
to PCI, clopidogrel in addition to aspirin significantly
lowered the risk of CV death, MI or urgent revascu-
larization within 30 days after PCI compared to
aspirin alone (4.5% vs. 6.4%), with no significant dif-
ference in major bleeding.20 One year after PCI, the
incidence of death, MI or stroke was still significantly
lower (8.5% vs. 11.5%) in patients who received both
drugs than in those who received aspirin alone.21 Use

32 Treatment Guidelines from The Medical Letter • Vol. 6 ( Issue 69) • May 2008

of clopidogrel in addition to aspirin for at least 12
months appears to be especially important in patients
implanted with drug-eluting stents.22
The SYNERGY trial in high-risk patients with non-ST
segment elevation acute coronary syndrome undergo-
ing angioplasty and often PCI or CABG found that
enoxaparin was as effective as UFH but was associated
with more bleeding.23 In another trial in patients with
UA/NSTEMI, fondaparinux was as effective as enoxa-
parin in preventing recurrent thrombosis, major
ischemic events and death, and 50% less likely to cause
major bleeding.24
High-risk patients often receive a GPIIb/IIIa inhibitor
as well; in one study at one year after UA/NSTEMI,
there was no significant difference in outcome between
patients receiving routine upstream GPIIb/IIIa
inhibitors and those who received them only if and
when they underwent PCI.25
ACUTE MI (STEMI) — In patients treated with fib-
rinolysis within 12 hours after an acute ST-elevation
myocardial infarction (STEMI), the primary endpoint
of an occluded infarct-associated artery on angiogra-
phy, recurrent MI or death before angioplasty occurred
in 15.0% of patients treated with clopidogrel and
aspirin and 21.7% of those treated with aspirin alone.26
In patients presenting within 24 hours of an acute MI,
death, reinfarction or stroke occurred in 9.2% of
patients treated with clopidogrel in addition to aspirin
and 10.1% of those treated with aspirin alone for up to
28 days, also a significant difference.27 In both of these
studies, serious bleeding did not occur significantly
more with addition of clopidogrel.
In 20,506 patients with STEMI, enoxaparin was supe-
rior to UFH as an adjunct to fibrinolytic therapy, but
with an increase in major bleeding episodes.28
In a prespecified subgroup analysis of the OASIS-6
trial, fondaparinux in patients with STEMI not receiv-
ing reperfusion treatment reduced the risk of death or
re-infarction without an increase in severe bleeding
compared to UFH or placebo.29 However, in patients
who underwent PCI, fondaparinux was ineffective and
was associated with more catheter thrombosis.30,31
PCI — Patients who undergo elective PCI should
receive aspirin, clopidogrel and short-term UFH or
LMWH; they may also benefit from a GPIIb/IIIa
inhibitor.
In one randomized trial in patients with UA/NSTEMI
undergoing PCI, bivalirudin alone was as effective as
heparin plus a GPIIb/IIIa inhibitor in preventing
ischemic events (in patients pretreated with clopido-
grel), with a lower incidence of serious bleeding.32
Treatment Guidelines from The Medical Letter • Vol. 6 ( Issue 69) • May 2008
Antiplatelet and Anticoagulant Drugs
A study in 2,399 patients undergoing elective PCI with
stent placement found that patients who received abcix-
imab had a 30-day primary endpoint (death, MI or
urgent revascularization) rate of 5.3% versus 10.8%
with placebo.33 Among 300 patients undergoing urgent
PCI with stent placement for acute MI, abciximab
reduced the incidence of the same endpoint from 14.6%
(with placebo) to 6.0%.34 However, a trial in 2,159 low-
to-intermediate risk patients pre-treated with clopido-
grel before elective PCI found no difference between
abciximab and placebo in the endpoint.35
A randomized, double-blind study in 2,064 patients
undergoing elective PCI with stent placement compared
eptifibatide with placebo; both groups were pretreated
with aspirin plus a thienopyridine. Eptifibatide reduced
the 48-hour primary endpoint (death, MI, or urgent
revascularization) from 10.5% with placebo to 6.6% and
the 30-day secondary endpoint from 10.5% to 6.8%.36 A
randomized, double-blind trial of abciximab versus
tirofiban in PCI found a significantly higher incidence
of death, non-fatal MI or urgent revascularization with
tirofiban (7.6% vs. 6.0%) after 30 days, but after 6
months the outcome was similar with either drug.37,38
TREATMENT OF VTE — Anticoagulant treatment of
patients with deep vein thrombosis (DVT) or pulmonary
embolism (PE) can prevent new or recurrent PE and
death.39 For initial treatment of DVT, LMWH is gener-
ally preferred to UFH. Whether LMWH is superior to
UFH in terms of recurrence rates or the incidence of
major bleeding remains to be determined.40,41 In one
study, however, weight-based, fixed-dose subcutaneous
UFH that did not require PTT monitoring was as effec-
tive and safe as LMWH.42 Fondaparinux is a reasonable
alternative for initial treatment of VTE; in a randomized
trial it was as effective and safe as enoxaparin.43
Table 3. Drugs for Treatment of VTE
Drug Dosage
Unfractionated Heparin Initial: 80 units/kg IV bolus
then 18 units/kg/hr
Enoxaparin1 1.0 mg/kg SC bid or
1.5 mg/kg once daily
Dalteparin1 100 IU/kg SC bid or
200 IU/kg once daily
Tinzaparin1 175 IU/kg SC once daily
Warfarin 2-5 mg PO2
Fondaparinux1 5-10 mg SC3 daily
1. Dosing adjustments may be necessary in renal insufficiency.
2. Monitored daily until results in therapeutic range (INR 2-3) for
>24 hours.
3. 5 mg daily if <50 kg, 10 mg daily if >100 kg
33
Antiplatelet and Anticoagulant Drugs
Table 4. Drugs for Prevention of VTE
Drug Dosage
Unfractionated heparin 5000 units SC q8-12h
Fondaparinux1 2.5 mg SC once daily
Enoxaparin1 30 mg bid SC or
40 mg once daily SC
Dalteparin1 2500 IU-5000 IU
SC once daily
Tinzaparin1 175 IU/kg SC
1. Dosage adjustment may be required in renal insufficiency.
For chronic anticoagulant treatment, which can pre-
vent recurrent VTE and death, it is not clear whether
an oral vitamin K antagonist such as warfarin is supe-
rior to subcutaneous injections of LMWH, but war-
farin is usually preferred because of the convenience
of oral dosing. In patients with cancer, long-term ther-
apy with an LMWH once daily subcutaneously has
been shown to be superior to warfarin in preventing
recurrent VTE without increasing the risk of bleed-
ing.44 The optimal duration of anticoagulant therapy
for patients with VTE is unclear45; the risk of recur-
rent VTE is greatest in the first 6 months.
PREVENTION OF VTE — Hospitalized Medical
Patients — Many studies have shown that prophylac-
tic anticoagulation of hospitalized medical patients
confined to bed or with other risk factors prevents
symptomatic DVT and PE, but they have not shown
that it decreases all-cause mortality.46 LMWH has
been more effective than UFH in preventing DVT but
not PE, and both have increased the risk of bleeding.47
General Surgery — Moderate-to-high risk patients
undergoing general surgery have a lower incidence of
DVT and PE if they are given anticoagulation prophy-
laxis. Preoperative subcutaneous low-dose UFH (5000
units tid) or LMWH, combined with use of compression
stockings or intermittent pneumatic compression
devices, can be used. Postoperative fondaparinux can
also be used for this indication.48 LMWH is preferred in
trauma.
Major Orthopedic Surgery — Patients undergoing
total hip replacement, total knee arthroplasty and hip
fracture surgery have an increased risk of VTE and
(especially with hip fracture surgery) PE. Many stud-
ies have shown that prophylactic anticoagulation
markedly decreases the incidence of these events.48
For all of these indications, enoxaparin has been
more effective than UFH or warfarin, and fonda-
parinux has been more effective than enoxaparin,
with little or no increase in the risk of clinically rele-
vant bleeding.49-51
34 Treatment Guidelines from The Medical Letter • Vol. 6 ( Issue 69) • May 2008
ATRIAL FIBRILLATION (AF) — Anticoagulation
can reduce the risk of thromboembolic stroke in
patients with AF by 60% or more and has been shown
to be more effective for this indication than antiplatelet
therapy.52 With an annual rate of major bleeding of
about 2% and an absolute increase in the rate of
intracranial hemorrhage of about 0.2%, the benefits of
warfarin far surpass the risks. Warfarin is more effec-
tive than aspirin and more effective than aspirin plus
clopidogrel in preventing stroke in patients with parox-
ysmal or sustained atrial fibrillation.53,54 The main
drawback of warfarin is the need for close monitoring
to keep the international normalized ratio (INR)
between 2 and 3.
ISCHEMIC STROKE — Antiplatelet drugs can
reduce the incidence of ischemic stroke in patients
who have had a TIA or previous ischemic stroke, but
not as dramatically as anticoagulants decrease the
incidence of thromboembolic stroke in patients with
atrial fibrillation. The relative risk reduction in most
studies is between 15% and 20%.55 Aspirin is gener-
ally used; no optimal dose has been established, but
most experts use between 50 and 325 mg per day. The
combination of aspirin 25 mg with 200 mg extended-
release dipyridamole (Aggrenox) taken twice daily
has been more effective in some studies in preventing
recurrent stroke than aspirin alone, without increasing
the risk of serious bleeding. Concurrent use of aspirin
and clopidogrel has not been shown to prevent stroke
more effectively than clopidogrel or aspirin alone,
and in one study it doubled the incidence of life-
threatening hemorrhage.17 Clopidogrel alone can be
used as initial therapy in patients with aspirin allergy.
PERIPHERAL ARTERIAL DISEASE —
Antiplatelet therapy has been shown to prevent MI
and stroke in patients with peripheral arterial dis-
ease. 56 Addition of an oral anticoagulant to an
antiplatelet drug in such patients did not, in one
study, significantly decrease the incidence of stroke,
MI or cardiovascular death, and it markedly
increased the incidence of life-threatening bleed-
ing.57 Whether addition of a second antiplatelet drug
would lower the incidence of ischemic events with-
out increasing the risk of serious bleeding remains to
be determined.
DRUGS OF CHOICE
For some indications, the anticoagulant and
antiplatelet drugs of choice are clearly established.
For others, the choice varies with clinical circum-
stances or is not clear. Nevertheless, the table that fol-
lows may be helpful.
 Antiplatelet and Anticoagulant Drugs

13. PF Boudes. The challenges of new drugs benefits and risks analysis:
Table 5. Antiplatelet and Anticoagulant Drugs lessons from the ximelagatran FDA Cardiovascular Advisory
of Choice Committee. Contemp Clin Trials 2006; 27:432.
14. Aspirin for primary prevention of cardiovascular disease (Revisited).
Indication Drugs
Med Lett Drug Ther 2006; 48:53.
Primary Prevention 15. ESPRIT Study Group. Aspirin plus dipyridamole versus aspirin alone
Risk Factors Aspirin after cerebral ischaemia of arterial origin (ESPRIT): randomised con-
No Risk Factors None1 trolled trial. Lancet 2006; 367:1665.
Secondary Prevention 16. CAPRIE Steering Committee. A randomised, blinded, trial of clopido-
Recent MI Aspirin2 grel versus aspirin in patients at risk of ischaemic events (CAPRIE).
CAPRIE Steering Committee. Lancet 1996; 348:1329.
Ischemic Stroke Aspirin + dipyridamole
17. HC Diener et al. Aspirin and clopidogrel compared with clopidogrel
alone after recent ischaemic stroke or transient ischaemic attack in
UA/NSTEMI Aspirin + clopidogrel
high-risk patients (MATCH): randomized, double-blind, placebo-con-
+ UFH, enoxaparin, trolled trial. Lancet 2004; 364:331.
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vention of atherothrombotic events. N Engl J Med 2006; 354:1706.
Acute MI (STEMI) Aspirin plus clopidogrel 19. S Yusuf et al. Effects of clopidogrel in addition to aspirin in patients
plus UFH, enoxaparin with acute coronary syndromes without ST-segment elevation. N Engl J
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21. SR Steinhubl et al. Early and sustained dual oral antiplatelet therapy
VTE Treatment LMWH, UFH or fondaparinux following percutaneous coronary intervention: a randomized controlled
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VTE Prevention 22. EL Eisenstein et al. Clopidogrel use and long-term clinical outcomes
after drug-eluting stent implantation. JAMA 2007; 297:159.
Hospitalized Medical Patients LMWH or UFH 23. JJ Ferguson. Enoxaparin vs. unfractionated heparin in high-risk patients
General Surgery Low-dose UFH, LMWH or with non-ST segment elevation acute coronary syndromes managed
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Hip Fracture Surgery Fondaparinux 24. Fifth Organization to Assess Strategies in Acute Ischemic Syndromes
Atrial Fibrillation Warfarin Investigators; S Yusuf et al. Comparison of fondaparinux and enoxa-
parin in acute coronary syndromes. N Engl J Med 2006; 354:1461.
Peripheral Arterial Disease Aspirin 25. GW Stone et al. Antithrombotic strategies in patients with acute coro-
1. Some clinicians offer aspirin to women >65 and men >45 years. nary syndromes undergoing early invasive management: one-year
2. Or, if intolerant to aspirin, clopidogrel. results from the ACUITY trial. JAMA 2007; 298:2497.
3. Fondaparinux should not be used in patients undergoing PCI. 26. MS Sabatine et al. Effect of clopidogrel pretreatment before percuta-
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6. G Montalescot et al. Enoxaparin versus unfractionated heparin in elec- farction in patients with acute ST-segment elevation myocardial infarc-
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7. AG Turpie et al. Superiority of fondaparinux over enoxaparin in pre- 31. RM Califf. Fondaparinux in ST-segment elevation myocardial infarc-
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Antiplatelet and Anticoagulant Drugs

35. A Kastrati et al. A clinical trial of abciximab in elective percutaneous

coronary intervention after pretreatment with clopidogrel. N Engl J Coming Soon in Treatment Guidelines:
Med 2004; 350:232
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Drugs for Epilepsy – June 2008
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Lancet 2000; 356:2037.
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tirofiban and abciximab during percutaneous coronary revasculariza-
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39. H Tran et al. Anticoagulant treatment of deep vein thrombosis and pul- from The Medical Letter

monary embolism. Clin Geriatr Med 2006; 22:113.

40. JB Segal et al. Management of venous thromboembolism: a systematic EDITOR: Mark Abramowicz, M.D.
EXECUTIVE EDITOR: Gianna Zuccotti, M.D., M.P.H., Weill Medical College
review for a practice guideline. Ann Intern Med 2007; 146:211. of Cornell University
41. HR Büller, et al. Antithrombotic therapy for venous thromboembolic DEPUTY EDITOR: Jean-Marie Pflomm, Pharm.D.
disease. The Seventh ACCP Conference on Antithrombotic and ASSISTANT EDITOR, DRUG INFORMATION: Susan Morey, Pharm.D.
CONTRIBUTING EDITOR: Eric J. Epstein, M.D., Albert Einstein College of Medicine
Thrombolytic Therapy. Chest 2004; 126 (3Suppl):401S.
CONTRIBUTING EDITOR, DRUG INTERACTIONS: Philip D. Hansten, Pharm.D.,
42. C Kearon et al. Comparision of fixed-dose weight-adjusted unfraction- University of Washington
ated heparin and low-molecular-weight heparin for acute treatment of ADVISORY BOARD:
venous thromboembolism. JAMA 2006; 296:935. Jules Hirsch, M.D., Rockefeller University
David N. Juurlink, BPhm, M.D., PhD, Sunnybrook Health Sciences Centre
43. HR Büller et al. Fondaparinux or enoxaparin for the initial treatment of
Richard B. Kim, M.D., University of Western Ontario
symptomatic deep venous thrombosis: a randomized trial. Ann Intern Gerald L. Mandell, M.D., University of Virginia School of Medicine
Med 2004; 140:867. Hans Meinertz, M.D., University Hospital, Copenhagen
44. AY Lee et al. Low-molecular-weight heparin versus a coumarin for the Dan M. Roden, M.D., Vanderbilt University School of Medicine
F. Estelle R. Simons, M.D., University of Manitoba
prevention of recurrent venous thromboembolism in patients with can- Neal H. Steigbigel, M.D., New York University School of Medicine
cer. N Engl J Med 2003; 349:146. SENIOR ASSOCIATE EDITORS: Donna Goodstein, Amy Faucard
45. BA Hutton and MH Prins. Duration of treatment with vitamin K antag- ASSOCIATE EDITOR: Cynthia Macapagal Covey
onists in symptomatic venous thromboembolism. Cochrane Database EDITORIAL FELLOWS:
Vanessa K. Dalton, M.D., M.P.H., University of Michigan Medical School
Syst Rev 2006; (1):CD001367. Lauren K. Schwartz, M.D., Mount Sinai School of Medicine
46. F Dentali et al. Meta-analysis: anticoagulant prophylaxis to prevent DRUG INTERACTIONS FELLOW: Emily Ung, BScPhm, Children’s Hospital of
symptomatic venous thromboembolism in hospitalized medical Western Ontario
EDITORIAL ASSISTANT: Liz Donohue
patients. Ann Intern Med 2007; 146:278.
PRODUCTION COORDINATOR: Cheryl Brown
47. L Wein et al. Pharmacological venous thromboembolism prophylaxis in MANAGING EDITOR: Susie Wong
hospitalized medical patients: a meta-analysis of randomized controlled
trials. Arch Intern Med 2007; 167:1476. EXECUTIVE DIRECTOR OF SALES: Gene Carbona
FULFILLMENT AND SYSTEMS MANAGER: Cristine Romatowski
48. WH Geerts et al. Prevention of venous thromboembolism: the Seventh
DIRECTOR OF MARKETING COMMUNICATIONS: Joanne F. Valentino
ACCP Conference on Antithrombotic and Thrombolytic Therapy. VICE PRESIDENT AND PUBLISHER: Yosef Wissner-Levy
Chest 2004; 126(3 suppl):338S. Founded in 1959 by
49. AG Turpie et al. Postoperative fondaparinux versus postoperative Arthur Kallet and Harold Aaron, M.D.
enoxaparin for prevention of venous thromboembolism after elective
hip-replacement surgery: a randomised double-blind trial. Lancet 2002; Copyright and Disclaimer: The Medical Letter is an independent nonprofit organ-
ization that provides healthcare professionals with unbiased drug prescribing rec-
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ommendations. The editorial process used for its publications relies on a review of
50. KA Bauer et al. Fondaparinux compared with enoxaparin for the pre- published and unpublished literature, with an emphasis on controlled clinical trials,
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51. BI Eriksson et al. Fondaparinux compared with enoxaparin for the pre-
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36 Treatment Guidelines from The Medical Letter • Vol. 6 ( Issue 69) • May 2008
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Issue 69 Questions
1. Aspirin inhibits platelet activation and aggregation for: 2. Clopidogrel is used more than ticlopidine because it is:
a. 4-6 hours a. more effective
b. 1-2 days b. less toxic
c. 5-7 days c. less expensive
d. 10-30 days d. none of the above
Page: 29 Page: 29

Continues on next page >>

Treatment Guidelines from The Medical Letter • Vol. 6 ( Issue 69) • May 2008
 Treatment Guidelines: Online Continuing Medial Education
(www.medicalletter.org/tgcme)
3. Disadvantages of unfractionated heparin (UFH) compared to low 8. Patients who undergo an elective PCI are usually treated with:
molecular weight heparins (LMWH) include: a. aspirin plus an anticoagulant
a. a more variable anticoagulant response b. aspirin plus clopidogrel
b. higher cost c. aspirin plus clopidogrel plus an anticoagulant
c. more renal toxicity d. none of the above
d. all of the above Page: 33
Page: 29, 31

4. Advantages of UFH over LMWH include:

a. rapidly neutralizable anticoagulant effect 9. Some high-risk patients undergoing PCI may benefit
b. not cleared by kidneys from addition of:
c. may be more effective in preventing thrombi a. a GPIIb/IIIa inhibitor
caused by catheters b. fondaparinux
d. all of the above c. dipyridamole
Page: 31 d. none of the above
Page: 33

5. Unlike heparins and fondaparinux, direct thrombin 10. VTE could be treated with:
inhibitors such as bivalirudin: a. fixed-dose weight-based subcutaneous UFH
a. can cause thrombocytopenia b. enoxaparin
b. can be given orally c. fondaparinux
c. have a long half-life d. any of the above
d. inhibit clot-bound as well as circulating thrombin Page: 33,34
Page: 31

6. In patients with coronary artery disease, aspirin prophylaxis 11. Prophylactic anticoagulation of hospitalized medical
reduces the incidence of myocardial infarction and/or death by patients confined to bed:
a. <5% a. has been shown to prevent DVT and PE
b. 15-20% b. has not been shown to prevent DVT and PE
c. 50% c. does not increase the risk of bleeding
d. >50% d. none of the above
Page: 31 Page: 34

12. To reduce the risk of thromboembolic stroke in patients

7. Current guidelines recommend treating patients with with atrial fibrillation:
UA/NSTEMI with: a. aspirin is as effective as anticoagulation
a. aspirin b. aspirin plus clopidogrel is as effective as anticoagulation
b. aspirin plus an anticoagulant c. warfarin is more effective than aspirin alone or with
c. aspirin plus clopidogrel clopidogrel
d. aspirin plus clopidogrel plus an anticoagulant d. neither antiplatelet therapy nor anticoagulation
Page: 32 is indicated
Page: 34

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Treatment Guidelines from The Medical Letter • Vol. 6 ( Issue 68) • May 2008