Manejo de La Terapia Antitrombotica

Juan Carlos Uribe O.
MD
Internista CES
Fellow Cardiologa CES

Informes:
CES-CARDIOLOGA Cr. 43 No 36 - 02 Of. 1101 Tels: (4) 4447378 (4) 576 73 86
Aliar Comunicaciones (Firma operadora del evento) Tel: (4) 444 22 60.

PROGRAMACIN

XVI CONGRESO ESTADO ACTUAL EN ENFERMEDADES CARDACAS Y VASCULARES
2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013

Mircoles 14 de Agosto

Salones 5 y 6

Simposio:
Hemodinamia, Cardiologa Intervencionista y Vascular Perifrico
2 a 6 p.m.: Coordinador Csar Hernndez, MD.

2:00 - 2:30 p.m. Ablacin simptica renal, muchos dispositivos pocos pacientes
lvaro Escobar, MD.
2:30 - 3:00 p.m. Cierre de Foramen Ovale, Decisin multidisciplinaria?
Diego Velsquez, MD.
3:00 - 3:30 p.m. Stents medicados: Estado Actual
Csar Hernndez, MD.
3:30 - 4:00 p.m. Intervencin percutnea en vlvula mitral: Mitraclip y ms
Ivn Rendn, MD.

4:00 - 4:30 p.m. Descanso

4:30 - 5:00 p.m. Actualizacin en antiplaquetarios: un medicamento para cada
paciente?
Csar Hernndez, MD.
5:00 - 5:50 p.m. Revascularizacin coronaria en Diabticos. Debate.
Quirrgica Luis Andrs Vlez, MD.
Percutnea lvaro Escobar, MD.
Manejo Mdico Alex Londoo, MD.

MANEJO DE LA TERAPIA ANTITROMBTICA
EN PACIENTES SOMETIDOS A
PROCEDIMIENTOS QUIRRGICOS

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

martes, 10 de septiembre de 13
Poblacin anticoagulada en aumento.
Warfarina.
Nuevos anticoagulantes.
TAPD por SCA y stents ! en aumento.
10% - 20% ! Qx o procedimientos invasivos que requieren la suspensin temporal.
Meta ! minimizar eventos tromboemblicos y hemorragias mayores peri

procedimiento.
200
400
600
800
1000
1200
1400
1980 1985 1990 1995 2000 2005 2009
Aos
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n

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e
s
Coronariografas
PCI
Circulation 2012;125(1):e2- e220.
Anticoagulados
INTRODUCCIN

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Antiplaquetarios
Vida
media
Bloqueo
del Rc
Inicio de
accin
Fin
accin
ASA
Irreversible 30 min 7 d
Inhibidores P2Y
12
Inhibidores P2Y
12
Inhibidores P2Y
12
Inhibidores P2Y
12
Inhibidores P2Y
12
Clopidogrel
6 h Irreversible 2 - 8 h 7 d
Prasugrel
7 h Irreversible 30 min - 4 h 7 d
Ticagrelor
8 - 12 h Reversible 30 min - 2 h 5 d
practise is signicantly diminished as the consequence of
new approaches to clopidogrel dosing (i.e. pretreatment,
high loading doses), the availability of more potent anti-
platelet agents than clopidogrel (i.e. prasugrel and ticagre-
lor), and the lower risk of bleeding with alternative
antithrombotic option (i.e. bivalirudin) [20].
Limitations of aspirin, clopidogrel, and glycoprotein
IIb/IIIa inhibitors have prompted a search for novel anti-
platelet agents with a more favorable riskbenet ratio.
This article is aimed at providing an overview on new an-
tiplatelet drugs in the setting of ACS and PCI, including
the most recent advances on recently approved agents as
well as on emerging compounds in clinical development
(Figs 1 and 2). A description of more established antiplat-
elet therapies, including aspirin, clopidogrel, and glyco-
protein IIb/IIIa inhibitors, antiplatelet drugs which do
not have an approved indication for ACS/PCI (i.e.
pentoxifylline, cilostazol, dipyridamole) as well as novel
anticoagulant agents with no direct action on platelets go
beyond the scope of this manuscript and will not be
discussed.
Thromboxane a2 pathway inhibitors
Aspirin has been the cornerstone of treatment for patients
with various atherosclerotic disease manifestations. It
exerts its effects by blocking the COX-1 enzyme and thus
inhibiting the synthesis of TXA2 from arachidonic acid
[21,22]. Despite the undisputable clinical benets of aspi-
rin, the notion that a proportion of patients experience
suboptimal antiplatelet effects while on aspirin therapy
has prompted investigations to identify agents that more
effectively inhibit thromboxane-mediated platelet activa-
tion processes [23].
Thromboxane and prostaglandin endoperoxide (TP)
receptors are expressed in platelets, inammatory cells,
vascular wall, and atherosclerotic plaques [24]. This may
explain why TP receptor inhibitors may exert additional
effects beyond those on platelets, including regulating
endothelial cell activation and vascular smooth muscle
cell contraction [25]. Blockage of TP receptors not only
inhibits the platelet interaction with TXA2 but also bind-
ing of its cyclic endoperoxide precursors. Importantly,
although aspirin blocks TXA2 synthesis in most individu-
als, shuttling of endoperoxide intermediates to platelets
from other cells may account for some variability in the
clinical response to aspirin. For this reason, blocking TP
receptors is theoretically more effective than simply
reducing the generation of TXA2 at the COX-1 level [26].
Moreover, many TXA2 pathway inhibitors exert a dual
pharmacological action, since they inhibit both TP recep-
tors and TXA2 synthase, thereby resulting in a more com-
ADP
CURRENTLY AVAILABLE ANTIPLATELET AGENTS
T
h
r
o
m
b
in
A
D
P
5
H
T
2
A
P
G
E
AA
G
P13K
cox-1
G
G
G
G
G
Ticlopidine
Clopidogrel
Prasugrel
Ticagrelor
fibrinogen
Intracellular signaling
GPVI GPlb/IX/V
GP llb/IIIa
GP llB/IIIA INHIBITORS
Abciximab
Tirofiban
Eptifibatide
TxA
2
INHIBITORS
P2Y
12
INHIBITORS
cox-1 Inhibitors
Aspirin
T
x
A
2
T
x
A
2
Fig. 1. Sites of action of currently available agents for acute coronary syndromes or percutaneous coronary intervention. 5HT2A, serotonin;
AA, arachidonic acid; ADP, adenosine diphosphate; COX-1, cyclooxygenase-1; G, G-protein; GP, glycoprotein; PG, prostaglandin; PI3K,
phosphatidylinositol 3-kinase; TxA2, thromboxane A2. Reproduced with permission from Ferreiro et al., Circ Cardiovasc Interv. 2012;5:43345
[20].
2013 International Society on Thrombosis and Haemostasis
New directions in antiplatelet therapy 317
J Thromb Haemost 2013; 11 (Suppl. 1): 31629.
ANTIPLAQUETARIOS

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Warfarina.
Nuevos anticoagulantes:
Vida media
Excrecin
renal
Rivaroxabn 5 - 13 h 66%
Apixabn 8 - 15 h 25%
Dabigatrn 12 - 14 h 80%
Anesthesiology 2013; 118:1466-74
Anesthesiology 2013, 118:1466-74 1467 Levy et al.
EDUCATION
increasingly replacing older parenteral agents and vitamin K
antagonists in clinical practice, it is important to consider that
patients treated with these agents will be exposed to dier-
ent clinical situations (spontaneous or postoperative bleeding,
overdose, trauma, and elective or emergent surgical proce-
dures) that require an intervention. Tere are also increasing
concerns about managing patients on these therapeutic agents
following trauma or in a perioperative setting. Te purpose
of this review is (1) to examine the NOACs, focusing on key
pharmacologic properties, and (2) to provide management
approaches for users of NOACs in the perioperative and criti-
cal care settings based on the available literature.
Oral Direct Thrombin Inhibitors
Trombin has a pivotal role in hemostasis, making it an
appealing target for anticoagulant drugs. When thrombin is
activated from prothrombin, it converts soluble brinogen
to insoluble brin; activates coagulation factors V, VIII, and
XI (which generate more thrombin); and activates platelets
(g. 1).
3
Dabigatran is a reversible direct thrombin inhibitor
that directly inhibits free and brin-bound thrombin without
the need for antithrombin. Dabigatran etexilate is a prodrug
that has a rapid onset of action, no reported food interactions,
few drug interaction, and does not require routine
coagulation monitoring. Te peak plasma concentration
is reached 1.253 h after administration, and it has a half-
life of 1214 h in healthy volunteers.
4
Dabigatran is 35%
bound to plasma proteins and undergoes renal excretion,
with 80% of the drug entering the urine unchanged. Te
anticoagulant eect of dabigatran accumulates in the setting
of renal insuciency, and such bioaccumulation correlates
well with the degree of renal dysfunction.
5
In contrast to
other NOACs that are highly protein bound, the relatively
low protein binding of dabigatran allows it to be eliminated
to a large extent by hemodialysis.
6
In cases of moderate
hepatic impairment, dabigatran can be administered safely
and no dose adjustment is necessary.
7
Dabigatran is approved in the United States, Canada,
Europe, and Japan for stroke prevention in patients with
non-valvular AF based on the results of the Randomized
Evaluation of Long-term anticoagulant therapY (RE-LY)
trial in which 150 mg of dabigatran twice-daily was superior
to dose-adjusted warfarin with a similar rate of major bleed-
ing.
8
Dabigatran, 75 mg twice-daily, is approved for use in
the United States for patients with severe renal insuciency
(CrCl 1530 ml/min), based on indirect pharmacokinetic
modeling and the assumed anticoagulant eect with this
level of renal dysfunction. In Europe and Canada, the 75-mg
dose is not approved for clinical use and dabigatran is con-
traindicated in patients with a CrCl < 30 ml/min. Dabiga-
tran is also is approved for VTE prophylaxis following total
hip or knee replacement surgery in Europe and Canada, but
not the United States. A recent indirect network meta-analy-
sis suggests that treatment with dabigatran oers benet for
the prevention of stroke, systemic embolism, and mortality
over antiplatelets and placebo without increased intracranial
or extracranial hemorrhage compared to antiplatelet agents.
9

Further investigations are needed to conrm these results.
Oral Direct Factor Xa Inhibitors
Factor Xa is another important target for anticoagulant
drugs due to its role as the rate-limiting factor in throm-
bin generation and amplication, generating the Xa com-
plex that converts prothrombin to thrombin (g. 1).
2
Te
direct factor Xa inhibitors inhibit free Factor Xa, Factor Xa
in the prothrombinase complex, and Factor Xa found in
clots, independent of an antithrombin cofactor.
2,10
Tis is
in contrast to low-molecular-weight heparin, unfractionated
heparin, and fondaparinux, which all are dependent on anti-
thrombin to inhibit Factor Xa.
Rivaroxaban
Rivaroxaban is an oral, direct Factor Xa inhibitor that has
good bioavailability (80%), is highly protein-bound, and
has few drug interactions. Peak plasma concentrations occur
within 24 h of administration, and rivaroxaban has a half-
life of 59 h in healthy subjects and 1113 h in the elderly.
10

It is selective for Factor Xa in relation to other serine prote-
ases.
2
Clearance of rivaroxaban may be decreased to some
extent in patients with renal impairment,
11
but its primary
mode of clearance is by non-renal mechanisms. It should be
noted that although some reports may indicate that approxi-
mately 67% of rivaroxaban is eliminated by the kidney, such
total renal clearance reects 33% clearance of active drug
and 33% clearance of inactive rivaroxaban, which is not clin-
ically important. Tus, two-thirds of the active rivaroxaban
Fig. 1. Effect sites of anticoagulation agents. The new oral an-
ticoagulation agents directly inhibit one of two major targets in
the coagulation cascade. Rivaroxaban and apixaban directly
inhibit factor Xa, and dabigatran directly inhibits thrombin.
The parenteral anticoagulants that inhibit factor Xa include
low-molecular-weight heparin (LMWH) and fondaparinux
by antithrombin (AT)-dependent binding. Parenteral direct
thrombin inhibitors include argatroban, bivalirudin, and de-
sirudin that also directly inhibit thrombin independent of AT.
ANTICOAGULANTES

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Conocer:
Riesgo de sangrado.
Riesgo tromboemblico.
Terapia puente.
Cundo suspender y reiniciar la terapia antitrombtica.

Valorar el riesgo de eventos trombticos durante el perodo en
que se suspenden los agentes antitrombticos.
CONCEPTOS GENERALES

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Depende principalmente del tipo de procedimiento.
Factores de riesgo asociados al paciente:
Efecto residual de los antitrombticos.
Cncer activo o QxTx.
Historia de sangrado.
Reintervencin.
HAS-BLED " 3.
VALORACIN DEL RIESGO DE
SANGRADO
J Thromb Haemost 2012;10:261- 7
J Thromb Haemost. 2012;108:6573
Caracterstica Puntos
HTA 1
Alteracin renal y/o heptica 1 o 2
ACV (Stroke) 1
Sangrado (Bleeding) 1
INR Labil 1
Edad 1
Drogas u OH 1 o 2

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Alto riesgo ! riesgo > 1.5%.
Procedimientos intracraneales, intraespinales, cmara posterior del ojo,

retroperitoneo, intratorcicos.
SANGRADO
Circulation. 2012;126:486-490.

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.


SANGRADO
Circulation. 2012;126:486-490.

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Dentales
Extracciones no complicadas
Endodoncias
Prtesis
Terapia periodoncia
Oftalmolgicas
Qx de catarata
Trabeculectoma
Gastrointestinal
Endoscopia superior c/s Bx.
Enteroscopia
Colonoscopia
Bajo Riesgo

SANGRADO
Circulation. 2012;126:486-490.

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Dentales
Endodoncias
Prtesis
Terapia periodoncia
Oftalmolgicas
Qx de catarata
Trabeculectoma
Gastrointestinal
Enteroscopia
Colonoscopia
Bajo Riesgo
N
o

s
u
s
p
e
n
d
e
r

a
n
t
i
t
r
o
m
b
t
i
c
o
s

Alto Riesgo
CABG o Reemplazo valvular
Qx intracraneal o espinal
Reparo de AA
Puentes arteriales perifricos
Qx vascular mayor
Qx ortopdica mayor
Qx plstica reconstructiva
Qx mayor de cancer
Qx de prstata o vejiga
Bx de prstata o rin
SANGRADO
Circulation. 2012;126:486-490.

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Dentales
Endodoncias
Prtesis
Terapia periodoncia
Oftalmolgicas
Qx de catarata
Trabeculectoma
Gastrointestinal
Enteroscopia
Colonoscopia
Bajo Riesgo
N
o

s
u
s
p
e
n
d
e
r

a
n
t
i
t
r
o
m
b
t
i
c
o
s

Alto Riesgo
CABG o Reemplazo valvular
Qx intracraneal o espinal
Reparo de AA
Puentes arteriales perifricos
Qx vascular mayor
Qx ortopdica mayor
Qx plstica reconstructiva
Qx mayor de cancer
Qx de prstata o vejiga
Bx de prstata o rin
SANGRADO
C
o
n
s
i
d
e
r
a
r

T
e
r
a
p
i
a
P
u
e
n
t
e
Circulation. 2012;126:486-490.

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Dentales
Endodoncias
Prtesis
Terapia periodoncia
Oftalmolgicas
Qx de catarata
Trabeculectoma
Gastrointestinal
Enteroscopia
Colonoscopia
Bajo Riesgo
N
o

s
u
s
p
e
n
d
e
r

a
n
t
i
t
r
o
m
b
t
i
c
o
s
Guidelines for the management of patients
on oral anticoagulants requiring dental surgery
BRITISH DENTAL JOURNAL VOLUME 203 NO. 7 OCT 13 2007
Sangrado Trombosis
Riesgo de sangrado bajo con INR 2 - 3.
Realizar INR 24 h previo al procedimiento.
Uso de surgicel, esponjas de colgeno y

suturas para disminuir el sangrado.
Enjuages con Ac tranexmico al 5%.
No prescribir AINEs o COX-2.

0
0,2
0,4
0,6
0,8
1
Riesgo (%)
Sangrado Trombosis


0
0,2
0,4
0,6
0,8
1
Riesgo (%)
Sangrado Trombosis


0
0,2
0,4
0,6
0,8
1
Riesgo (%)
Sangrado Trombosis


Evaluation of the need to discontinue antiplatelet
and anticoagulant medications before cataract
surgery
J Cataract Refract Surg 2010; 36:11151119
0
5
10
15
20
H subconjuntival
Hifema
Hemorragia retiniana
En terapia Sin terapia
P = 0.0309
P = 0.3572
P = 0.6187
Continuar terapia antitromboemblica.
Anestesia local y/o sub tenoniana.

Riesgo extrapolado segn CHADS

2
y CHA
2
DS
2
-VASc.
Puntaje Riesgo
0, 1 o 2 Bajo
" 3, Stroke o ICT en
los 3 meses previos o
enf. valvular severa
Alto
VALORACIN DEL RIESGO TROMBOEMBLICO
Fibrilacin Auricular
JAMA. 2001 Jun 13;285(22):2864-70.
CHEST 2010; 137(2):263272.
Factor de Riesgo Puntaje
Falla Cardaca 1
HTA 1
Edad (Age): 65 - 74 aos 1
Diabetes 1
ACV/ICT/Tromboembolismo (Stroke) 2
Enfermedad Vascular 1
Edad (Age): " 75 aos 2
Sexo (Femenino) 1

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Riesgo depende de:
Tipo de vlvulas, nmero, localizacin.
Patologas asociadas: FA, falla cardaca, historia de tromboembolismo o

trombos intracavitarios.
En TEV mayor riesgo dentro de los primeros 3 meses.

comparison with a baseline study or serial postoperative Doppler
echocardiographic studies is often helpful, particularly when the func-
tion of the valve is in question (Table 2).
1. Clinical Data. The reason for the echocardiographic study and
the patients symptoms should be clearly documented. Furthermore,
because Doppler ndings and interpretation depend on the type and
size of the replacement valve, this information and the date of surgery
should be incorporated in the report when available, as this can be
used in subsequent studies. Blood pressure and heart rate should be
measured. The heart rate of the cardiac cycles used for Doppler mea-
surements is particularly important in mitral and tricuspid prosthetic
valves, because the mean gradient is dependent on the diastolic lling
period. Finally, the patients height, weight, and body surface area
should be recorded to assess whether PPM is present and to interpret
cardiac chamber size.
2. Echocardiographic Imaging. The echocardiographic assess-
ment of patients with prosthetic valves includes standardized mea-
surement and evaluation of the size of cardiac chambers, LV wall
thickness and mass, and indices of LV systolic and diastolic function
per guidelines of the ASE.
10
In patients with aortic prostheses, mea-
surements of the aortic root and ascending aorta are recommended.
Valves should be imaged from multiple views, with particular atten-
tion to the following:
the opening and closing motion of the moving parts of the prosthesis (leaf-
lets for bioprosthesis and occluders for mechanical prostheses);
the presence of leaet calcications or abnormal echo density attached to
the sewing ring, occluder, leaets, stents, or cage; and
the appearance of the sewing ring, including careful inspection for regions of
separation fromthe native annulus and for abnormal rocking motion during
the cardiac cycle.
In general, magnication of real-time images is necessary for better
visualization of the leaets or occluder mechanism. Mild thickening is
often the rst sign of primary failure of a biologic valve and is a signal
to follow the patient more carefully.
11
Occluder motion of a mechan-
ical valve may not be well visualized by transthoracic echocardiogra-
phy (TTE) because of artifact and reverberations. Nevertheless,
optimal 2-dimensional (2D) echocardiographic visualization of oc-
cluder motion in tilting disc valves in the mitral or tricuspid position
frequently necessitates incremental rotation of the imaging plane
Figure 1 Examples of bileaet, single-leaet, and caged-ball mechanical valves and their transesophageal echocardiographic char-
acteristics taken in the mitral position in diastole (middle) and in systole (right). The arrows in diastole point to the occluder mechanism
of the valve and in systole to the characteristic physiologic regurgitation observed with each valve. Videos 1 to 6 showthe motion and
color ow patterns seen with these valves. View video clips online.
978 Zoghbi et al Journal of the American Society of Echocardiography
September 2009
Riesgo Bajo
Riesgo
Moderado
Riesgo Alto
Vlvulas
mecnicas
Prtesis Articas sin
FA, stroke o eventos
emblicos o trombos
intracardacos
conocidos.
Prtesis articas
bivalvas y FA.
Cualquier prtesis
mitral, otras prtesis
articas, mltiples
vlvulas mecnicas,
ACV, ICT o eventos
cardioemblicos.
TEV
TEV > 12 m y sin
otros FR.
TEV 3 - 12 m,
trombofilia no severa
o TEV recurrente
TEV < 3 m,
trombofilia severa,
TVE no provocado o
cncer activo.
Vlvulas mecnicas y TEV
N Engl J Med 2013;368:2113-24.

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Suspensi n premat ura ! ri esgo de

trombosis del stent.
Muerte e infarto ! 75%.
Muerte 25%.
Stents convencionales mayor riesgo en las

primeras 6 semanas.
DES mayor riesgo en los primeros 6 meses.
SCA terapia antiplaquetaria dual al menos 1

ao.
Stents coronarios
Circulation 2011;124(23):e574-e651
Journal of Cardiology (2011) 57, 231238

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Suspensi n premat ura ! ri esgo de

trombosis del stent.
Muerte e infarto ! 75%.
Muerte 25%.
Stents convencionales mayor riesgo en las

primeras 6 semanas.
DES mayor riesgo en los primeros 6 meses.
SCA terapia antiplaquetaria dual al menos 1

ao.
Stents coronarios
Circulation 2011;124(23):e574-e651
Journal of Cardiology (2011) 57, 231238
Effect of coronary endothelial function on outcomes in patients undergoing percutaneous coronary intervention 233
3
2
stent Sirolimus
Bare-metal stent
1
P
r
o
b
a
b
i
l
i
t
y

o
f

S
t
e
n
t

T
h
r
o
m
b
o
s
i
s

(
%
)
0
5 4 3 2 1 0
Years after Minimum Duration of Recommended
Dual Antiplatelet Therapy
Figure 1 KaplanMeier curves for stent thrombosis in the
pooled population according to stent type and the duration of
dual antiplatelet therapy. The graph shows the probability of
stent thrombosis after the use of a trial-dened minimum dura-
tion of recommended dual antiplatelet therapy, according to
stent type.
Adapted from Kastrati et al. [14].
for reintervention after the use of SES, the risk of stent
thrombosis with SES is at least as great as that seen with
BMS [14] (Fig. 1). Joner et al. [15] reported that rst-
generation DES caused a signicant delay in arterial healing
as a result of persistent brin deposition and delayed re-
endothelialization when compared with BMS implantation.
Indeed, LST in the context of rst-generation DES is due
to a variety of factors, including delayed arterial healing,
withdrawal of antiplatelet therapy, malapposition, incom-
plete apposition, and bifurcation stenting. Finn et al. [16]
reported that the most powerful histological predictor of
stent thrombosis was endothelial coverage on stent struts
(Fig. 2). Non-uniformity of healing is a common nding in
rst-generation DES with LST and VLST. Thus, incomplete
healing of the stented segment may play a major role in the
pathophysiology of LST.
DES and coronary endothelial dysfunction
In the rst published clinical study of coronary endothe-
lial dysfunction related to rst-generation DES, Togni et al.
[17] assessed exercise-induced coronary vasodilator func-
tion in patients with known coronary artery disease after DES
implantation. This study indicated that vasodilatory capac-
ity recovered quickly in atherosclerotic arteries stented
with BMS, but not in those stented with SES. Addition-
ally, other studies used an acetylcholine provocation test to
show that rst-generation DES induced focal dysfunction of
endothelium-dependent vasodilation in both proximal and
distal non-stented reference segments of coronary arter-
ies for 612 months post-stent implantation [18,19]. Obata
et al. [20] investigated coronary vasomotor function at two
weeks post-SES implantation following successful reperfu-
sion therapy after acute MI. More severe constriction of
distal epicardial coronary arteries in response to acetyl-
choline was seen in patients with SES when compared with
100
90
80
70
60
50
40
P
e
r
c
e
n
t
a
g
e

E
n
d
o
t
h
e
l
i
a
l
i
z
e
d
30
20
10
0
>40 20 17 16 15 11 9 8 7 6 5 4 3 2 1
Duration in months
DES
BMS
Figure 2 Line chart comparing the percentage of endothe-
lialization in drug-eluting stents (DES) versus bare-metal stent
(BMS) as a function of time. Note that DES (solid line) consis-
tently shows less endothelialization when compared with BMS
(dashed line), regardless of time point. Even beyond 40 months,
DES are not fully endothelialized, whereas BMS are completely
endothelialized by six to seven months.
Adapted from Joner et al. [15].
those with BMS. Furthermore, coronary blood ow and
vascular endothelial growth factor levels were also sig-
nicantly diminished in patients with SES than in those
with BMS. The authors concluded that SES implantation
had an adverse effect on endothelium-dependent vasodi-
lation in both epicardial and resistance coronary arteries
and reduced vascular endothelial growth factor secretion.
Kim et al. [21] reported that paclitaxel-eluting stent (PES)
and SES both resulted in greater endothelium-dependent
vasoconstriction at corresponding segments when compared
with BMS, but that there was no signicant difference in
endothelium-independent vasodilation when comparing the
different stents.
The rst-generation DES is associated with increased
vasoconstriction when compared with BMS, and this
vasoconstriction can have adverse effect on myocardial per-
fusion. Indeed, severe diffuse coronary artery spasm after
either SES or PES has been well documented in clinical
case reports [22,23]. Coronary vasoconstriction would result
in reduction of coronary blood ow and deterioration of
non-laminar ow within the stented vessel, which may be
associated with an increase in inammation and thrombosis.
Secondary prevention in the era of DES
Effect of DES on prevention of cardiac events
DES result in decreased late luminal loss and angio-
graphic restenosis when compared with BMS. This decrease
reduces the need for subsequent revascularization pro-
cedures [24,25]. In spite of these benets, DES is
associated with several adverse arterial responses, including
delayed endothelialization and hypersensitivity to the poly-
meric coating that regulates drug-dose-and-release kinetics

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INTEGRACIN DEL RIESGO
CONTINUAR
TERAPIA
CONTINUAR
TERAPIA
SUSPENDER
TERAPIA
TERAPIA PUENTE
Bajo
Alto
Alto
Bajo
TROMBOEMBOLISMO
S
A
N
G
R
A
D
O

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Condicin Terapia puente No terapia puente
Vlvulas
mecnicas
Mitral, 2 o ms vlvulas,
Reemplazo Ao (1 disco)
o con otros FR.
Prtesis articas (2
discos) sin FR adicionales.
FA no valvular
ACV o evento emblico,
trombos intracardacos,
CHADS
2
! 3.
No eventos emblicos,
trombos o CHADS
2
< 3.
TEV
TEV < 3 m o trombolia
severa.
TEV > 3 m o no FR
adicionales.
TERAPIA PUENTE
Circulation 2012; 126:1630-9.
Thromb Haemost 2012;108: 213-6.
Chest 2012;141:2 Suppl:e326S- e350S.

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paciente?
Csar Hernndez, MD.

En pacientes de alto riesgo de sangrado.
Intervalo sin terapia anticoagulante lo mas corto posible.
Considerar otros factores sobre la duracin del efecto anticoagulante:
Falla renal ! dabigatran, rivaroxaban, apixaban, HBPM.
Falla heptica ! warfarina, rivaroxaban y apixaban.

CUNDO SUSPENDER LOS
ANTITROMBTICOS?
Thromb Haemost 2012;107:803-5.

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93% de los pacientes con INR 2 - 3.5 tienen un INR de 1.5 luego de 5 das de
suspendida la warfarina.
Hemostasia normal con INR de 1.5.
INR < 1.5 ! seguro para procedimientos de alto riesgo.
INR < 1.2 ! procedimientos de alto riesgo de sangrado en espacios cerrados.
INR > 2 ! # en el riesgo de sangrado.

CUNDO SUSPENDER LOS ANTITROMBTICOS?
Warfarina
Thromb J 2008;16:15

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Rivaroxaban
Fx renal normal ! 1 d.
TFG 60 - 90 mL/min ! 2 d.
TFG 30 - 59 mL/min ! 3 d.
TFG 15 - 29 ! 4 d.
Apixaban
TFG > 60 mL/min ! 1 - 2 d.
TFG 50 - 59 mL/min ! 3 d.
TFG 30 - 49 mL/min ! 5d.
Dabigatran
TFG " 50 mL/min ! 1 - 2 d.
TFG < 50 mL/min ! 3 - 5 d.
Nuevos anticoagulantes
Circulation 2012;126:343-8
Circulation. 2012;126:1573-1576

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Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Rivaroxaban
TFG 60 - 90 mL/min ! 2 d.
TFG 30 - 59 mL/min ! 3 d.
TFG 15 - 29 ! 4 d.
Apixaban
TFG > 60 mL/min ! 1 - 2 d.
TFG 50 - 59 mL/min ! 3 d.
TFG 30 - 49 mL/min ! 5d.
Dabigatran
TFG " 50 mL/min ! 1 - 2 d.
TFG < 50 mL/min ! 3 - 5 d.
Circulation. 2012;126:1573-1576

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Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

patients who require periprocedural interruption of oral anti-
coagulation and bridging. How should these data should be
interpreted and incorporated in clinical practice? A major
limitation of the analysis is the heterogeneity of the data,
which is a reflection of the high variation in current clinical
practice. Under the term bridging, several different regimes
were used, including intermediate or prophylactic doses.
Moreover, a number of different procedures have been
assessed with a wide range of periprocedural bleeding risk.
Similarly, a variety of events were pooled under the terms
bleeding and thromboembolism. Most importantly, it is un-
clear how the estimated baseline risk for thromboembolism or
bleeding affected outcomes, because the indications for
anticoagulation varied and high risk was variably defined in
each study.
Also, Siegal et al
11
assessed the outcome of bridging
therapy in vitamin K antagonisttreated patients only, but the
increasing availability of novel oral anticoagulants, either
direct thrombin or factor Xa inhibitors, brings the question of
bridging therapy with the use of these drugs. Their shorter
half-life compared with coumarins suggests that the manage-
ment of bleeding complications and the antithrombotic regi-
men during operations and invasive procedures could poten-
tially become simpler with these drugs.
13,14
Nevertheless, the
optimal periprocedural management strategies of patients
taking the novel oral anticoagulants undergoing invasive
procedures need to be based on adequate quality evidence,
which is not currently available.
Only randomized trials can perhaps address the remaining
uncertainty in periprocedural anticoagulation. Currently, the
PERIOP-2 (A Double Blind Randomized Control Trial of
Post-Operative Low Molecular Weight Heparin Bridging
Therapy Versus Placebo Bridging Therapy for Patients
Who Are at High Risk for Arterial Thromboembolism),
BRIDGE (Effectiveness of Bridging Anticoagulation for
Surgery), and BRUISECONTROL (Bridge or Continue
Coumadin for Device Surgery Randomized Controlled
Trial), randomized trials comparing bridging with no
bridging strategies in warfarin-treated patients who require
elective surgery, are ongoing.
1517
These ongoing studies
are designed to answer relevant questions on periproce-
dural anticoagulation in specific settings using specific
regimes. Moreover, they will evaluate periprocedural
bridging using clearly defined efficacy and safety end
points.
BRIDGE is a prospective randomized, double-blinded study
which aims to recruit 3600 patients with atrial fibrillation/
flutter and a major risk factor for thromboembolism who require
elective surgery or invasive procedure necessitating interruption
of their oral anticoagulant therapy.
16
Patients will be random-
ized perioperatively to receive either subcutaneous dalteparin
or placebo, and primary end points include arterial thrombo-
Chronic oral anticoagulation
VKA
New OAC
Assessing thrombotic
risk
low Non low
Pre-operative:
- no bridgning
- stop warfarin 5 days prior
- check INR morning of surgery
Post-operative:
- assess haemostasis
- restart warfarin when
feasible
- VTE prophylaxis if needed
Pre-operative:
- LMWH when INR subtherapeutic
- therapeutic dose/12h if MHV
- therapeutic dose daily if AF/VTE
- half dose 1 day prior
Post-operative:
- restart warfarin when feasible
- delay LMWH restart 48h
Elective procedure scheduled
Assess creatinine
clearance
<50mL/min
50mL/min
Stop dabigatran 7 days prior
Stop rivaroxaban 5 days
prior
prior
Pre-operative:
- no bridging therapy needed
- if high bleeding risk procedure, check
haemostasis on morning of procedure
Post-operative:
- re-assess creatinine
clearance
- delay restart 48h
Figure. Bridging algorithm for vitamin K antagonists and new oral anticoagulants. Adapted from Wysokinski et al.
8
AF indicates atrial
brillation; INR, International Normalized Ratio; LMWH, low-molecular-weight heparin; MHV, mechanic heart valve; OAC, oral anticoag-
ulants; VKA, vitamin K antagonist; and VTE, venous thromboembolism.
1574 Circulation September 25, 2012
by guest on August 15, 2013 http://circ.ahajournals.org/ Downloaded from
Rivaroxaban
TFG 60 - 90 mL/min ! 2 d.
TFG 30 - 59 mL/min ! 3 d.
TFG 15 - 29 ! 4 d.
Apixaban
TFG > 60 mL/min ! 1 - 2 d.
TFG 50 - 59 mL/min ! 3 d.
TFG 30 - 49 mL/min ! 5d.
Dabigatran
TFG " 50 mL/min ! 1 - 2 d.
TFG < 50 mL/min ! 3 - 5 d.
Circulation. 2012;126:1573-1576

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

patients who require periprocedural interruption of oral anti-
coagulation and bridging. How should these data should be
interpreted and incorporated in clinical practice? A major
limitation of the analysis is the heterogeneity of the data,
which is a reflection of the high variation in current clinical
practice. Under the term bridging, several different regimes
were used, including intermediate or prophylactic doses.
Moreover, a number of different procedures have been
assessed with a wide range of periprocedural bleeding risk.
Similarly, a variety of events were pooled under the terms
bleeding and thromboembolism. Most importantly, it is un-
clear how the estimated baseline risk for thromboembolism or
bleeding affected outcomes, because the indications for
anticoagulation varied and high risk was variably defined in
each study.
Also, Siegal et al
11
assessed the outcome of bridging
therapy in vitamin K antagonisttreated patients only, but the
increasing availability of novel oral anticoagulants, either
direct thrombin or factor Xa inhibitors, brings the question of
bridging therapy with the use of these drugs. Their shorter
half-life compared with coumarins suggests that the manage-
ment of bleeding complications and the antithrombotic regi-
men during operations and invasive procedures could poten-
tially become simpler with these drugs.
13,14
Nevertheless, the
optimal periprocedural management strategies of patients
taking the novel oral anticoagulants undergoing invasive
procedures need to be based on adequate quality evidence,
which is not currently available.
Only randomized trials can perhaps address the remaining
uncertainty in periprocedural anticoagulation. Currently, the
PERIOP-2 (A Double Blind Randomized Control Trial of
Post-Operative Low Molecular Weight Heparin Bridging
Therapy Versus Placebo Bridging Therapy for Patients
Who Are at High Risk for Arterial Thromboembolism),
BRIDGE (Effectiveness of Bridging Anticoagulation for
Surgery), and BRUISECONTROL (Bridge or Continue
Coumadin for Device Surgery Randomized Controlled
Trial), randomized trials comparing bridging with no
bridging strategies in warfarin-treated patients who require
elective surgery, are ongoing.
1517
These ongoing studies
are designed to answer relevant questions on periproce-
dural anticoagulation in specific settings using specific
regimes. Moreover, they will evaluate periprocedural
bridging using clearly defined efficacy and safety end
points.
BRIDGE is a prospective randomized, double-blinded study
which aims to recruit 3600 patients with atrial fibrillation/
flutter and a major risk factor for thromboembolism who require
elective surgery or invasive procedure necessitating interruption
of their oral anticoagulant therapy.
16
Patients will be random-
ized perioperatively to receive either subcutaneous dalteparin
or placebo, and primary end points include arterial thrombo-
Chronic oral anticoagulation
VKA
New OAC
Assessing thrombotic
risk
low Non low
Pre-operative:
- no bridgning
Post-operative:
- restart warfarin when
feasible
Pre-operative:
- LMWH when INR subtherapeutic
- therapeutic dose/12h if MHV
- therapeutic dose daily if AF/VTE
- half dose 1 day prior
Post-operative:
- restart warfarin when feasible
- delay LMWH restart 48h
Elective procedure scheduled
Assess creatinine
clearance
<50mL/min
50mL/min
prior
prior
Pre-operative:
- no bridging therapy needed
- if high bleeding risk procedure, check
haemostasis on morning of procedure
Post-operative:
- re-assess creatinine
clearance
- delay restart 48h
Figure. Bridging algorithm for vitamin K antagonists and new oral anticoagulants. Adapted from Wysokinski et al.
8
AF indicates atrial
brillation; INR, International Normalized Ratio; LMWH, low-molecular-weight heparin; MHV, mechanic heart valve; OAC, oral anticoag-
ulants; VKA, vitamin K antagonist; and VTE, venous thromboembolism.
1574 Circulation September 25, 2012
by guest on August 15, 2013 http://circ.ahajournals.org/ Downloaded from
?
En pacientes con depuracin de Cr < 30 se prefiere la HNF.
Protocolo con HBPM:
Suspender warfarina 5 das antes del procedimiento de alto riesgo.
En pacientes con nuevos anticoagulantes iniciar 12 horas luego de la ltima dosis.
Iniciar HBPM cuando el INR est por debajo del rango teraputico:
Vlvulas mecnicas o FA ! Enoxa 1mg/kg o Dalte 100U/kg cada 12 horas.
TEV !1.5mg/kg o Dalte 200U/kg cada 24 horas.
24 h antes del
procedimiento }
TERAPIA PUENTE
Transfusion 2012;52:Suppl 1: 45S-55S
Chest 2012;141:2 Suppl:e326S- e350S

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Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

HNF
Vida $ IV ! 60 - 90 min.
Suspender 4 - 6 h antes de procedimientos de alto riesgo.
HBPM
Vida $ 4 horas.
Suspender 24 horas antes del procedimiento.

Heparinas
Chest 2012;141:2 Suppl:e326S- e350S

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Csar Hernndez, MD.

ASA
Dosis bajas solas ! no aumento importante del riesgo de sangrado.
Cilostazol
No aumento del riesgo cuando se usa solo.

Antiplaquetarios
N Engl J Med 2013;368:2113-24.

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ASA 7 das
Cilostazol 2 das
Inhibidores P2Y
12
Clopidogrel o ticagrelor 5 das.
Prasugrel 7 das.
Antiplaquetarios

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Csar Hernndez, MD.

Thrombosis and Haemostasis 105.5/2011
743 Schattauer 2011 Consensus Document
Peri-operative management of antiplatelet therapy in patients
with coronary artery disease
Joint position paper by members of the working group on Perioperative Haemostasis of the
Society on Thrombosis and Haemostasis Research (GTH), the working group on Perioperative
Coagulation of the Austrian Society for Anesthesiology, Resuscitation and Intensive Care
(GARI) and the Working Group Thrombosis of the European Society for Cardiology (ESC)
Wolfgang Korte
1
; Marco Cattaneo
2
; Pierre-Guy Chassot
3
; Sabine Eichinger
4
; Christian von Heymann
5
; Niklaus Hofmann
6
;
Hans Rickli
7
; Michael Spannagl
8
; Bernhard Ziegler
9
; Freek Verheugt
10
; Kurt Huber
11

1
Center for Laboratory Medicine, Kantonsspital St. Gallen, Switzerland;
2
Medicina 3, Ospedale San Paolo, Department of Medicine, Surgery and Dentistry,
Universit degli Studi di Milano, Milan, Italy;
3
Departement of Anesthesiology, University Hospital Lausanne, Switzerland;
4
Department of Medicine I, Division of Hematology,
Medical University of Vienna, Austria;
5
Department of Anesthesiology and Intensive Care, Charit-Universittsmedizin Berlin, Germany;
6
Department of Anesthesiology,
Diakonissen-Krankenhaus Salzburg, Austria;
7
Division of Cardiology, Kantonsspital St. Gallen, Switzerland;
8
Division of Haemostaseology, University of Munich, Germany;
9
Department of Anesthesiology, Landeskliniken Salzburg, Austria;
10
Department of Cardiology, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands;
11
3
rd
Medical
Department, Cardiology and Emergency Medicine, Wilhelminenspital, Vienna, Austria
Summary
An increasing number of patients suffering from cardiovascular dis-
ease, especially coronary artery disease (CAD), are treated with aspirin
and/or clopidogrel for the prevention of major adverse events. Unfor-
tunately, there are no specific, widely accepted recommendations for
the perioperative management of patients receiving antiplatelet ther-
apy. Therefore, members of the Perioperative Haemostasis Group of the
Society on Thrombosis and Haemostasis Research (GTH), the Perioper-
ative Coagulation Group of the Austrian Society for Anesthesiology,
Reanimation and Intensive Care (GARI) and the Working Group
Thrombosis of the European Society of Cardiology (ESC) have created
this consensus position paper to provide clear recommendations on the
perioperative use of anti-platelet agents (specifically with semi-urgent
and urgent surgery), strongly supporting a multidisciplinary approach
to optimize the treatment of individual patients with coronary artery
disease who need major cardiac and non-cardiac surgery. With planned
Correspondence to:
PD Dr. Wolfgang Korte
Center for Laboratory Medicine
Kantonsspital St. Gallen
CH-9007 St. Gallen, Switzerland
Tel.: +41 71 494 39 33, Fax: +41 71 494 39 00
E-mail: wolfgang.korte@ikch.ch
surgery, drug eluting stents (DES) should not be used unless surgery can
be delayed for 12 months after DES implantation. If surgery cannot be
delayed, surgical revascularisation, bare-metal stents or pure balloon
angioplasty should be considered. During ongoing antiplatelet therapy,
elective surgery should be delayed for the recommended duration of
treatment. In patients with semi-urgent surgery, the decision to pre-
maturely stop one or both antiplatelet agents (at least 5 days pre-oper-
atively) has to be taken after multidisciplinary consultation, evaluating
the individual thrombotic and bleeding risk. Urgently needed surgery
has to take place under full antiplatelet therapy despite the increased
bleeding risk. A multidisciplinary approach for optimal antithrombotic
and haemostatic patient management is thus mandatory.
Keywords
Antiplatelet agents, surgery, atherothrombosis, coronary syndrome,
atherosclerosis
Financial support:
The meeting that allowed this manuscript to be formulated was supported by sanofi
aventis (suisse) sa (a manufacturer of clopidogrel and enoxaparin). However, sanofi
aventis had no influence whatsoever on the contents of this mansucript.

Received: April 7, 2010
Accepted after major revision: January 28, 2011
Prepublished online: March 24, 2011
doi:10.1160/TH10-04-0217
Thromb Haemost 2011; 105: 743749
Introduction
An increasing number of patients who are suffering from or are at
risk for cardiovascular disease, especially coronary artery disease
(CAD), is treated with aspirin or clopidogrel for the prevention of
major adverse events. In congruence, the number of patients that
receive percutaneous coronary intervention (PCI) with stent im-
plantation continues to increase and therefore, the need for treat-
ment with dual antiplatelet therapy (usually aspirin plus clopido-
grel) is also augmented. In addition, an increased use of new and
possibly more effective antiplatelet agents, e.g. prasugrel or ticagre-
lor, can be expected in the near future (1, 2). At present, 68% of
patients with dual antiplatelet therapy also need oral anticoagu-
lation with vitamin K antagonists (VKA) due to atrial fibrillation,
mechanical heart valves or a history of venous thromboembolism.
Given these facts, physicians nowadays face situations in which the
peri-operative bleeding risk has to be balanced against the individ-
ual risk of thrombotic complications. Although the pathophysiol-
For personal or educational use only. No other uses without permission. All rights reserved.
Downloaded from www.thrombosis-online.com on 2013-07-08 | IP: 190.29.20.198
Qx menor: No suspender TAP.
HBPM: No son tiles para la inhibicin plaquetaria.
Qx mayor y Que hacer Excepciones Que hacer
ASA para
prevencin primaria
Suspender ASA 5 d
antes de la ciruga
ASA en pacientes
de alto riesgo
Continuar ASA
Qx en espacios
cerrados o alto
riesgo de sangrado
Suspender ASA 5 d antes de
la ciruga.
Considerar el reinicio a las
24 horas.
ASA + Clopidogrel
en pacientes de
alto riesgo
1. Qx electiva: Aplazar.
2. Qx semi urgente: contine
ASA Clopidogrel segn
sea el caso.
3. Qx urgente (24 horas):
Contine ASA y
clopidogrel.
Qx en espacios
cerrados o alto
riesgo de sangrado
Si no es posible aplazar la Qx /
Qx semi urgente:
1. Suspender el clopidogrel 5 d
antes.
2. Considerar continuar ASA.
3. Considerar reinicio de TAPD
lo antes posible.
Thromb Haemost 2011; 105: 743749
Determinante del riesgo de sangrado postQx.
Profilaxis ! reiniciar una vez se garantice la hemostasia.
Heparina ! reiniciar a las 24 - 48 horas.
Warfarina ! reiniciar al da siguiente del procedimiento.
Dabigatran, rivarixaban o apixaban ! reiniciar a las 48 horas luego de

procedimientos de alto riesgo de sangrado.
Clopidogrel ! 24 h luego del procedimiento.

CUNDO REINICIAR LOS
ANTITROMBTICOS?
N Engl J Med 2013;368:2113-24.

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.

Procedimiento
de bajo riesgo
de sangrado
Warfarina TAPD
Continuar Continuar
Bajo riesgo
tromboembl
Suspender
warfarina
Reiniciar al otro
da del
procedimiento.
Medir INR a la
semana.
Procedimiento
de alto riesgo de
sangrado
Warfarina TAPD
Alto riesgo
tromboembl
Bajo riesgo
tromboembl
Alto riesgo
tromboembl
Terapia
puente
Suspender
clopidogrel 5
das antes.
Continuar ASA.
Considerar
suspender
clopidogrel y/o
ASA 5 das
antes.
Considerar
Terapia puente.
EN RESUMEN...

Informes:

PROGRAMACIN

2013.

Plaza Mayor Medelln
14,15 y 16 de Agosto de 2013


Salones 5 y 6

Simposio:

lvaro Escobar, MD.
Diego Velsquez, MD.
Csar Hernndez, MD.
Ivn Rendn, MD.


paciente?
Csar Hernndez, MD.


Manejo de La Terapia Antitrombotica

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Manejo de La Terapia Antitrombotica

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Juan Carlos Uribe O.

Poblacin anticoagulada en aumento.

TAPD por SCA y stents ! en aumento.

10% - 20% ! Qx o procedimientos invasivos que requieren la suspensin temporal.

Meta ! minimizar eventos tromboemblicos y hemorragias mayores peri

Cundo suspender y reiniciar la terapia antitrombtica.

Depende principalmente del tipo de procedimiento.

Factores de riesgo asociados al paciente:

Efecto residual de los antitrombticos.

Cncer activo o QxTx.

Alto riesgo ! riesgo > 1.5%.

Procedimientos intracraneales, intraespinales, cmara posterior del ojo,

Alto riesgo ! riesgo > 1.5%.

Procedimientos intracraneales, intraespinales, cmara posterior del ojo,

Alto riesgo ! riesgo > 1.5%.

Procedimientos intracraneales, intraespinales, cmara posterior del ojo,

Alto riesgo ! riesgo > 1.5%.

Procedimientos intracraneales, intraespinales, cmara posterior del ojo,

Alto riesgo ! riesgo > 1.5%.

Procedimientos intracraneales, intraespinales, cmara posterior del ojo,

Riesgo de sangrado bajo con INR 2 - 3.

Realizar INR 24 h previo al procedimiento.

Uso de surgicel, esponjas de colgeno y

Enjuages con Ac tranexmico al 5%.

No prescribir AINEs o COX-2.

Riesgo de sangrado bajo con INR 2 - 3.

Realizar INR 24 h previo al procedimiento.

Uso de surgicel, esponjas de colgeno y

Enjuages con Ac tranexmico al 5%.

No prescribir AINEs o COX-2.

Riesgo de sangrado bajo con INR 2 - 3.

Realizar INR 24 h previo al procedimiento.

Uso de surgicel, esponjas de colgeno y

Enjuages con Ac tranexmico al 5%.

No prescribir AINEs o COX-2.

Riesgo de sangrado bajo con INR 2 - 3.

Realizar INR 24 h previo al procedimiento.

Uso de surgicel, esponjas de colgeno y

Enjuages con Ac tranexmico al 5%.

No prescribir AINEs o COX-2.

Continuar terapia antitromboemblica.

Riesgo de sangrado bajo con INR 2 - 3.

Realizar INR 24 h previo al procedimiento.

Anestesia local y/o sub tenoniana.

Riesgo extrapolado segn CHADS

Riesgo depende de:

Tipo de vlvulas, nmero, localizacin.

Patologas asociadas: FA, falla cardaca, historia de tromboembolismo o

En TEV mayor riesgo dentro de los primeros 3 meses.

Suspensi n premat ura ! ri esgo de

Muerte e infarto ! 75%.

Stents convencionales mayor riesgo en las

DES mayor riesgo en los primeros 6 meses.

SCA terapia antiplaquetaria dual al menos 1

Suspensi n premat ura ! ri esgo de

Muerte e infarto ! 75%.

Stents convencionales mayor riesgo en las

DES mayor riesgo en los primeros 6 meses.

SCA terapia antiplaquetaria dual al menos 1

En pacientes de alto riesgo de sangrado.

Intervalo sin terapia anticoagulante lo mas corto posible.

Considerar otros factores sobre la duracin del efecto anticoagulante:

Falla renal ! dabigatran, rivaroxaban, apixaban, HBPM.

Falla heptica ! warfarina, rivaroxaban y apixaban.