Antithrombotics and endoscopy

GUIDELINE
The management of antithrombotic agents for patients
undergoing GI endoscopy
Prepared by: ASGE STANDARDS OF PRACTICE COMMITTEE
Ruben D. Acosta, MD, Neena S. Abraham, MD, MSCE, FASGE (invited content expert, ad-hoc member),
Vinay Chandrasekhara, MD, Krishnavel V. Chathadi, MD, Dayna S. Early, MD, FASGE,
Mohamad A. Eloubeidi, MD, MHS, FASGE, John A. Evans, MD, Ashley L. Faulx, MD, FASGE,
Deborah A. Fisher, MD, MHS, FASGE, Lisa Fonkalsrud, BSN, RN, CGRN, Joo Ha Hwang, MD, PhD, FASGE,
Mouen A. Khashab, MD, Jenifer R. Lightdale, MD, MPH, FASGE, V. Raman Muthusamy, MD, FASGE,
Shabana F. Pasha, MD, John R. Saltzman, MD, FASGE, Aasma Shaukat, MD, MPH, FASGE,
Amandeep K. Shergill, MD, Amy Wang, MD, Brooks D. Cash, MD, FASGE, previous Committee Chair,
John M. DeWitt, MD, FASGE, Chair
This document was reviewed and approved by the Governing Board of the American Society for Gastrointestinal
Endoscopy.
This is one of a series of statements discussing the use of
GI endoscopy in common clinical situations. The Stan-
dards of Practice Committee of the American Society for
Gastrointestinal Endoscopy (ASGE) prepared this text. In
preparing this guideline, a search of the medical litera-
ture was performed using PubMed and the Cochrane
Database, with dates of search from August 1966 to
December 2014. Additional references were obtained
from the bibliographies of the identified articles and
from recommendations of expert consultants. When
limited or no data exist from well-designed prospective
trials, emphasis is given to results from large series and
reports from recognized experts. Guidelines for appro-
priate use of endoscopy are based on a critical review
of the available data and expert consensus at the time
the guidelines are drafted. Further controlled clinical
studies may be needed to clarify aspects of this guideline.
This guideline may be revised as necessary to account for
changes in technology, new data, or other aspects of clin-
ical practice. The recommendations were based on re-
viewed studies and were graded on the strength of the
supporting evidence (Table 1).1
This guideline is intended to be an educational device
to provide information that may assist endoscopists in
providing care to patients. This guideline is not a rule
and should not be construed as establishing a legal stan-
dard of care or as encouraging, advocating, requiring,
or discouraging any particular treatment. Clinical deci-
sions in any particular case involve a complex analysis
of the patient’s condition and available courses of action.
Therefore, clinical considerations may lead an endoscop-
ist to take a course of action that varies from these
guidelines.
Antithrombotic therapy is used to reduce the risk of
thromboembolic events in patients with conditions such as
atrial fibrillation (AF), acute coronary syndrome (ACS),
deep vein thrombosis (DVT), hypercoagulable states, and
endoprostheses. Antithrombotics include medications classi-
fied as anticoagulants or antiplatelet agents (APAs). Anticoag-
ulants prevent the clotting of blood by interfering with the
native clotting cascade and include the following 4 drug
classes: vitamin K antagonists (eg, warfarin), heparin deriva-
tives (eg, unfractionated [UFH] and low molecular weight
[LMWH], fondaparinux [Arixtra, GlaxoSmithKline, Research
Triangle Park, NC, USA]), direct factor Xa inhibitors (eg, ri-
varoxaban [Xarelto, Janssen Pharmaceuticals, Inc, Raritan,
NJ, USA], apixaban [Eliquis, Bristol-Myers Squibb Company,
Princeton, NJ, USA], edoxaban [Savaysa, Daiichi Sankyo
Co, LTD, Tokyo, Japan]), and direct thrombin inhibitors
(eg, dabigatran [Pradaxa, Boehringer Ingelheim Pharmaceu-
ticals Inc, Ridgefield, Conn, USA], hirudins, argatraban
[Acova, Abbott Laboratories, North Chicago, Ill, USA]).
APAs decrease platelet aggregation, thus preventing
thrombus formation. APAs include the thienopyridines (eg,
clopidogrel, [Plavix, Bristol-Myers Squibb/Sanofi Pharmaceu-
ticals Partnership, Bridgewater, NJ, USA], prasugrel [Effient,
Eli Lilly and Company, Indianapolis, Ind, USA], ticlopidine
[Ticlid, Roche Pharmaceuticals, Nutley, NJ, USA], and ticagre-
lor [Brilinta, AstraZeneca, Wilmington, Del, USA]), the
protease-activated receptor-1 (PAR-1) inhibitor vorapaxar
(Zontivity, Merck Sharp & Dohme Corp, Whitehouse Station,
NJ, USA), glycoprotein IIb/IIIa receptor inhibitors (GPIIb/IIIa
inhibitors) (eg, abciximab [ReoPro, Eli Lilly and Company, In-
dianapolis, Ind, USA], eptifibatide [Integrilin, Merck Sharp &
Dohme Corp, Whitehouse Station, NJ, USA], and tirofiban
[Aggrastat, Medicure Pharma, Inc, Somerset, NJ, USA]),
Copyright ª 2016 by the American Society for Gastrointestinal Endoscopy
0016-5107/$36.00
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www.giejournal.org Volume 83, No. 1 : 2016 GASTROINTESTINAL ENDOSCOPY 3

aspirin (acetylsalicylic acid [ASA]), and nonsteroidal anti-
inﬂammatory drugs. The duration of action and reversal
routes for the antithrombotic drug classes are described in
Table 2.
Adverse events of antithrombotic therapy include GI
bleeding,2,3
and their use increases the risk of hemorrhage
after some endoscopic interventions.4-6
For patients taking
these medications who require endoscopy, one should
consider the following important factors: (1) the urgency
of the procedure, (2) the bleeding risk of the procedure,
(3) the effect of the antithrombotic drug(s) on the bleeding
risk, and (4) the risk of a thromboembolic event related
to periprocedural interruption of antithrombotic agents.7
PROCEDURE RISKS
Common endoscopic procedures vary in their potential
to induce bleeding, and these have been outlined in other
TABLE 1. System for rating the quality of evidence for guidelines
Quality of evidence Definition Symbol
High quality Further research is very unlikely to change our confidence in the estimate of effect. 4444
Moderate quality Further research is likely to have an important impact on our confidence in the estimate of
effect and may change the estimate.
444O
Low quality Further research is very likely to have an important impact on our confidence in the estimate of
effect and is likely to change the estimate.
44OO
Very low quality Any estimate of effect is very uncertain. 4OOO
Adapted from Guyatt et al.1
TABLE 2. Antithrombotic drugs: duration of action and approach to reversal when indicated
Drug class Specific agent(s) Duration of action
Approach to reversal based on procedural urgency
Elective Urgent
APAs Aspirin 7-10 days NA Hold, can give platelets
NSAIDs Varies NA Hold
Dipyridamole (Persantine) 2-3 days Hold Hold
Cilostazol (Pletal, Otsuka Pharmaceutical
Co., Ltd., Tokushima, Japan)
2 days Hold Hold
Thienopyridines: clopidrogrel (Plavix)
prasugrel (Effient) ticlodipine (Ticlid)
ticagrelor (Brilinta)
5-7 days: clopidogrel, 3-5
days: ticagrelor
5-7 days: prasugrel
10-14 days98
: ticlopidine
Hold Hold
GPIIb/IIIa inhibitors: tirofiban (Aggrastat)
abciximab (ReoPro)
eptifibatide (Integrilin)
tirofiban: 1-2 seconds
abciximab: 24 hours
eptifibitide: 4 hours
NA Hold
HD: tirofiban
PAR-1 inhibitor: vorapaxar (Zontivity) 5-13 days Hold Hold
Anticoagulants Warfarin (Coumadin) 5 days Hold Vitamin K, PCC
UFH IV 2-6 hours
SQ 12-24 hours
Hold Protamine sulfate* (partial)
LMWH:
enoxaparin (Lovenox)
dalteparin (Fragmin, Pfizer Inc,
New York, NY, USA)
24 hours Hold Protamine sulfate, consider rVIIa
Fondaparinux (Arixtra) 36-48 hours Protamine sulfate, consider rVIIa
Direct factor Xa Inhibitor: rivaroxaban
(Xarelto) apixaban (Eliquis)
edoxaban (Savaysa)
See Tables 7 and 8 Hold Charcoal (if last intake within 2-3 hours);
nonactivated PCC or activated PCC
Direct thrombin inhibitor, oral: dabigatran
(Pradaxa)
IV: Desirudin (Iprivask, Aventis
Pharmaceuticals Inc.,
Bridgewater, NJ, USA)
See Table 9 Hold Charcoal (if last intake within 2-3 hours);
nonactivated PCC or activated PCC; HD
NSAIDs, Nonsteroidal anti-inflammatory drugs; NA, not applicable; HD, hemodialysis; PCC, prothrombin complex concentrate; rVIIa, recombinant factor VIIa.
*Caution: Can cause severe hypotension and anaphylaxis.
Management of antithrombotic agents for patients undergoing GI endoscopy
4 GASTROINTESTINAL ENDOSCOPY Volume 83, No. 1 : 2016 www.giejournal.org

ASGE guidelines (Table 3).8
Studies on postprocedural
bleeding risks have been conducted in patients who are not
on complex antithrombotic regimens and thus may not
accurately reﬂect the bleeding risk of patients using newer
antithrombotic therapies. Traditionally, low-risk procedures
have included diagnostic EGD, colonoscopy, ERCP without
sphincterotomy, biliary stent placement, and push or
balloon-assisted enteroscopy. Mucosal biopsy sampling per-
formed as part of these procedures confers a low risk of GI
bleeding. Similarly, EUS without FNA, capsule endoscopy,
and argon plasma coagulation8
are low risk. Nonachalasia
esophageal dilation has been associated with a low risk of
bleeding in large series9,10,11
; however, the safety of dilation
while on anticoagulants is unknown, and the potential for
an inaccessible site of bleeding argues for caution in this
setting. High-risk endoscopic procedures are associated with
a potential for bleeding that requires an intervention, such as
hospitalization, transfusion, endoscopic treatment, or sur-
gery.12
These high-risk procedures include polypectomy,13,14
therapeutic balloon-assisted enteroscopy (other than argon
plasma coagulation),15,16
endoscopic sphincterotomy,17
EUS
with FNA, percutaneous endoscopic gastrostomy,18-20
percuta-
neous endoscopic jejunostomy,21
tumor ablation
(esophagus, stomach, colon, and rectum),22
endoscopic
submucosal dissection,23
EMR,24
pneumatic balloon dilation
for achalasia,25
treatment of varices,26
ampullary resection,
per-oral endoscopic myotomy,27
cystoenterostomy,28
and
endoscopic therapy of Zenker’s diverticulum.29
The risk of
bleeding after polypectomy ranges from .3% to 10% and
depends on a number of factors, including the polyp size,
location, morphology (nonpolypoid, sessile, pedunculated),
resection technique (cold or hot forceps, cold snare, or
snare cautery), and type of cautery used.
There is controversy with regard to whether enteral
stent placement is high or low risk. One retrospective re-
view of 85 patients with esophageal stents described a
bleeding risk as high as 5.3%.30
However, subsequent
prospective multicenter studies as well as systematic
reviews have described bleeding rates in the range of
.5% to 1% in a variety of GI locations.31,32
CONDITION RISKS
The probability of a thromboembolic event related to the
temporary interruption of antithrombotic therapy for an
endoscopic procedure depends on the indication for
TABLE 3. Procedure risk for bleeding (overall)
Higher-risk procedures Low-risk procedures
Polypectomy Diagnostic (EGD, colonoscopy, flexible sigmoidoscopy) including mucosal biopsy
Biliary or pancreatic sphincterotomy ERCP with stent (biliary or pancreatic) placement or papillary balloon dilation without sphincterotomy
Treatment of varices
PEG placement* Push enteroscopy and diagnostic balloon-assisted enteroscopy
Therapeutic balloon-assisted enteroscopy Capsule endoscopy
EUS with FNAy Enteral stent deployment (Controversial)
Endoscopic hemostasis EUS without FNA
Tumor ablation Argon plasma coagulation
Cystgastrostomy Barrett’s ablation
Ampullary resection
EMR
Endoscopic submucosal dissection
Pneumatic or bougie dilation
PEJ
PEJ, Percutaneous endoscopic jejunostomy.
*PEG on aspirin or clopidogrel therapy is low risk. Does not apply to DAPT.
yEUS-FNA of solid masses on ASA/NSAIDs is low risk.
TABLE 4. CHA2DS2-VASc scoring system
CHA2DS2-VASc score or
assessment
Risk of stroke
(CVA)
% Risk of annual
CVA
0 Low 0
1 Moderate 1.3
2 High 2.2
3 High 3.2
4 High 4.0
5 High 6.7
6 High 9.8
7 High 9.6
8 High 6.7
9 High 15.2
CHA2DS2-VASc, Congestive heart failure [1 point], Hypertension [1 point], Age ! 75
years [2 points], Diabetes mellitus [1 point], Stroke [2 points], Vascular disease [1
point], Age 65-74 years [1 point], Sex category, ie, female sex [1 point].
CVA, cerebrovascular accident.

antithrombotic therapy and individual patient characteristics.
For example, in patients with nonvalvular AF, important de-
terminants of risk for a cerebrovascular accident (CVA) are
included in the CHA2DS2-VASc index (Table 4).33
This score
ranges from 0 to 9 and considers thromboembolic risk
factors of congestive heart failure (1 point), hypertension
(1 point), age ! 75 years (2 points), diabetes (1 point),
stroke (2 points), vascular disease (prior myocardial
infarction [MI], peripheral artery disease, or aortic plaque)
(1 point), age 65 to 74 years (1 point), and sex category
(female) (1 point). The higher the score, the greater the
thromboembolic risk, and patients with a score of !2 are
considered to be at high risk of thromboembolism
(>2.2%/year). These patients are frequently prescribed an
anticoagulant to mitigate thromboembolic risk.
High thrombosis risk scenarios for patients on APA ther-
apy include placement of drug-eluting coronary stents
12 months previously or bare metal coronary stents 1
month previously. For patients with ACS, a bare metal coro-
nary stent placed 12 months previously is considered a
high-risk setting.4
Endoscopists should be aware of
specific clinical risk factors that will predispose a patient to
higher rates of stent occlusion beyond 1 year after stent
insertion and approach modification of antiplatelet
regimens cautiously in these cases. These patients include
those with a prior history of stent occlusion, because 1 in 5
patients who experience a first thrombosis will experience
a second stent occlusion at a rate of .6% per year over the
first 3 years,34,35
with a cumulative risk of cardiac death of
27.9%. Patients with ACS or ST elevation MI, multivessel
percutaneous coronary intervention, diabetes, renal failure,
or diffuse coronary artery disease are also at higher risk of
stent occlusion or ACS events with alteration of antithrom-
botic therapy.36
Patients with previous venous thromboembolism (VTE)
on anticoagulation or 1 or more mechanical heart valves
have different risk factors for thromboembolic events
(Table 5). Specific clinical variables divide patients into
low-, medium-, and high-risk groups. Among patients with
VTE, time from initial VTE, history of recurrent VTE with an-
tithrombotic interruption, and presence of underlying
thrombophilia are most predictive of future thromboem-
bolic risk. For patients with mechanical heart valves the
type, number, and location of valvular prostheses and the
presence or absence of associated heart failure and AF deter-
mine the annual risk of thromboembolic events. Bio-
prosthetic valves are considered low risk.37
ANTIPLATELET AGENTS
ASA is a cyclooxygenase inhibitor that is used alone or in
combination with other APAs. It is used to inhibit platelet
aggregation for prophylaxis of secondary cardioembolic
phenomena after occurrence of a stroke or MI. In patients
with a >10% 10-year risk of heart attack or stroke,38
primary cardioprophylaxis with low-dose ASA therapy is
recommended. ASA causes irreversible inhibition of the cy-
clooxygenase 1 and 2 enzyme systems. After cessation of
ASA, 7 to 9 days are required to regain full platelet
function.39
Dipyridamole (Persantine, Teva Pharmaceuticals USA,
Sellersville, Pa, USA) reversibly inhibits platelet aggrega-
tion. This drug is used in combination with ASA in the sec-
ondary prevention of stroke and off-label for primary
stroke prevention. The mechanism of action of this drug
is controversial40
; both inhibition of cyclic nucleotide
phosphodiesterase and blockade of the uptake of
adenosine have been suggested. Dipyridamole has an
elimination half-life of 12 hours and duration of action of
about 2 days after discontinuation.
The most common APAs used after ASA therapy are the
thienopyridine agents. These drugs bind to the P2Y12
component of the ADP receptors, which prevents activa-
tion of the GPIIb/IIIa receptor complex, thereby reducing
platelet aggregation. The class includes ticlopidine (Ticlid),
TABLE 5. Risk for thromboembolic event in patients with mechanical heart valve(s) or VTE on anticoagulation37
Clinical indication for warfarin therapy
Annual
risk Mechanical heart valve VTE
High Any mitral valve prosthesis
Any caged-ball or tilting disc aortic valve prosthesis
Recent (within 6 months) CVA or TIA
Recent (within 3 months) VTE
Severe thrombophilia (deficiency of protein C, protein S, or
antithrombin; antiphospholipid antibodies; multiple
abnormalities)
Medium Bileaflet aortic valve prosthesis and one or more of the following risk
factors: AF, prior CVA or TIA, hypertension, diabetes, congestive heart
failure, age ! 75 years
VTE within the past 3-12 months
Nonsevere thrombophilia (heterozygous factor V Leiden or
prothrombin gene mutation)
Recurrent VTE
Active cancer (treated within 6 months or palliative)
Low Bileaflet aortic valve prosthesis without AF and no other risk factors
for CVA
VTE 12 months previous and no other risk factors
VTE, venous thromboembolism; CVA, cerebrovascular accident; TIA, Transient ischemic attack; AF, atrial fibrillation.

clopidogrel (Plavix), prasugrel (Effient), and ticagrelor
(Brilinta). Ticlopidine (Ticlid), the first widely available
thienopyridine agent, has largely been supplanted in clin-
ical use by newer second-generation agents because of
concerns regarding hematologic side effects (such as neu-
tropenia, thrombotic thrombocytopenia purpura, and he-
molytic uremic syndrome). Clopidogrel (Plavix) is
approved for secondary prevention of MI or stroke and
in the primary management of established peripheral
vascular disease. Clopidogrel (Plavix) efficacy can be
limited by variations of the ABCB13435 TT and CYP2C19
genotypes of cytochrome P450 enzymes, which alter he-
patic metabolism of the clopidogrel prodrug to its active
thiol metabolite.41,42
This altered metabolism results in var-
iable antiplatelet effects and adverse cardiac events,43
including stent thrombosis44
and post–percutaneous
coronary intervention ischemic events.45
The minimum
duration of discontinuation of clopidogrel that allows for
restoration of normal platelet aggregation is 5 to 7 days.37
Third-generation thienopyridine agents include prasu-
grel (Effient) and ticagrelor (Brilinta). Similar to clopidog-
rel (Plavix), prasugrel (Effient) is a prodrug that requires
conversion by the cytochrome P450 hepatic enzymes;
however, unlike clopidogrel’s (Plavix) multistep conversion
process to an active metabolite, the activation of prasugrel
(Effient) occurs in a single hepatic step. The pharmaco-
logic characteristics of prasugrel (Effient) overcome some
of the limitations of clopidogrel (Plavix) but at the risk of
increased bleeding. Because of this, the U.S. Food and
Drug Administration (FDA) approved the drug with a black
box warning specifically noting that prasugrel (Effient)
should not be used in patients with active bleeding, a his-
tory of transient ischemic attack or CVA, or likely to un-
dergo urgent coronary bypass graft surgery. Similar to
clopidogrel (Plavix), the mechanism of action is the irre-
versible inhibition of the P2Y12 receptor; thus, the mini-
mum duration of discontinuation of prasugrel that allows
for restoration of normal platelet aggregation is 5 to 7
days. Unlike clopidogrel (Plavix), prasugrel (Effient)
achieves a much higher level of platelet inhibition and is
unaffected by variants of the CYP2C19 or ABCB1 geno-
types.46-48
Ticagrelor (Brilinta) is the first reversible oral P2Y12
antagonist and an alternative therapy for ACS. This
drug is quickly absorbed, does not require metabolic
activation, and has a rapid antiplatelet effect that closely
parallels drug-exposure levels. Unlike clopidogrel (Pla-
vix) and prasugrel (Effient), the reversible inhibition of
the P2Y12 receptor permits a shorter interval of discon-
tinuation, 3 to 5 days, to recover adequate platelet
function.49
In January 2014 the FDA approved a first-in-class anti-
platelet medication, vorapaxar (Zontivity). This agent is a
competitive and selective inhibitor of PAR-1, the major
thrombin receptor on human platelets. It has been shown
in clinical trials to reduce the risk of MI, stroke, CV death,
and need for revascularization procedures in patients with
a previous MI or peripheral artery disease when prescribed
in conjunction with traditional dual antiplatelet therapy
(DAPT).50
However, this intensification of antiplatelet
effect, via a novel pathway, is associated with an
increased risk of moderate or severe bleeding in 4.2%
versus 2.5% (placebo) and a 66% increased risk of
bleeding overall. Currently, this agent is associated with a
black box warning identifying a high risk of bleeding and
contraindication in patients with a history of stroke,
transient ischemic attack, or intracranial hemorrhage.
Vorapaxar displays significant inhibition of platelet
aggregation that remains up to 4 weeks after
discontinuation.51
The actual impact of this drug on the
GI tract is relatively unknown, and postmarketing data
are needed to identify these risks.
ANTICOAGULANT AGENTS
Warfarin
Warfarin (Coumadin, Bristol-Myers Squibb Company,
Princeton, NJ, USA) is an oral anticoagulant that inhibits
the vitamin K–dependent clotting factors II, VII, IX, and
X and proteins C and S. Its activity is measured via the In-
ternational Normalized Ratio (INR). The INR decreases
to 1.5 in approximately 93% of patients within 5 days of
discontinuing therapy.52
Novel oral anticoagulants
The novel oral anticoagulants (NOACs) include the
direct thrombin inhibitor dabigatran and the direct factor
Xa inhibitors (eg, rivaroxaban [Xarelto], apixaban [Eliquis],
edoxaban [Savaysa]) (Table 2). Dabigatran (Pradaxa) was
the first NOAC approved in the United States for
prevention of CVA and systemic embolism in patients
with nonvalvular AF. It is metabolized and excreted
primarily by the kidneys, reaching maximum effect 1.25
to 3 hours after ingestion, with a half-life of 12 to 14 hours.
Assessment of the degree of anticoagulation is best
achieved by assessment of the Ecarin Clotting Time or
the dilute thrombin time, neither of which is readily avail-
able in the acute clinical setting. Partial thromboplastin
time and prothrombin time vary in their sensitivities to da-
bigatran depending on the reagents used and can be
normal in spite of circulating therapeutic levels of dabiga-
tran. However, a normal activated partial thromboplastin
time effectively rules out a clinically significant circulating
drug level. Timing of discontinuation before an endoscopic
procedure is dictated by the patient’s creatinine clearance
because 80% of excretion occurs via the kidneys
(Table 6).53
Rivaroxaban (Xarelto) is approved in the United States
for prevention of VTE after orthopedic surgery, treat-
ment of VTE, and prevention of CVA and systemic embo-
lism in patients with AF. Apixaban (Eliquis) is FDA

approved for prevention of systemic embolism in AF pa-
tients, postorthopedic surgery prevention of VTE, and
for treatment and reduction of recurrence of VTE. Edox-
aban (Savaysa) is FDA approved for AF and VTE treat-
ment indications. The effect of the anti-Xa
anticoagulants is best assessed by measuring anti-Xa
levels with drug-specific calibrators. Prothrombin time
and activated partial thromboplastin time are crude mea-
sures of drug effect and are insensitive tests, often only
minimally prolonged or even normal in spite of thera-
peutic drug levels. However, normal test results rule
out high circulating drug levels. There is no reliable
serum assay to assess the degree of anticoagulant activ-
ity with these agents at this time. Caution should be
used in interpretation of the activated partial thrombo-
plastin time in situations of drug toxicity because the
assay is subject to a ceiling effect and does not reliably
capture the severity of the anticoagulant effect.53
In the periendoscopic period there are 3 important phar-
macodynamic considerations when holding and restarting
an anticoagulant: (1) time to maximum effect, (2) half-life,
and (3) excretion of the drug. Rivaroxaban (Xarelto), apixa-
ban (Eliquis), and edoxaban (Savaysa) all have a relatively
short time to maximal effect (eg, 2-4 hours with rivaroxaban
[Xarelto], 1-3 hours with apixaban [Eliquis]), a half-life
ranging from 8 to 15 hours, and variable excretion by the kid-
neys (rivaroxaban [Xarelto] 66% and apixaban [Eliquis]
25%). To minimize the risk of bleeding, these medications
should be stopped for at least 2 half-lives before high-risk
procedures, and their dosing should be adjusted in the
setting of renal impairment (Tables 7-9).54
An antidote for dabigatran (Pradaxa) has been approved
following accelerated review by the FDA.55
This antidote is
idarucizumab (Praxbind, Boehringer Ingelheim, Inc,
Ridgefield, CT, USA) and is approved for use in cases of life-
threatening, uncontrolled bleeding or prior to emergency
surgery. Another reversal agent that is currently under
evaluation is Aripazine (PER977, Perosphere, Inc, Danbury,
CT, USA), which binds to UFH and LMWH; factor Xa
inhibitors; edoxaban (Savaysa); rivaroxaban (Xarelto) and
apixaban (Eliquis); and dabigatran (Pradaxa).56
Animal
studies and pharmacodynamics studies with Aripazine have
demonstrated reversal of edoxaban (Savaysa) to 10% of
baseline values within 10 minutes of drug delivery. Finally,
Andexanet alfa has been studied in a phase II trial and
shows promise as yet another reversal agent, by decreasing
anti-Xa activity and reducing plasma concentrations of free
apixaban (Eliquis) in healthy volunteers.57
Future studies
are needed to demonstrate efficacy in humans and in the
setting of major hemorrhage.
Parenteral and subcutaneously administered
anticoagulants
UFH administered intravenously has a half-life of 60 to
90 minutes, and anticoagulant effects dissipate 3 to 4 hours
after discontinuation. LMWH (enoxaparin [Lovenox, Sanofi-
Aventis U.S., LLC, Bridgewater, NJ, USA] and dalteparin
[Fragmin, Pfizer Inc, New York, NY, USA]) is administered
subcutaneously at therapeutic doses for bridging and for
the treatment of VTE. It is also prescribed at reduced doses
for the prevention of VTE in low-risk patients. The last dose
of these agents should be given 24 hours before the antic-
ipated procedure at 50% of the total daily dose.37
Fondaparinux (Arixtra) is a synthetic and specific inhib-
itor of factor Xa. It is approved in the United States for
TABLE 6. Periprocedural management of dabigatran (Pradaxa)53
Creatinine
clearance (mL/min)
Time to onset
of action (h) Half-life (h)
Timing of discontinuation before procedure
Moderate procedural
bleeding risk (2-3 half-lives)
High procedural bleeding
risk (4-5 half-lives)
80 1.25-3 13 (11-22) 1-1.5 days 2-3 days
50-80 1.25-3 15 (12-34) 1-2 days 2-3 days
30-49 1.25-3 18 (13-23) 1.5-2 days 3-4 days
29 1.25-3 27 (22-35) 2-3 days 4-6 days
TABLE 7. Periprocedural management of apixaban (Eliquis)54
Creatinine
clearance
(mL/min)
Time to onset of
action (h)
Timing of discontinuation before
high-risk endoscopic procedure
(day)
60 1-3 1 or 2
30-59 1-3 3
15-29 1-3 4
TABLE 8. Periprocedural management of rivaroxaban (Xarelto)54
Creatinine
clearance
(mL/min)
Time to onset
of action (h)
Timing of discontinuation
before high-risk
endoscopic
procedure (day)
90 2-4 !1
60-90 2-4 2
30-59 2-4 3
15-29 2-4 4

perioperative DVT prophylaxis and for the initial treatment
of acute DVT/pulmonary embolism. It is administered sub-
cutaneously and is distinct from LMWH. Fondaparinux
(Arixtra) has a high affinity for antithrombin III, which po-
tentiates inhibition of factor Xa. The minimum recommen-
ded time for discontinuation of this drug before a high-risk
procedure is 36 hours.58
Desirudin (Iprivask, Aventis Pharmaceuticals Inc.,
Bridgewater, NJ, USA) is a direct thrombin inhibitor
approved for DVT prophylaxis after hip replacement and
is administered subcutaneously. Recommendations are to
discontinue this medication 10 hours before a high-risk
procedure.59
COMMON ELECTIVE ENDOSCOPIC PROCEDURES
IN PATIENTS ON ANTITHROMBOTIC THERAPY
Because of the paucity of high-quality evidence
regarding bleeding risks associated with antithrombotic
therapies prescribed in dual (ASA þ thienopyridine;
ASA þ anticoagulant) and triple combinations (ASA þ
thienopyridine þ anticoagulant), a “one-size-fits-all
approach” to recommendations regarding the periproce-
dural management of antithrombotic agents undergoing
endoscopy is not possible at this time. A summary of the
available evidence is presented below (Table 10), with
the awareness that additional research is required and
will likely influence future recommendations regarding
periendoscopic management of third-generation thieno-
pyridines, PAR-1 inhibitors, and NOAC prescribed in com-
bination with ASA.60
With regard to polypectomy, there are modest data to
support the use of cold snare rather than conventional
polypectomy in those patients anticoagulated with
warfarin (Coumadin). In a small study of warfarin (Cou-
madin), 70 patients with 159 polyps up to 10 mm were
randomized to cold polypectomy versus conventional
snare. Delayed bleeding requiring hemostasis occurred
less commonly after cold snare polypectomy than conven-
tional polypectomy despite continuation of anticoagulants
(0% vs 14%, P Z .027).61
Further data in the area of
optimal endoscopic technique for patients prescribed
antithrombotic agents are necessary to better inform
endoscopic decisions and clinical best practice.
RISK OF STOPPING ANTITHROMBOTIC
THERAPY BEFORE ELECTIVE ENDOSCOPY
When antithrombotic therapy is required for a short
period of time (ie, after VTE or bare metal stent insertion),
elective procedures should be delayed until such therapy is
no longer indicated. In patients who need antithrombotic
therapy for a longer period of time (ie, after drug-eluting
stent placement or post-ACS), careful consideration of
the cardioembolic risk must be made before temporary
drug cessation to avoid spontaneous stent occlusion,
ACS, and death.62-64
Decisions about discontinuing or tem-
porary cessation of these agents should be individualized
and discussed, before the endoscopic procedure, with
the patient and, optimally, the prescribing provider (cardi-
ologist, neurologist, hematologist, primary care physician).
It is important to recognize that in some high-risk patients,
antithrombotic agents may not be able to be stopped.
Cessation of anticoagulant
Current guidelines from the American College of Chest
Physicians (ACCP) regarding the management of anticoa-
gulation in patients with AF and/or valvular heart disease
undergoing elective invasive procedures are summarized
in Table 6.42
The absolute risk of an embolic event in
patients whose anticoagulation is interrupted for 4 to 7
days is approximately 1%.65,66
After temporary discontinu-
ation of warfarin (Coumadin), reinitiation of drug should
occur within 4 to 7 days of initial drug discontinuation to
ensure no increased risk of thromboembolic event and
can occur on the same day in many patients.67
Role of bridge therapy
To reduce the risk of thromboembolic events, patients
on warfarin (Coumadin) may be switched to a shorter-
acting (ie, bridge [Table 11]) anticoagulant in the
periendoscopic period. Evidence for the use of UFH and
LMWH (enoxaparin) as bridge therapies for endoscopic
procedures in patients on warfarin (Coumadin) is limited.
One study of 98 patients undergoing endoscopy (EGD
and/or colonoscopy) with bridge therapy using
bemiparin, an ultra-LMWH, found no thromboembolic
events and only 2 major bleeding episodes that were unre-
lated to endoscopy.68
Current guidelines (2011 American
College of Cardiology Foundation/American Heart
Association [AHA]/Heart Rhythm Society guideline on AF
and the 2014 AHA/American College of Cardiology [ACC]
guideline on valvular heart disease) regarding the
management of anticoagulation in patients with AF and/
or valvular heart disease undergoing elective invasive
procedures are summarized in Table 10.69,70
A meta-anal-
ysis71
showed that vitamin K antagonist–treated patients
receiving periprocedural bridging therapy with heparin
appear to be at increased risk of both overall and major
TABLE 9. Periprocedural management of edoxaban (Savaysa)99
Creatinine
clearance
(mL/min)
Time to
onset
of action (h)
Half-life
(h)
Timing of discontinuation
before high-risk procedure
(h)
60 1-2 8.6 At least 24
30-60 1-2 9.4 At least 24
15-30 1-2 16.9 At least 24
15 1-2 No data No data

bleeding and at similar risk of thromboembolic events
compared with nonbridged patients.
A recently published randomized controlled trial72
sought to better define the role of periprocedural heparin
bridging in 1884 patients with nonvalvular AF undergoing
an elective invasive procedure. Patients were randomized
to bridging versus no-bridging, and results demonstrated
the heparin-bridged group experienced more major
bleeding (3.2% vs 1.3%) than the nonbridged group, with
no difference in arterial thromboembolism (.3% vs .4%).
Of note, these data should not be applied to those patients
with higher risk for thromboembolism, such as patients
with valvular AF, mechanical valves, left ventricular assist de-
vices, recently diagnosed thromboembolism, AF with
congestive heart failure, or in the post-ACS setting.72
Cessation of APA (including DAPT)
The most common antithrombotic strategy prescribed
in the United States with regard to patients on DAPT is
to hold the thienopyridine in the periendoscopic period
and continue the aspirin. Eisenberg et al73
performed a
systematic review of 161 reported cases of late stent
thrombosis (30 days but 1 year after stent placement)
and very late stent thrombosis (1 year after stent
placement). Patients who discontinued both ASA and a
thienopyridine had a median time to event of 7 days. In
those who discontinued thienopyridine but remained on
ASA, the median time to an event was 122 days. There
were a total of 6 cases (6%) of stent thrombosis within
10 days of thienopyridine cessation, suggesting short-
term discontinuation between 30 days and 1 year from
drug-eluting coronary stent placement (late stent throm-
bosis) might be relatively safe but still carry some risk.
Best practice recommendations for the management of
DAPT (ie, ASA þ thienopyridine APA) are summarized in
the American College of Cardiology Foundation and Amer-
ican College of Gastroenterology consensus statement
(Table 12).36
REINITIATION OF ANTITHROMBOTIC AGENTS
AFTER ELECTIVE ENDOSCOPY
There is consensus that antithrombotic therapy should
be resumed upon completion of the procedure.36,74
The benefits of immediate reinitiation of antithrombotic
therapy for the prevention of thromboembolic events
should be weighed against the risk of hemorrhage associ-
ated with the specific agent, the time to onset of the medi-
cation, and on procedure-specific circumstances (eg, risk
of bleeding after sphincterotomy, polypectomy, or EMR).
Most existing literature on this topic addresses reinitiation
of warfarin or heparin and heparin-like products. Less is
known regarding timing to reinitiation of APAs and NOACs.
In 1 study involving 94 patients who had undergone 109
colonoscopies (including hot biopsy or snare polypectomy
in 47%), patients were instructed to restart warfarin (Cou-
madin) therapy on the day after endoscopy.75
Only 1 case
(0.9%) of procedure-related bleeding occurred after 7 days
of warfarin (Coumadin) therapy and required hospitaliza-
tion and transfusion. None of the patients undergoing diag-
nostic colonoscopy experienced bleeding. Conversely, a
second study involving 173 patients found that resuming
warfarin (Coumadin) or heparin within 1 week after poly-
pectomy was associated with an increased risk of bleeding
(OR 5.2; 95% CI, 2.2-12.5).76
Because of the ongoing risk of
thromboembolic events, the 2014 AHA/ACC guideline (on
the management of valvular heart disease) recommends
that warfarin (Coumadin) be restarted within 24 hours of
the procedure in patients with valvular heart disease and
a low-risk for thromboembolism. In patients at high risk
TABLE 10. Summary for available evidence for bleeding risk with common endoscopic procedures on antithrombotic agents
Therapeutic warfarin/heparin Thienopyridine ASA/NSAID
Diagnostic EGD/colonoscopy þ/- biopsy Low risk100
Low112
Low104
Colonoscopic polypectomy High risk75,101-109
High113
Low75,98,115
Sphincterotomy High110
Unknown Low17
EUS/FNA High111
Unknown Low111
PEG (does not apply to DAPT) Unknown Low for clopidogrel only114
Low114
ASA, acetylsalicylic acid, or aspirin; NSAID, nonsteroidal anti-inflammatory drug; DAPT, dual antiplatelet therapy.
TABLE 11. Approach to bridge therapy for warfarin (Coumadin)69-70
Condition Associated diagnosis Management
AF None
CHA2DS2-VASc score 2
No bridge
recommended
Mechanical valves
History of CVA
CHA2DS2-VASc score ! 2
Bridge therapy
recommended
Valvular heart
disease
Bileaflet mechanical AVR No bridge
recommended
Mechanical AVR and any
thromboembolic risk factor
Older-generation mechanical AVR
Mechanical mitral valve
replacement
Bridge therapy
recommended
AF, atrial fibrillation; CHA2DS2-VASc, Congestive heart failure, Hypertension, Age 75
years [2 points], Diabetes Mellitus, Stroke [2 points], Vascular disease, Age 65-74
years, Sex category [ie, female sex]; CVA, cerebrovascular accident; AVR, aortic valve
replacement.

for thromboembolism, UFH or LMWH should be restarted
as soon as “bleeding stability allows” and continued until
the INR reaches an appropriate therapeutic level.70
UFH
may be restarted 2 to 6 hours after a therapeutic
procedure. The optimal time to restart LMWH after
endoscopy has not been determined. The 2012 ACCP
guidelines recommend delaying reinitiation of LMWH 48
to 72 hours after surgery in patients believed to be at
high risk for bleeding adverse events.37
There are no data to inform optimal timing of resump-
tion of NOACs after endoscopic procedures. Because these
agents have a short onset of action (Tables 7-10), if a NOAC
cannot be restarted within 24 hours after a high-risk proce-
dure because of concern regarding the adequate hemosta-
sis, then thromboprophylaxis (ie, UFH bridge)
should be considered for patients at high risk for
thromboembolism.53,54
Cardiac ASA should not be discontinued in most cases.
Other APAs should be resumed once hemostasis has been
achieved (Table 12).
ENDOSCOPIC PROCEDURES IN THE ACUTELY
BLEEDING PATIENT ON ANTITHROMBOTIC
THERAPY
Endoscopic evaluation and therapy in patients using an-
tithrombotics with active GI bleeding is both warranted
and safe.7
The most common etiologies for upper GI
blood loss in these patients are peptic ulcer disease and
erosive diseases of the esophagus, stomach, and
duodenum.77
Diverticular bleeding is the most common
cause of lower GI bleeding.78,79
Anticoagulants
In 1 retrospective series of 52 patients, correction of the
INR to between 1.5 and 2.5 allowed successful endoscopic
diagnosis and therapy at rates comparable with those
achieved in non-anticoagulated patients.80
In a large
series in which 95% of patients had an INR between 1.3
and 2.7, endoscopic therapy achieved initial success in
95% of patients (233/246) using a variety of hemostatic
techniques, including injection therapy, heater probe,
and hemoclips.81
Although the rebleeding rate in this
series was 23%, the INR level before endoscopy was not
a predictor of rebleeding. In another retrospective study,
rates of rebleeding in patients with supratherapeutic INRs
(!4.0) were not signiﬁcantly different from those with
INRs in the therapeutic range (2.0-3.9).79
Finally, in a
systematic review of 1869 patients with nonvariceal
upper GI bleeding, INR at initial presentation was found
not to predict the risk of rebleeding.82
These data
suggest that endoscopic hemostatic therapy is very
effective even in patients with moderately elevated INR,
normalizing the INR does not reduce rebleeding but
does delay time to endoscopy, and INR at the time of
endoscopy may not be predictive of rebleeding. Pending
further data, performing endoscopic therapy in bleeding
patients with INRs 2.5 is reasonable.
The decision to stop, reduce, and/or reverse antithrom-
botic therapy (and thereby risking thromboembolic conse-
quences) must be weighed against the risk of continued
bleeding. The risk of thromboembolic events was shown
to be low in 2 small studies that withheld warfarin (Couma-
din) for 4 to 15 days before endoscopy (1/27 patients and
0/28 patients, respectively).83,84
The ACCP recommends
that warfarin (Coumadin) be held and rapid reversal of an-
ticoagulation with 4-factor prothrombin complex (PCC) be
used for patients with vitamin K antagonist-associated ma-
jor bleeding rather than fresh frozen plasma. They also sug-
gest the additional use of vitamin K be given (5-10 mg by
slow IV) rather than reversal with coagulation factors
alone.85
PCC contains the vitamin K–dependent factors
II, VII, IX, and X either in nonactivated form
(nonactivated PCCs) or partially activated form (activated
PCCs; individual drug: Feiba). Some of the nonactivated
PCCs contain relatively little factor VII, and these PCCs
are referred to as 3-factor PCCs (Bebulin, Baxter Healthcare
Corporation, Westlake Village, Calif, USA; Proﬁlnine, Gri-
fols Biologicals Inc, Los Angeles, Calif, USA). In 2012 the
FDA approved a 4-factor PCC (Kcentra, CSL Behring LLC,
Kankakee, Ill, USA) for vitamin K antagonist reversal in pa-
tients with acute major bleeding or need for an urgent sur-
gery/invasive procedure. For warfarin (Coumadin) reversal,
the 4-factor PCC is the appropriate reversal agent. Howev-
er, a combination of 3-factor PCC and low dose of recom-
binant factor VIIa can also be used when the 4-factor agent
is unavailable.86
The 2014 AHA/ACC guideline on the
management of valvular heart disease recommends that
fresh frozen plasma (which is not recommended in the
ACCP 2012 guideline on the management of
anticoagulant therapy, mentioned earlier in this
paragraph) or PCC is reasonable in patients with
TABLE 12. Best practice recommendations for the management of
DAPT36
Avoid cessation of all antiplatelet therapies after PCI with stent
placement.
Avoid cessation of clopidogrel (even when aspirin is continued) within
the first 30 days after PCI and either DES or BMS placement when
possible.
Defer elective endoscopic procedures, possibly up to 12 months, if
clinically acceptable from the time of PCI to DES placement.
Perform endoscopic procedures, particularly those associated with
bleeding risk, 5-7 days after thienopyridine drug cessation. ASA
should be continued.
Resume thienopyridine and ASA drug therapy after the procedure
once hemostasis is achieved. A loading dose of the former should be
considered among patients at risk for thrombosis.
Continue platelet-directed therapy in patients undergoing elective
endoscopy procedures associated with a low-risk for bleeding.
DAPT, dual antiplatelet therapy; BMS, Bare metal stent(s); DES, drug-eluting stent(s);
PCI, percutaneous coronary intervention; ASA, acetylsalicylic acid, or aspirin.

mechanical valves and uncontrollable bleeding who
require reversal of anticoagulation. High-dose vitamin K
should not be given routinely because this may create a hy-
percoagulable condition.70
In the event of massive hemorrhage, hemodialysis can
be used in patients receiving dabigatran (Pradaxa) but
not for rivaroxaban (Xarelto), edoxaban (Savaysa), and
apixaban (Eliquis) because of their decreased renal excre-
tion and because they are highly protein bound. Although
factor VIIa and 4-factor PCC have been used in these situ-
ations, their value in reversing the clinical anticoagulant ef-
fects, and controlling clinical hemorrhage is uncertain.87
Antiplatelet agents
For patients on APAs with life-threatening or serious
bleeding, options include stopping these agents and/or
administration of platelets. Most patients will require
resumption of antithrombotic therapy after endoscopic con-
trol of GI bleeding. There are very limited data to guide the
timing of reinitiation of antiplatelet therapy; however, cur-
rent multidisciplinary cardiac and GI society consensus
statements recommend reinitiation of antiplatelet therapy
as soon as hemostasis is achieved.36,74
For patients who
develop ASA-related peptic ulcer disease bleeding, resump-
tion of ASA with concurrent proton pump inhibitor therapy
is superior to switching to clopidogrel alone for the preven-
tion of recurrent GI bleeding.88,89
The importance of prompt
resumption of cardiac aspirin is critical as demonstrated by a
randomized control trial by Sung et al90
that showed no
increased risk of postprocedural bleeding associated with
continued ASA use but a clear increase in 30-day mortality
in cardiac patients in whom ASA was not resumed.
ENDOSCOPY IN THE PATIENT WITH
INTRACORONARY STENTS OR ACS TAKING
ANTITHROMBOTIC DRUGS
Elective endoscopy in the patient with an
intracoronary stent
Use of DAPT may confer a 3-fold increase in the risk of
upper GI bleeding over single-agent antithrombotic ther-
apy.2,3,91
Given the current evidence, all elective high-risk
endoscopic procedures in patients on DAPT should be de-
layed until the patient has received the minimum length of
therapy as recommended by American College of Cardiol-
ogy Foundation/ACG guidelines.36
Once this period has
elapsed, the decision to proceed with such procedures
should be made after discussion of the associated risks
and benefits with the patient and relevant medical
professionals.
Urgent endoscopy in the patient with ACS or
recently placed vascular stent
Antithrombotic agents are commonly used in the man-
agement of ACS in patients with recently placed intracoro-
nary stents. Many of these patients receive several agents
simultaneously, including the potent platelet GPIIb/IIIa re-
ceptor antagonists. It is estimated that 1% to 3% of patients
with an ACS will present with or develop GI bleeding dur-
ing their index hospitalization.92-95
Patients who develop
GI bleeding in the setting of ACS have an almost 4- to 7-
fold increased risk of in-hospital mortality over patients
with ACS and no GI bleeding.93,94
In this context, clinicians
are faced with the dilemma with proceeding with endo-
scopic evaluation in a patient at an increased risk of proce-
dural complications. Despite the clinical significance of GI
bleeding during ACS, there are sparse data on outcomes of
patients with GI bleeding in the setting of ACS. In 1 retro-
spective case-control study, 200 patients underwent endos-
copy within 30 days (mean, 9.1 Æ 8.9) of an acute MI.94
Serious adverse events (fatal ventricular tachycardia and
near respiratory arrest) occurred in 2 patients (1%). In
another study, ACS patients with an upper GI bleed were
associated with markedly increased mortality.96
Patients may develop an acute MI after a GI bleed,
and these patients are likely to benefit from endoscopic
evaluation. A retrospective study showed that patients
who presented with upper GI bleeding leading to acute
MI were more likely to require endoscopic therapy
than patients who developed GI bleeding after being
treated for acute MI (OR 3.9; 95% CI, 1.8-8.5).95
Other
factors associated with the need for endoscopic therapy
included hemodynamic instability and hematemesis
on presentation. The benefit of endoscopy in the
patient with significant GI bleeding in the setting of
acute MI is supported by a decision analysis that
showed upper endoscopy before cardiac catheterization
to be beneficial in patients who presented with overt
GI bleeding in the setting of ACS, reducing overall
deaths from 600 to 97 per 10,000 patients. However,
endoscopy was not found to be beneficial in patients
who presented with occult GI bleeding and acute MI.97
Our understanding of the safety of endoscopy in
patients with ACS and/or recently placed intracoronary
stents on antithrombotic medications, including
DAPT and GPIIb/IIIa inhibitors, is rapidly evolving and
is likely to change as knowledge and experience are
accumulated.
RECOMMENDATIONS (SUMMARIZED
IN TABLE 13)
A. Elective endoscopic procedures
Patients receiving anticoagulant therapy
1. We recommend that elective endoscopic procedures be
deferred until short-term anticoagulation therapy (eg,
warfarin for VTE) is completed. 444B
2. We suggest discontinuing anticoagulation (ie, warfarin
[Coumadin], NOACs) for the appropriate drug-specific
interval in the periendoscopic period if high-risk

endoscopic procedures are planned in a patient at low
risk for thromboembolic events. 44BB
3. We suggest continuing warfarin and NOAC in the peri-
endoscopic period in patients undergoing low-risk
endoscopic procedures. 44BB
4. We suggest bridge therapy for patients undergoing
high-risk endoscopic procedures who are at high risk
for thromboembolic events. 44BB
5. We suggest that warfarin (Coumadin) be restarted on
the same day as the procedure in all patients who do
not have ongoing bleeding. 44BB
6. We suggest that the reinitiation of NOACs after high-risk
endoscopic procedures be delayed until adequate he-
mostasis is ensured, given their rapid onset of action
and lack of reversal agents. If therapeutic doses of
NOACs cannot be restarted within 12 to 24 hours after
a high-risk endoscopic procedure, thromboprophylaxis
(ie, UFH bridge) should be considered to decrease
risk of thromboembolism, given the short half-life of
the NOAC agent, in those with a high risk for thrombo-
embolism. 44BB
Patients receiving APA therapy
1. We suggest that continuation of low doses of ASA and
nonsteroidal anti-inﬂammatory drugs may be continued
safely in the periendoscopic period. 444B
2. We recommend that thienopyridines be continued for
all low-risk endoscopic procedures. 444B
3. We recommend discontinuation of thienopyridines at
least 5 to 7 days before high-risk endoscopic procedure
or switching to ASA monotherapy and continuing until
the thienopyridine can be safely resumed. 444B
4. We recommend that elective endoscopic procedures be
deferred in patients with recently placed intracoronary
stents and/or ACS until the patient has received
antithrombotic therapy for the minimum recommended
duration. 444B
5. We suggest that thienopyridines be withheld for at least
5 to 7 days (ticagrelor 3-5 days) before high-risk endo-
scopic procedures and that ASA be continued for pa-
tients requiring dual APA. 444B
B. Urgent and emergent endoscopic
procedures
Patients receiving anticoagulant therapy
1. We recommend patients with acute GI bleeding on anti-
coagulation therapy have anticoagulant agents held to
facilitate achievement of hemostasis. 444B
2. We recommend either (1) 4-factor PCC and vitamin K or
(2) fresh frozen plasma be given for life-threatening GI
bleeding in patients on warfarin anticoagulant therapy.
Please note the ACCP only advocates option 1. The
AHA/ACC supports option 1 or 2. 444B
3. We suggest endoscopic therapy not be delayed in pa-
tients with serious GI bleeding and an INR 2.5.
44BB
4. We suggest patients who require anticoagulation receive
UFH because of its relatively short half-life after success-
ful endoscopic hemostasis for high-risk stigmata.
44BB
Patients receiving APA therapy
1. We recommend consultation with the prescribing
specialist (or their colleague) before stopping APAs in
situations of signiﬁcant GI bleeding in patients (1)
with recently (1 year) placed drug eluting intracoro-
nary stents, (2) within 30 days after insertion of a bare
metal intracoronary stent, or (3) within 90 days of
ACS. The risk of an adverse cardiac event associated
TABLE 13. Management of antithrombotic agents in the elective endoscopic setting
Endoscopy-induced bleeding risk
Low High
CV risk
Low AC 1. Continue warfarin and NOAC AC 1. Discontinue AC
2. Restart warfarin on same day of procedure
3. Delay reinitiating NOACs until adequate hemostasis is achieved
APA 1. Continue standard doses of ASA/NSAIDs
2. Continue thienopyridines
APA 1. Continue standard doses of ASA/NSAIDs*
2. Discontinue thienopyridines at least 5 days before switch to ASAy
3. Dual APA, hold thienopyridines for at least 5 days, continue ASAy
High AC 1. Continue warfarin and NOAC AC 1. Discontinue AC
2. Bridge therapyz
3. Restart warfarin on same day of procedure
4. Delay reinitiating NOACs until adequate hemostasis is achieved
2. Continue thienopyridines
2. Discontinue thienopyridines at least 5 days before
endoscopy or switch to ASAy
3. Dual APA, hold thienopyridines for at least 5 days, continue ASAy
AC, Anticoagulants; APA, antiplatelet agent; NOAC, novel oral anticoagulant; ASA, acetylsalicylic acid, or aspirin; NSAID, nonsteroidal anti-inflammatory drug; CV, cardiovascular.
*There is evidence to hold APA in patients undergoing ESD and EMR who have a low risk for a thromboembolic event.116
yTicagrelor should be held for 3-5 days, and all other thienopyridines should be held for 5-7 days.
zIn moderate-risk patients (from Table 5), the decision to use bridging therapy and the degree of intensity should be individualized and the patient’s wishes considered.40

with cessation of the APA therapy likely exceeds the
benefit of decreasing postendoscopic bleeding.444B
2. We recommend patients on APAs with life-threatening
or serious GI bleeding should have these agents held af-
ter discussion with their cardiologist. 444B
DISCLOSURE
The following authors disclosed financial relationships
relevant to this publication: K. V. Chathadi is a consultant
for Boston Scientific. J. H. Hwang is a speaker for Novar-
tis, a consultant for US Endoscopy, and has received a
research grant from Olympus. M. A. Khashab is a consul-
tant for Boston Scientific and Olympus America, and has
received a research grant from Cook Medical. All other
authors disclosed no financial relationships relevant to
this publication.
Abbreviations: ACS, acute coronary syndrome; AF, atrial fibrillation;
APA, antiplatelet agent; ASA, acetylsalicylic acid, or aspirin; CVA,
cerebrovascular accident; DAPT, dual antiplatelet therapy; DVT, deep
vein thrombosis; FDA, U.S. Food and Drug Administration; GP,
glycoprotein; INR, International Normalized Ratio; LMWH, low-
molecular-weight heparin; MI, myocardial infarction; NOAC, novel
oral anticoagulant; PAR-1, protease-activated receptor-1; PCC,
prothrombin complex concentrate; UFH, unfractionated heparin; VTE,
venous thromboembolism.
REFERENCES
1. Guyatt G, Oxman AD, Akl EA, et al. GRADE guidelines: introduction-
GRADE evidence profiles and summary of findings tables. J Clin Epi-
demiol 2011;64:383-94.
2. Abraham NS, Hartman C, Richardson P, et al. Risk of lower and upper
gastrointestinal bleeding, transfusions, and hospitalizations with
complex antithrombotic therapy in elderly patients. Circulation
2013;128:1869-77.
3. Holster IL, Valkhoff VE, Kuipers EJ, et al. New oral antigcoagulants in-
crease risk for gastrointestinal bleeding: a systematic review and
meta-analysis. Gastroenterology 2013;145(1):105-12.e15.
4. Jneid H, Anderson JL, Wright RS, et al. 2012 ACCF/AHA Focused up-
date of the guideline for the management of patients with unstable
angina/non-ST-elevation myocardial infarction (updating the 2007
guideline and replacing the 2011 focused update). JACC 2012;60:
645-81.
5. Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in
patients with acute coronary syndromes. N Engl J Med 2009;361:
1045-57.
6. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidog-
rel in patients with acute coronary syndromes. N Engl J Med
2007;357:2001-15.
7. Abraham NS, Castillo DL. Novel anticoagulants: bleeding risk and
management strategies. Curr Opin Gastroneterol 2013;29:676-83.
8. ASGE Standards of Practice committee; Anderson MA, Ben-Menac-
hem T, Gan SI, et al. Management of antithrombotic agents for endo-
scopic procedures. Gastrointest Endosc 2009;70:1060-70.
9. Perreira-Lima JC, Ramires RP, Zamin I, et al. Endoscopic dilation of
benign esophageal strictures: report on 1043 procedures. Am J Gas-
troenterol 1999;94:1497-501.
10. Raymond R, Perreira-Lima JC, Valves A, et al. Endoscopic dilation of
benign esophageal strictures without fluoroscopy: experience of
2750 procedures. Hepatogastroenterology 2008;55:1342-8.
11. Polese L, Angriman I, Bonello E, et al. Endoscopic dilation of benign
esophageal strictures in a surgical unit: a report on 95 cases. Surg
Laparosc Endosc Percutan Tech 2007;17:477-81.
12. ASGE Standards of Practice committee; Eisen GM, Baron TH, Dominitz
JA, et al. Guideline on the management of anticoagulation and anti-
platelet therapy for endoscopic procedures. Gastrointest Endosc
2002;55:775-9.
13. Rubin PH, Waye JD. Colonoscopic polypectomy: a critical review of
recent literature. Curr Gastroenterol Rep 2006;8:430-3.
14. Vatansever S, Akpinar Z, Alper E, et al. Gastric polyps and polypoid
lesions: Retrospective analysis of 36650 endoscopic procedures in
29940 patients. Turk J Gastroenterol 2015;26:117-22.
15. Mensink PB, Haringsma J, Kuchrzik T, et al. Complications of double
balloon enteroscopy: a multicenter survey. Endoscopy 2007;39:613-5.
16. May A, Nachbar L, Pohl J, et al. Endoscopic interventions in the small
bowel using double balloon enteroscopy: feasibility and limitations.
Am J Gastroenterol 2007;102:527-35.
17. Cotton PB, Garrow DA, Gallagher J, et al. Risk factors for complications
after ERCP: a multivariate analysis of 11,497 procedures over 12 years.
Gastrointest Endosc 2009;70:80-8.
18. Horiuchi A, Nakayama Y, Tanaka N, et al. Prospective randomized trial
comparing the direct method using a 24 Fr bumper-button-type de-
vice with the pull method for percutaneous endoscopic gastrostomy.
Endoscopy 2008;40:722-6.
19. Rahnemai-Azar AA, Rahnemaiazar AA, Naghshizadian R, et al. Percu-
taneous endoscopic gastrostomy: indications, technique and man-
agement. World J Gastroenterol 2014;20:7739-51.
20. Lee SP, Lee KN, Lee OY, et al. Risk factors for complications of percu-
taneous endoscopic gastrostomy. Dig Dis Sci 2014;59:117-25.
21. Zopf Y, Rabe C, Bruckmoser T, et al. Percutaneous endoscopic jeju-
nostomy and jejunal extension tube through percutaneous endo-
scopic gastrostomy: a retrospective analysis of success,
complications and outcome. Digestion 2009;79:92-7.
22. Kozarek RA. Endoscopic palliation of esophageal malignancy. Endos-
copy 2003;35:S9-13.
23. Cao Y, Liao C, Tan A, et al. Meta-analysis of endoscopic submucosal
dissection versus endoscopic mucosal resection for tumors of the
gastrointestinal tract. Endoscopy 2009;41:751-7.
24. Heresbach D, Kornhauser R, Seyrig JA, et al. A national survey of
endoscopic mucosal resection for superficial gastrointestinal
neoplasia. Endoscopy 2010;42:806-13.
25. Lynch KL, Pandolfino JE, Howden CW, et al. Major complications of
pneumatic dilation and Heller myotomy for achalasia: single center
experience and systematic review of the literature. Am J Gastroenter-
ol 2012;107:1817-25.
26. Pai G, Cipolleta, Claar M, et al. Prophylactic sclerotherapy of high risk
esophageal varices: results of a multicentric prospective controlled
trial. Hepatology 1988;8:1495-500.
27. Cai MY, Zhou PH, Yao LQ, et al. Peroral endoscopic myotomy for idio-
pathic achalasia: randomized comparison of water-jet assisted versus
conventional dissection technique. Surg Endosc 2014;28:1158-65.
28. Fabbri C, Luigiano C, Maimone A, et al. Endoscopic ultrasound-guided
drainage of pancreatic fluid collections. World J Gastrointest Endosc
2012;4:479-88.
29. Katzka DA, Baron TH. Transoral flexible endoscopic therapy of Zen-
ker’s diverticulum: is it time for gastroenterologists to stick their
necks out? Gastrointest Endosc 2013;77:708-10.
30. Kozarek RA, Ball TJ, Branbaur JJ, et al. Expandable versus conventional
esophageal prostheses: easier insertion may not preclude subse-
quent stent-related problems. Gastrointest Endosc 1996;43:204-8.
31. Dormann A, Meisner S, Verin N, et al. Self-expanding stents for gastro-
duodenal malignancies: systematic review of clinical effectiveness.
Endoscopy 2004;36:543-50.
32. Telford JJ, Carr-Locke DL, Baron TH, et al. Palliation of patients with
malignant gastric outlet obstruction with the enteral Wallstent: out-
comes from a multicenter study. Gastrointest Endosc 2004;60:
916-20.

33. Lip GY, Nieuwlaat R, Pisters R, et al. Refining clinical risk stratification
for predicting stroke and thromboembolism in atrial fibrillation using
a novel risk factor-based approach: the Euro Heart Survey on atrial
fibrillation. Chest 2010;137:263-72.
34. van Werkum JW, Heestermans AACM, de Korte FI, et al. Long-term clin-
ical outcome after a first angiographically confirmed coronary stent
thrombosis, an analysis of 431 cases. Circulation 2009;119:828-34.
35. Daemen J, Wenaweser P, Tsuchida K, et al. Early and late coronary
stent thrombosis of sirolimus-eluting and paclitaxel-eluting stents
in routine clinical practice: data from a large two-institutional cohort
study. Lancet 2007;369:667-78.
36. Becker RC, Scheiman J, Dauerman HL, et al. Management of platelet-
directed pharmacotherapy in patients with atherosclerotic coronary
artery disease undergoing elective endoscopic gastrointestinal proce-
dures. Am J Gastroenterol 2009;104:2903-17.
37. Douketis JD, Spyropoulos AC, Spencer FA, et al. Perioperative man-
agement of 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.
38. D’Agostino RB, Vasan RS, Pencina MJ, et al. General cardiovascular risk
profile for use in primary care: the Framingham Heart Study. Circula-
tion 2008;117:743-53.
39. Patrono C, Ciabattoni G, Patrignani P, et al. Clinical pharmacology of
platelet cyclooxygenase inhibition. Circulation 1985;72:1177-84.
40. Born G, Patrono C. Antiplatelet drugs. Br J Pharmacol
2006;147(Suppl 1):S241-51.
41. Simon T, Verstuyft C, Mary-Krause M, et al. Genetic determinants of
response to clopidogrel and cardiovascular events. N Engl J Med
2009;360:363-75.
42. Cayla G, Hulot JS, O’Connor SA, et al. Clinical, angiographic, and ge-
netic factors associated with early coronary stent thrombosis. JAMA
2011;306:1765-74.
43. Serebuany VL, Steinhubl SR, Berger PB, et al. Variability in platelet
responsiveness to clopidogrel among 544 individuals. J Am Coll Car-
diol 2005;45:246-51.
44. Muller I, Besta F, Shulz C, et al. Prevalence of clopidogrel nonre-
sponders among patients with stable angina pectoris scheduled for
elective coronary stent placement. Thromb Haemost 2003;89:783-7.
45. Matetzky S, Shenkman B, Guetta V, et al. Clopidogrel resistance is
associated with increased risk of recurrent atherothrombotic events
in patients with acute myocardial infarction. Circulation 2004;109:
3171-5.
46. Wiviott SD, Trenk T, Frelinger AL, et al. Prasugrel compared with high
loading-and maintenance-dose clopidogrel in patients with planned
percutaneous coronary intervention, the prasugrel in comparison to
clopidogrel for inhibition of platelet activation and aggregationd
thrombolysis in myocardial infarction 44 trial. Circulation 2007;116:
2923-32.
47. Bliden KP, Tantry US, Storey RF, et al. The effect of ticagrelor versus
clopidogrel on high on-treatment platelet reactivity: combined anal-
ysis of the ONSET/OFFSET and RESPOND studies. Am Heart J
2011;162:160-5.
48. Cayla G, Silvain J, O’Connor SA, et al. Current antiplatelet options for
NSTE-ACS patients. Q J Med 2012;105:935-48.
49. Gurbel PA, Bliden KP, Butler K, et al. Randomized double-blind assess-
ment of the ONSET and OFFSET of the antiplatelet effects of ticagre-
lor versus clopidogrel in patients with stable coronary artery disease:
the ONSET/OFFSET study. Circulation 2009;120:2577-85.
50. Morrow DA, Braunwald E, Bonaca MP, et al. Vorapaxar in the second-
ary prevention of atherothrombotic events. N Engl J Med 2012;366:
1404-13.
51. Ueno M, Ferreiro JL, Angiolillo DJ. Mechanism of action and clinical
development of platelet thrombin receptor antagonists. Exp Rev Car-
diovasc Ther 2010;8:1191-200.
52. Schulman S, Elbazi R, Zondag M, et al. Clinical factors influencing the
normalization of prothrombin time after stopping warfarin: a retro-
spective cohort study. Thromb J 2008;16:15.
53. Weitz JI, Quinlan DJ, Eikelboom JW. Periprocedural management and
approach to bleeding in patients taking dabigatran. Circulation
2012;126:2428-32.
54. Dzik WS. Reversal of drug-induced anticoagulation: old solutions and
new problems. Transfusion 2012;52(Suppl 1):25S-55S.
55. FDA approves Praxbind, the first reversal agent for the anticoagulant
Pradaxa. Available at: http://www.fda.gov/NewsEvents/Newsroom/
PressAnnouncements/ucm467300.htm. Accessed October 15, 2015.
56. Ansell JE, Bakhru SH, Laulicht BE, et al. Use of PER977 to reverse the
anticoagulant effect of edoxaban. N Engl J Med 2014;371:2141-2.
57. Crowther M, Kitt M, Lorenz T, et al. A phase 2 randomized, double-
blind, placebo-controlled trial of PRT064445, a novel, universal anti-
dote for direct and indirect factor Xa inhibitors. J Thromb Haemost
2013;11:30.
58. Landenhed M, Johansson M, Erlinge D, et al. Fondaparinux or enox-
aparin: a comparative study of postoperative bleeding in coronary ar-
tery bypass grafting surgery. Scand Cardiovasc J 2010;44:100-6.
59. Baron TH, Kamath PS, McBane RD. Management of antithrombotic
therapy in patients undergoing invasive procedures. N Engl J Med
2013;368:2113-24.
60. Bhatt DL, Hulot JS, Moliterno DJ, et al. Antiplatelet and anticoagula-
tion therapy for acute coronary syndromes. Circ Res 2014;114:
1929-43.
61. Horiuchi A, Nakayama Y, Kajiyama M, et al. Removal of small colo-
rectal polyps in anticoagulated patients: a prospective randomized
comparison of cold snare and conventional polypectomy. Gastroint-
est Endosc 2014;79:417-23.
62. Williams DO, Abbott JD, Kip LE. DEScover Investigators. Outcomes of
6905 patients undergoing percutaneous coronary intervention in the
era of drug-eluting stents: report of the DEScover Registry. Circulation
2006;114:2154-62.
63. Iakovou I, Schmidt T, Bonizzoni E, et al. Incidence, predictors, and
outcome of thrombosis after successful implantation of drug-
eluting stents. JAMA 2005;293:2126-30.
64. Mauri L, Hsieh WH, Massaro JM, et al. Stent thrombosis in randomized
clinical trials of drug-eluting stents. N Engl J Med 2007;356:1020-9.
65. Garcia DA, Regan S, Henault LE, et al. Risk of thromboembolism with
short-term interruption of warfarin therapy. Arch Intern Med
2008;168:63-9.
66. Blacker DJ, Wijdicks EF, McLelland RL. Stroke risk in anticoagulated
patients with atrial fibrillation undergoing endoscopy. Neurology
2003;61:964-8.
67. Witt DM, Delate T, Garcia DA, et al. Risk of thromboembolism, recur-
rent hemorrhage, and death after warfarin therapy interruption for
gastrointestinal tract bleeding. Arch Intern Med 2012;172:1484-91.
68. Constans M, Santamaria A, Mateo J, et al. Low-molecular-weight hep-
arin as bridging therapy during interruption of oral anticoagulation in
patients undergoing colonoscopy or gastroscopy. Int J Clin Pract
2007;61:212-7.
69. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline
for the management of patients with atrial fibrillation. J Am Coll Car-
diol 2014;64:e1-76.
70. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for
the management of patients with valvular heart disease: a report of
the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines. Circulation 2014;129:e521-643.
71. Siegal D, Yudin J, Kaatz S, et al. Periprocedural heparin bridging in pa-
tients receiving vitamin K antagonists. Circulation 2012;126:1630-9.
72. Douketis JD, Spyropoulos AC, Kaatz S, et al. Perioperative bridging an-
ticoagulation in patients with atrial fibrillation. N Engl J Med
2015;373:823-33.
73. Eisenberg MJ, Richard PR, Libersan D, et al. Safety of short-term
discontinuation of antiplatelet therapy in patients with drug-eluting
stents. Circulation 2009;119:1634-42.
74. Bhatt DL, Scheiman J, Abraham NS, et al. ACCF/ACG/AHA 2008 expert
consensus document on reducing the gastrointestinal risks of anti-
platelet therapy and NSAID use. Circulation 2008;118:1894-909.

75. Timothy SK, Hicks TC, Opelka FG, et al. Colonoscopy in the patient
requiring anticoagulation. Dis Colon Rectum 2001;44:1845-8; discus-
sion, 1848-9.
76. Sawhney MS, Salfiti N, Nelson DB, et al. Risk factors for severe delayed
postpolypectomy bleeding. Endoscopy 2008;40:115-9.
77. Taha AS, Angerson WJ, Knill-Jones RP, et al. Upper gastrointestinal
mucosal abnormalities and blood loss complicating low-dose aspirin
and antithrombotic therapy. Aliment Pharmacol Ther 2006;23:489-95.
78. Hashash JG, Shamseddeedn W, Skoury A, et al. Gross lower gastroin-
testinal bleeding in patients on anticoagulant and/or antiplatelet
therapy: endoscopic findings, management, and clinical outcomes.
J Clin Gastroenterol 2009;43:36-42.
79. Rubin TA, Murdoch M, Nelson DB. Acute GI bleeding in the setting of
supratherapeutic international normalized ratio in patients taking
warfarin: endoscopic diagnosis, clinical management, and outcomes.
80. Choudari CP, Rajgopal C, Palmer KR. Acute gastrointestinal haemor-
rhage in anticoagulated patients: diagnoses and response to endo-
scopic treatment. Gut 1994;35:464-6.
81. Wolf AT, Wasan SK, Saltzman JR. Impact of anticoagulation on re-
bleeding following endoscopic therapy for nonvariceal upper gastro-
intestinal hemorrhage. Am J Gastroenterol 2007;102:290-6.
82. Shingina A, Barkun AN, Razzaghi A, et al. Systematic review: the pre-
senting international normalized ratio (INR) as a predictor of outcome
in patients with upper nonvariceal gastrointestinal bleeding. Aliment
Pharmacol Ther 2011;33:1010-8.
83. Kuwada SK, Balm R, Gostout CJ. The role of withdrawing chronic an-
tithrombotic because of acute GI bleeding. Am J Gastroenterol
1996;91:1116-9.
84. Ananthasubramaniam K, Beattie JN, Rosman HS, et al. How safely and
how long can warfarin therapy be withheld in prosthetic heart valve
patients hospitalized with a major hemorrhage? Chest 2001;119:
478-84.
85. Holbrook A, Schulman S, Witt DM, et al. Evidence-based management
of anticoagulant therapy: antithrombotic therapy and prevention of
thrombosis, 9th ed: American College of Chest Physicians Evidence-
Based Clinical Practice Guidelines. Chest 2012;141:e152S-84S.
86. Sarode R, Matevosyan K, Bhagat R, et al. Rapid warfarin reversal: a 3-
factor prothrombin complex concentrate and recombinant factor VIIa
cocktail for intracerebral hemorrhage. J Neurosurg 2012;116:491-7.
87. Kaatz S, Kouides PA, Garcia DA, et al. Guidance on the emergent
reversal of oral thrombin and factor Xa inhibitors. Am J Hematol
2012;87(Suppl 1):S141-5.
88. Chan FK, Ching JY, Hung LC, et al. Clopidogrel versus aspirin and eso-
meprazole to prevent recurrent ulcer bleeding. N Engl J Med
2005;102:290-6.
89. Lai KC, Chu KM, Hui WM, et al. Esomeprazole with aspirin versus clo-
pidogrel for prevention of recurrent gastrointestinal ulcer complica-
tions. Clin Gastroenterol Hepatol 2006;4:860-5.
90. Sung JJY, Lau JYW, Ching JYL, et al. Continuation of low-dose aspirin
therapy in peptic ulcer bleeding. Ann Intern Med 2010;152:1-9.
91. Hallas J, Dall M, Andries A, et al. Use of single and combined antith-
rombotic therapy and risk of serious upper gastrointestinal bleeding:
population based case-control study. BMJ 2006;333:726.
92. Moscucci M, Fox KA, et al. Predictors of major bleeding in acute cor-
onary syndromes; the Global Registry of Acute Coronary Events
(GRACE). Eur Heart J 2003;24:1815-23.
93. Al-Mallah M, Bazari RN, Jankowski M, et al. Predictors and outcomes
associated with gastrointestinal bleeding in patients with acute coro-
nary syndromes. J Thromb Thrombo 2007;23:51-5.
94. Abbas AE, Brodie B, Dixon S, et al. Incidence and prognostic impact of
gastrointestinal bleeding after percutaneous coronary intervention
for acute myocardial infarction. Am J Cardiol 2005;96:173-6.
95. Lin S, Konstance R, Jollis J, et al. The utility of upper endoscopy in pa-
tients with concomitant upper gastrointestinal bleeding and acute
myocardial infarction. Dig Dis Sci 2006;51:2377-83.
96. Shalev A, Zahger D, Novack V, et al. Incidence, predictors, and out-
comes of upper gastrointestinal bleeding in patients with acute cor-
onary syndromes. Int J Cardiol 2012;157:386-90.
97. Yachimski P, Hur C. Upper endoscopy in patients with acute myocar-
dial infarction and upper gastrointestinal bleeding: results of a deci-
sion analysis. Dig Dis Sci 2009;54:701-11.
98. Hui AJ, Wong RM, Ching JY, et al. Risk of colonoscopic polypectomy
bleeding with anticoagulants and antiplatelet agents: analysis of
1657 cases. Gastrointest Endosc 2004;59:44-8.
99. Heidbuchel H, Verhamme P, Alings M, et al. European heart rhythm
association practical guide on the use of new oral anticoagulants in
patients with non-valvular atrial fibrillation. Europace 2013;15:625-51.
100. Gerson LB, Gage BF, Owens DK, et al. Effect and outcomes of the
ASGE guidelines on the periendoscopic management of patients
who take anticoagulants. Am J Gastroenterol 2000;95:1717-24.
101. Friedland S, Soetikno R. Colonoscopy with polypectomy in anticoagu-
lated patients. Gastrointest Endosc 2006;64:98-100.
102. Ko CW, Dominitz JA. Complications of colonoscopy: magnitude and
management. Gastrointest Endosc Clin North Am 2010;20:659-71.
103. Howell DA, Eswaran SL, Lowe BJ, et al. Use of hemostatic clips in pa-
tients undergoing colonoscopy in setting of Coumadin antithrom-
botic therapy [abstract]. Gastrointest Endosc 2006;63:AB98.
104. Sobrino-Faya M, Martinez S, Gomez Balado M, et al. Clips for the pre-
vention and treatment of postpolypectomy bleeding (hemoclips in
polypectomy). Rev Esp Enferm Dig 2002;94:457-62.
105. Friedland S, Sedehi D, Soetikno R, et al. Colonoscopic polypectomy in
anticoagulated patients. World J of Gastroenterol 2009;15:1973-6.
106. Liaquat H, Rohn E, Rex DK. Prophylactic clip closure reduced the risk
of delayed postpolypectomy hemorrhage: experience in 277 clipped
large sessile or flat colorectal lesions and 247 control lesions. Gastro-
intest Endosc 2013;77:401-7.
107. Parikh ND, Zanocco K, Keswani RN, et al. A cost-efficacy analysis of
prophylactic clip placement after endoscopic removal of large polyps.
Clin Gastroenterol Hepatol 2013;11:1319-24.
108. Repici A, Hassan C, De Paula Pessoa D, et al. Efficacy and safety of
endoscopic submucosal dissection for colorectal neoplasia: a system-
atic review. Endoscopy 2012;44:137-47.
109. Kouklakis G, Mpoumponaris A, Gatopoulou A, et al. Endoscopic resec-
tion of large pedunculated colonic polyps and risk of postpolypec-
tomy bleeding with adrenaline injection versus endoloop and
hemoclip: a prospective, randomized study. Surg Endosc 2009;23:
2732-7.
110. Hussain N, Alsulaiman R, Burtin P, et al. The safety of endoscopic
sphincterotomy in patients receiving antiplatelet agents: a case-
control study. Aliment Pharmacol Ther 2007;25:579-84.
111. Kien-Fong V, Chang F, Doig I, et al. A prospective control study of the
safety and cellular yield of EUS-guided FNA or Trucut biopsy in pa-
tients taking aspirin, nonsteroidal anti-inflammatory drugs, or pro-
phylactic low molecular weight heparin. Gastrointest Endosc
2006;63:808-13.
112. Singh M, Mehta N, Murthy UK, et al. Postpolypectomy bleeding in pa-
tients undergoing colonoscopy uninterrupted clopidogrel therapy.
113. Feagins LA, Iqbal R, Harford WV, et al. Low rate of postpolypec-
tomy bleeding among patients who continue thienopyridine ther-
apy during colonoscopy. Clin Gastroenterol Hepatol 2013;11:
1325-32.
114. Richter JA, Patrie JT, Richter RP, et al. Bleeding after percutaneous
endoscopic gastrostomy is linked to serotonin reuptake inhibitors,
not aspirin or clopidogrel. Gastrointest Endosc 2011;74:22-34.
115. Shiffman ML, Farrel MT, Yee YS. Risk of bleeding after endoscopic bi-
opsy or polypectomy in patients taking aspirin or other NSAIDs. Gas-
trointest Endosc 1994;40:458-62.
116. Tsuji Y, Ohata K, Ito T, et al. Risk factors for bleeding after endoscopic
submucosal dissection for gastric lesions. World J Gastroenterol
2010;16:2913-7.

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