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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3865_Библиотеки_им_академика_М_И_Перельмана
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350 Anticoagulation Therapy
https://t.me/med1917
VASc=0
2
DS
2
Oming
CHA
anthromboc
therapy is reasonable
VASc=1
2
DS
Minimal
CCB, BB, or digoxin
Control ventricular rate with
Yes
Symptoms?
than 48 hours
AF present for more
No
syncope)
failure, hypotension,
Severe (angina, heart
Cardioversion without prolonged ancoagulaon
(therapeuc IV UFH, LMWH or DOAC suggested at
presentaon if no contraindicaon to ancoagulaon)
maintained
DOAC suggested as soon as possible)
Follow with at least 4 weeks of therapeuc ancoagulaon if NSR
Emergency electrical cardioversion (therapeuc IV UFH, LMWH or
Rate control
(reasonable for older paents with persistent AF and stroke risk factors)
Rhythm control
symptomac despite adequate rate control)
(reasonable for younger paents with paroxysmal AF or who remain
Stroke risk?
Warfarin (INR 2-3) or DOAC
Screening TEE plus
immediate therapeuc
ancoagulaon with IV UFH,
2
CHA
VASc >1
2
DS
2
or CHA
Prior stroke/TIA/systemic
embolism or mitral stenosis
No
cardioversion
for at least 3 weeks
Electric or pharmacologic
No
seen?
Thrombus
LMWH or DOAC
Or
Oming
ASA alone
2-3) or DOAC
ASA + clopidogrel or
Chronic warfarin (INR
2-3) or DOAC
Chronic warfarin (INR
Yes
NSR?
Yes
cardioversion)
aempng later
(repeat TEE prior to
Postpone cardioversion
anthromboc
therapy is reasonable
IV=intravenous; UFH=unfraconated heparin; LMWH=low-molecular weight heparin;
NSR=normal sinus rhythm; CCB=calcium channel blocker (non-dihydropyridine); BB=beta
blocker; TEE=transesophageal echocardiogram; INR=internaonal normalized rao;
TIA=transient ischemic aack; ASA=aspirin; DOAC=direct oral ancoagulant
Yes
2-3) or DOAC
Chronic warfarin (INR
factors?
Stroke risk
No
Warfarin (INR 2-3) or
DOAC for at least 4 weeks
Warfarin (INR 2-3) or DOAC
FIGURE 14-1. Stroke Prevention in Atrial Fibrillation Treatment
Algorithm
ATRIAL FIBRILLATION 351
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Therefore, various risk stratification schemes have evolved with the
following goals:
Identifying AF patients at such low risk of stroke that anticoagulation
therapy-associated bleeding risk may outweigh stroke prevention
benefit.
Encouraging anticoagulation therapy use in AF patients at high risk
for stroke where benefit has been clearly demonstrated.
•
The CHADS2 score, which is well validated and easy to use, is the nonvalvular AF
stroke risk stratification tool used for recommendations of the 9th ed., American
College of Chest Physicians Evidence-Based Clinical Practice Guidelines (AT9).
Risk Factor Points
Congestive heart failure
Hypertension
b
Age ≥75 years of age = 1
c
Diabetes
Prior stroke/TIA/systemic embolus
a
Signs/symptoms of heart failure confirmed with objective evidence of cardiac dysfunction.
b
Resting BP >140/90 mmHg on at least 2 occasions or current antihypertensive pharmacologic
treatment.
c
Fasting glucose >125 mg/dL or treatment with oral hypoglycemic agent and/or insulin.
d
Includes any history of cerebral ischemia.
a
= 1
= 1
= 1
d
= 2
2
Example: An 82-year-old male with hypertension and prior stroke would
have a CHADS2 score = 4.
352 Anticoagulation Therapy
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Higher CHADS2 score = higher AF stroke risk
CHADS2 Score Stroke
Rate (%/
year)
0 1.9 No therapy is suggested rather than antithrombotic therapy
1 2.8 Warfarin (INR 2–3) or DOAC is recommended rather than
2 4 Warfarin (INR 2–3) or DOAC is recommended rather than no
3 5.9
4 8.5
5 12.5
6 18.2
AT9 Recommendations for Antithrombotic Therapy
(Grade 2B)
For patients choosing antithrombotic therapy, aspirin (75
mg–325 mg once daily) is suggested rather than warfarin (INR
2–3) or DOAC (Grade 2B) or combination therapy with aspirin
and clopidogrel (Grade 2B)
no therapy (Grade 1B) or aspirin (75 mg–325 mg once daily)
(Grade 2B) or combination therapy with aspirin and clopidogrel
(Grade 2B)
For patients unsuitable for or choosing not to take warfarin or
DOAC (for reasons other than concerns about major bleeding),
combination therapy with aspirin and clopidogrel is suggested
rather than aspirin (75 mg–325 mg once daily) (Grade 2B)
therapy (Grade 1A), aspirin (75 mg– 325 mg once daily) (Grade
1B), or combination therapy with aspirin and clopidogrel
(Grade 1B)
For patients unsuitable for or choosing not to take warfarin
or DOAC (for reasons other than concerns about major
bleeding), combination therapy with aspirin and clopidogrel
is recommended rather than aspirin (75–325 mg once daily)
(Grade 1B)
8
2
Grade 1A: strong recommendation, high-quality evidence; Grade 1B: strong recommendation,
moderate-quality evidence; Grade 2B: weak recommendation, moderate-quality evidence; Grade
2C: weak recommendation, low- or very low-quality evidence
•
A revised scoring approach (CHA2DS2-VASc) is the nonvalvular AF stroke risk
stratification tool used in recommendations from 2014 AHA/ACC/HRS Guideline
for the Management of Patients with Atrial Fibrillation: A Report of the Ameri
can College of Cardiology/American Heart Association Task Force on Practice
Guidelines and the Heart Rhythm Society.
-
1
ATRIAL FIBRILLATION 353
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Stroke Risk Factor Points
Congestive heart failure
Hypertension
b
a
= 1
= 1
Age ≥75 years of age = 2
c
Diabetes
Prior stroke/TIA/systemic embolus
Vascular disease
e
d
= 1
= 2
= 1
Age 65–74 = 1
Sex category (female) = 1
a
Signs/symptoms of heart failure confirmed with objective evidence of cardiac dysfunction.
b
Resting BP >140/90 mmHg on at least 2 occasions or current antihypertensive pharmacologic
treatment.
c
Fasting glucose >125 mg/dL or treatment with oral hypoglycemic agent and/or insulin.
d
Includes any history of cerebral ischemia, peripheral arterial embolism, or pulmonary embolism.
e
Prior myocardial infarction, peripheral artery disease, or aortic plaque.
The CHA2DS2-VASc identifies a lower risk population; the impact of the
approach over the CHADS2 has not been determined.
CHA2DS2-VASc
Score
Stroke Rate
(%/year)
AT9 Recommendations for Antithrombotic Therapy
2
0 0 Reasonable to omit antithrombotic therapy (Class IIa: B)
1 1.3 No antithrombotic therapy or treatment with warfarin (INR
2–3), or DOAC or aspirin may be considered (Class IIb: C)
2 2.2 Warfarin (INR 2–3) (Class I:A) or DOAC (Class I:B)
3 3.2
4 4
5 6.7
6 9.8
7 9.6
8 6.7
9 15.2
354 Anticoagulation Therapy
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Class I: A = recommendation that treatment is useful/effective, evidence from multiple
randomized trials; Class I: B = recommendation that treatment is useful/effective, evidence from
single randomized trial; Class IIa: B = recommendation in favor of treatment, some conflicting
evidence from single randomized trial or nonrandomized studies; Class IIb: C = recommendation’s
usefulness/efficacy less well established, only diverging expert opinion, case studies, or standard
of care.
•
Echocardiography is often used in treatment decision-making but has limited
proven value in determining the need for chronic oral anticoagulation therapy.
Echocardiography can detect the presence of features associ-
ated with thromboembolism. Anticoagulation therapy in patients
with these features has been shown to reduce stroke risk (e.g.,
impaired left ventricular systolic function, left atrial thrombus,
dense spontaneous echo contrast, “smoke,” or reduced velocity of
blood flow in the left atrial appendage); however, the absence of
these echocardiographic abnormalities has not been established as
identifying a low-risk group of AF patients who could safely forgo
warfarin therapy.
Echocardiography is valuable for detecting rheumatic mitral valve
1
disease (there is universal agreement that these patients should
receive warfarin therapy).
Detection of left atrial thrombus is a contraindication for cardiover-
1
sion of AF (see below).
Transesophageal echocardiography (TEE) is the most sensitive and
specific technique to detect left atrial (LA) thrombi as a potential
source of systemic embolism in AF and can be used to guide the
timing of cardioversion or catheter ablation procedures.
•
Risk stratification caveats
CHADS
nonvalvular AF.
No published risk stratification tool is ideal, and all can frequently
underestimate stroke risk.
Although risk stratification tools identify AF patients who will likely
and CHA2DS2-VASc are appropriate only for patients with
2
9
1
benefit most and least from warfarin therapy, the stroke versus
bleeding risk tipping point for anticoagulation therapy use is
controversial, especially for those at intermediate risk for stroke.
Use of CHADS
renal disease on dialysis is controversial.
No tool can incorporate all potential AF stroke risk factors. Risk
and CHA2DS2-VASc for patients with end-stage
2
stratification tools can, therefore, best be described as “rough
guides” to help inform clinicians.
Although bleeding risk stratification tools exist (e.g., HAS-BLED),
9
they are rarely used in clinical practice because many clinicians
error toward preventing cardioembolic stroke at the expense of
bleeding as it is more often fatal or severely debilitating compared
ATRIAL FIBRILLATION 355
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to most types of bleeding, with the exception of intracranial hemorrhage (ICH).
Patient perspectives and preferences should also factor into clinical
decision making.
10
1
Optimal Intensity of Warfarin Anticoagulation for AF
•
Optimal warfarin therapy intensity involves a careful balancing between maximizing protection against thromboembolism while minimizing bleeding risk (ICH in
particular rivals ischemic stroke in terms of clinical importance).
The risk of ischemic stroke is low at INR levels ≥2.
An INR >3.5 at ICH presentation doubles the risk for fatal ICH.
An INR of <2 at admission for a new stroke substantially increases
the likelihood of death and severe disability from AF-related
12
stroke.
There is virtually no evidence supporting a decreased risk of ICH
at INR levels <2.
•
Strong evidence supports the recommended INR target of 2.5 (range 2–3).
Narrower target ranges have been suggested in certain situations
10
(e.g., INR 2–2.5 has been recommended in patients requiring
warfarin, aspirin, and clopidogrel following percutaneous coronary
intervention).
13
Such narrow ranges are not supported by good
evidence, which makes achieving therapeutic INRs more difficult
and usually results in the need for more frequent INR testing.
Target INR range 2–3 should be used for most patients with AF.
10
11
10
Stroke Prevention Considerations During Cardioversion
•
Systemic embolism can complicate cardioversion whether NSR is reestablished
by electrical, pharmacologic, or spontaneous means (see Figure 14-2).
•
Conversion of AF to NSR, regardless of method, results in transient mechanical
dysfunction of the left atrium (“stunning”).
Recovery of mechanical function occurs over a period of days to
Thromboembolism after cardioversion can be due to migration
•
Although at least 4 weeks of warfarin (INR 2–3) or DOAC therapy is recommended
following successful cardioversion, patients with risk factors for thromboembo
lism should continue anticoagulation beyond 4 weeks unless there is convincing
evidence that NSR is maintained.
•
DOACs have been shown to be effective and safe to use prior to cardioversion—shocks can be delivered at any time during the dosing interval.
•
There are no randomized clinical trials to guide anticoagulation for emergency
cardioversion. Expert opinion suggests that hemodynamically unstable patients
requiring emergency cardioversion should receive therapeutic anticoagulation
1
weeks (depending in part on duration of AF prior to conversion).
of thrombi formed prior to cardioversion or to the formation and
subsequent migration of thrombi formed while atrial function is still
depressed in the period following cardioversion.
1
-
1
356 Anticoagulation Therapy
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No
DOAC
vs.
DOAC?
Warfarin
Warfarin (INR 2-3)
IV=intravenous; UFH=unfraconated heparin; LMWH=low-molecular weight heparin;
rao; DOAC=direct oral ancoagulant
NSR=normal sinus rhythm; TEE=transesophageal echocardiogram; INR=internaonal normalized
Convenonal
Elecve
planned
cardioversion
vs. TEE
guided?
Convenonal
TEE guided
weeks?
No missed
doses for 3
maintained
for 3
weeks?
INR ≥2.0
Warfarin (INR 2-3) or DOAC indefinitely
No
Yes
No
Yes
Aempt
cardioversion
No
successful?
Cardioversion
convincing evidence that NSR is
Chronic warfarin (INR 2-3) or DOAC unless
Yes
factors?
Stroke risk
No
FIGURE 14-2. Anticoagulation Therapy for Elective
Cardioversion Treatment Algorithm
Yes
seen?
Perform TEE
Thrombus
Postpone cardioversion, connue
before aempng later cardioversion
warfarin (INR 2-3) or DOAC , repeat TTE
weeks
Warfarin (INR 2-3) or DOAC for at least 4
ATRIAL FIBRILLATION 357
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with either intravenous (IV) unfractionated heparin (UFH), low molecular weight
heparin (LMWH), or DOAC therapy started as soon as possible, followed by at
least 4 weeks of warfarin (INR 2–3) or DOAC therapy.
The optimal strategy for initiating warfarin once patients are
1
hemodynamically stable is not known.
Bridging with UFH or LMWH during initiation of warfarin in patients
with AF has been shown to increase the risk of bleeding without
the benefit of preventing stroke.
The optimal intensity for heparin or dose of a LMWH has not been
14
assessed in clinical trials. Higher doses (e.g., similar to doses used
for venous thromboembolism [VTE] treatment or acute coronary
syndrome [ACS] treatment) have evolved out of the high concern
for a stroke, yet evidence supporting this strategy as a bridge to
warfarin therapy is currently limited.
Most stable patients do not require cross-coverage with parenteral
anticoagulants (bridge therapy).
Electrical versus Pharmacologic Cardioversion,
Implications for Anticoagulation Therapy
•
Anticoagulation therapy recommendations are similar for electrical and pharmacologic cardioversion.
•
Amiodarone is commonly used to maintain NSR in AF patients following
successful cardioversion and presents unique challenges for patients on warfarin
therapy.
15
Amiodarone inhibits the metabolism of warfarin leading to the
potential for excessive anticoagulation and increased bleeding risk.
Amiodarone may take hundreds of days to reach steady state due
to its very long half-life.
Co-administration of warfarin and amiodarone requires vigilant
INR monitoring (at least weekly for several weeks and as needed
thereafter). Some have advocated empiric warfarin dose reductions
(35–65%) when amiodarone is added to ongoing warfarin there-
15
apy;
however, optimal timing of empiric dose reductions are
challenging since the clinical onset of the interaction is often
delayed and becomes more significant over time
NONPHARMACOLOGIC PREVENTION OF AF
STROKE
•
Obliteration of the left atrial appendage (LAA) by direct surgical truncation,
amputation, or closure devices inserted into the LAA (e.g., WATCHMAN device)
are emerging second-line options for patients who are not suitable candidates
for chronic anticoagulation therapy.
After 3.8 years of follow-up, percutaneous LAA closure with the
1
WATCHMAN device met criteria for both noninferiority and superi
-
ority, compared with warfarin alone (INR 2–3), for preventing the
358 Anticoagulation Therapy
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combined outcome of stroke, systemic embolism, and cardiovascular death, as well as superiority for cardiovascular and mortality
from all causes.
Following implantation of the WATCHMAN device, antithrombotic
16
medication is required to allow endothelialization of the device
surface.
Continue warfarin for at least 45 days.
If device stability, flow leaks around the margins of the
filter, and thrombus formation are deemed satisfactory,
discontinue warfarin and substitute clopidogrel 75 mg/
day plus aspirin 81–325 mg/day until 6 months after
device implantation.
After 6 months, discontinue clopidogrel and continue
with aspirin alone.
FDA approved the WATCHMAN device in 2015.
Surgical-based procedures to exclude the LAA during cardiac
surgery are controversial because of the inconsistency of surgical
techniques, the highly variable rates of successful LAA occlusion/
closure, and the unknown impact of LAA occlusion/closure on
future, thromboembolic events.
1
Because of the risk for incomplete LAA occlusion/closure and subsequent thrombus formation,
anticoagulation therapy should probably be continued following
surgical LAA ligation unless contraindicated and occlusion/closure
of the LAA is confirmed via TEE.
The Lariat snare device has also been used for the exclusion of the
1
LAA but has not been evaluated in clinical trials specifically for this
indication, so there is no way to know if the device is safe or if it
prevents stroke.
•
Other nonpharmacologic measures aimed at restoring NSR, including the surgi-
17
cal Maze procedure and various catheter ablation techniques, are playing an
increasing role in AF management.
The current version of the Maze procedure involves cryotherapy
or bipolar radiofrequency ablation in the atria along with the
amputation of both atrial appendages to prevent the occurrence
of AF and restores NSR in over 90% of patients. The procedure
can be done in conjunction with other surgical procedures, such
as cardiac valve replacement or independently through a small
incision to access the atria.
The VATS/MAZE procedure is a video-assisted approach similar
1
to catheter-directed ablation; however, lines are drawn instead
of pinpoints
The primary indication for catheter AF ablation is the presence
of symptomatic AF refractory to or intolerant of antiarrhythmic
medication.
Ablation involves placing a catheter into the left atrium and either
1
using a heating or freezing technique to tissues surrounding the
ATRIAL FIBRILLATION 359
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pulmonary veins to disrupt their electrical conduction by blocking
or destroying abnormal electrical pathways and/or ectopic foci.
AF recurrence rates with catheter ablation are high and
may be asymptomatic, even among previously symptom
atic patients.
18
The procedure may need to be repeated
-
to fully ablate conduction.
AF patients with stroke risk factors should continue warfarin therapy
for a prolonged period after surgery or ablation procedures.
The Heart Rhythm Society/European Hearth Rhythm Association/
18
European Cardiac Arrhythmia Society Expert Consensus Statement
on Catheter and Surgical Ablation of Atrial Fibrillation makes the
following recommendations regarding anticoagulation therapy
during ablation procedures:
Recommendations regarding anticoagulation at the time
18
of cardioversion apply to patients who are in AF at the
time of the ablation procedure.
If adequate systemic anticoagulation has not been
maintained for at least 3 weeks prior to the AF ablation
procedure, a pre-ablation TEE should be performed
in all patients with AF >48 hours in duration or of an
unknown duration.
The presence of a left atrial thrombus is a contraindica-
tion to AF catheter ablation.
Performance of a TEE in patients in NSR or who have
been in AF for 48 hours or less prior to AF ablation may
be considered but is not mandatory.
Continuing therapeutic anticoagulation with warfarin
during performance of catheter ablation of AF should
be considered. Because of concerns for procedurerelated bleeding, including transeptal perforations, use
of DOACs has not been widely considered.
During AF ablation, UFH adjusted to achieve and
maintain an activated clotting time (ACT – low range)
of 300–400 seconds should be administered prior to or
immediately following transseptal puncture regardless
of whether the patient is anticoagulated with warfarin.
Administration of protamine following ablation to reverse
heparin should be considered.
Patients who are not therapeutically anticoagulated with
warfarin at the time of AF ablation should be bridged
with LMWH (a reduction of the dose to 0.5 mg/kg should
be considered to reduce bleeding risk) or IV UFH during
resumption of warfarin. Alternatively DOAC initiation
may be considered as a post-ablation anticoagulation
strategy.
Warfarin (INR 2–3) or DOAC is recommended for at least
2 months following an AF ablation procedure (consider
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