Investigations cardiaques et AVC-AIT

Investigations cardiaques et AVC-AIT
Jean-Martin Boulanger
Neurologue Hôpital Charles-Lemoyne
Septembre 2014
BI, Sanofi-Aventis,
BMS, Roche, Bayer,
Novartis, Solvay,
Allergan, Merz,
Octa-Pharma,
Servier
Objectifs-Plan
!  Savoir rechercher de façon optimale les
anomalies structurales emboligènes du
cœur et de l’aorte;
!  Déterminer l’investigation optimale des
arythmies cardiaques emboligènes en post
AVC- AIT;
!  Définir le type de patients susceptible de
bénéficier d’une investigation cardiaque en
post AVC-ICT.
Étiologie des AVC et ICT
25%
30%
15%
20%
Autres 10%
70%
Investigations cardiaques post
AVC-ICT
Cas clinique
!  Homme 82 ans
!  Épisode transitoire
d’aphasie
!  AP: HTA-MCAS –AVC
cérébelleux
!  IRM
!  Ancien AVC cérébelleux
!  Pluie de lésions DWI
territoire ACM gauche
!  Doppler -, ECG – , ETT N…
Questions?
!  Indice de « cardioembolicité » d’un AVC-ICT?
!  Utilité de l’échographie cardiaque?
!  ETT vs ETO?
!  Utilité des ECG sériés vs holter vs monitoring?
!  Rôle de l’enregistrement prolongé?
Bof…
Étude Framingham
Risque attribuable d AVC 30 Prévalence de FA Pourcentage (%) AVC aAribuables à la FA 20 10 0 50–59 60–69 70–79 Groupes d’âge (ans) Wolf PA, et al. Stroke 1991;22:983-988.
80–89 Troponin Elevation Predicts Atrial Fibrillation in Patients
with Stroke or Transient Ischemic Attack
Isabelle Beaulieu-Boire, MD,* Nancy Leblanc, MSc,† L!eo Berger, MD, FRCPC,†
and Jean-Martin Boulanger, MD, FRCPC†
Background: Atrial fibrillation (AF) is a major cause of ischemic stroke. Cardiac troponin (cTnI) is a marker of myocardial damage and may predict arrhythmia.I.We
BEAULIEU-BOIRE ET AL.
sought to determine if increased cTnI levels were a predictor of new-onset AF in
Table
2.stroke
Atrialorfibrillation
ontransient
electrocardiogram
or(TIA).
Holter
monitoring
Methods:
Consecuischemic
patients with
ischemic attack
tive patients who presented to Charles-Lemoyne Hospital between October 2006
and November 2010 with a diagnosis
of acute
ischemic stroke or TIA,Elevated
without atroponin,
hisNormal
troponin,
tory of AF, with a baseline measurement
of
cTnI
were
included
in
the
study.
The
#0.03 ug/L (n 5 362)
.0.03 ug/Lpri(n 5 46)
P value
mary outcome was new-onset AF on 24-hour Holter measurement within 1 week of
admission in patients without AF on the baseline electrocardiogram (ECG). SecondNew-onset AF on 24-hour Holter,
% (n)*
4.8 (12/250)
21.4 (6/28)
.0028
ary outcomes included AF on Holter measurement, death, myocardial infarction
AF on baseline ECG, % (n) (MI), and stroke within 3 months. Results:
6.4 (23/362)
21.7
(10/46)
.0009
A total of 408 patients were included.
AF on 24-hour Holter, % (n)Forty-six patients (11.3%) had elevated
5.9cTnI
(15/253)
(9/31)
.0001
levels. These patients were29.0
older
and
AF on baseline ECG or 24-hour
(n)
(35/362)
34.7
(16/46)
.0001
had aHolter,
higher %
prevalence
of coronary9.7
artery
disease and diabetes. AF on
baseline
ECG or 24-hour Holter measurement was present in 51 patients (12.5%) and was
more frequent
among patients with increased cTnI levels compared to patients
Abbreviations: AF, atrial fibrillation;
ECG, electrocardiogram.
with
normal
cTnI
(34.7%
vs 9.7%;
*AF on Holter monitoring in patients without AFlevels
on the
baseline
ECG.P 5 .004 multivariate analysis). Elevated
cTnI levels also predicted the composite outcome of stroke, MI, and death at 3
months (50.0% vs 16.1%; P 5 .0001). Conclusions: cTnI elevation predicts newonset AF
on 24-hourwith
Holter
measurementan
in established
patients with cause
acute ischemic
stroke
of stroke.
Nevertheless, it is virtually
The 90-day outcome was good
in patients
normal
or TIA and may indicate a poorer prognosis and a higher risk of stroke, MI, and
impossible to determine if AF is the cause or the effect of
cTnI levels but poor in those with high cTnI levels. In fact,
death at 3 months. Key Words: Acute stroke—atrial fibrillation—cardiac emboli—
theattack.
stroke. It remains possible that the stroke was respon64.0% of those with normal cTnI
levels hadaccident—transient
a mRS score of ischemic
cerebrovascular
! 2012 bywith
National
sible for AF in some cases, because an underlying brain
0 to 2, while only 39.1% of patients
highStroke
cTnIAssociation
levels
4
had a similar outcome (P 5 .002; after multivariate analysis P 5 .016; Table 3). In addition, patients with elevated
cTnI levels were more likely to die (39.1% vs 11.0%; P 5
Atrial fibrillation (AF) is a major cause of ischemic
.0001) and to have a new or recurrent MI (2.2% vs 0.6%;
stroke in adults. The identification of AF is important in
P 5 .035) the
within
3 months
when
compared
to patients
secondary
prevention
of stroke
or transient
ischemic
with normal
cTnI
levels.
Causes
deathmay
were
not from
differattack
(TIA)
because
these of
patients
benefit
antient between
groups;1 vascular
was
responsible
for
coagulation.
Testing fordeath
AF after
a stroke
or TIA usually
85.0% (34/40) and 72.2% (13/18; P 5 .290) of deaths in
From the *Division of Neurology, Centre Hospitalier Universitaire
insult influences the odds of having myocardial injury.
From a practical point of view, most neurologists and cardiologists would still prescribe anticoagulant medications
includes serial electrocardiograms (ECGs) or Holter refor these patients. The risk of myocardial injury may be
cording. Unfortunately, these tests are insensitive, and
higher
in SAHsuggest
than ischemic
stroke;monitoring
as many may
as 31% of
some studies
that prolonged
12
2,3
SAH
patients
hadyield,
elevated
levels
increase
diagnostic
but atcTnI
a higher
cost. in 1 study,
compared
to 12.5%I (cTnI)
in ourand
cohort
andT6%
to 7.8% in other
Cardiac troponin
troponin
are recognized
11,13 and specific markers of cardiac injury.4 Eleas sensitive
cohorts.
Still, there are conflicting results; some
vated levels of troponin have been described in about
Facteurs de risque de FA
Âge (intervalles de 7 ans)* 1,03 (1,00-­‐1,05) Sexe (hommes vs femmes) 1,02 (0,77-­‐1,35) 2,67 (1,57-­‐4,55) ICC* Cardiopathie valvulaire* AVC* 3,27 (2,23-­‐4,81) 1,57 (0,95-­‐2,60) Sténose mitrale* RégurgitaTon aorTque* Diamètre de l oreilleAe gauche* Hypertension* 0 * p < 0,05; IC 95 %
Furberg et al. Am J Cardiol 1994;74:236-241.
4,35 (1,42-­‐13,35) 1,62 (1,15-­‐2,29) 2,69 (2,21-­‐3,27) 1,39(1,05-­‐1,83) 4 8 12 16 In MRI veritas…
! Lacune = <1.5 cm
! Syndromes lacunaires cliniques:
!  59% ont une image lacunaire classique
!  22% ont des lésions dispersées dans un
terrritoire vasculaire ou ont une lésion >1.5cm
!  19% ont plusieurs lésions dans plusieurs
territoires vasculaires
Durée du monitoring cardiaque
Combien de
temps doit-on
enregistrer ce
foutu rythme
cardiaque?
The longer the better…but how much
longer….???
Improved Detection of Silent Atrial Fibrillation Using
72-Hour Holter ECG in Patients With Ischemic Stroke
A Prospective Multicenter Cohort Study
Martin Grond, MD; Marek Jauss, MD; Gerhard Hamann, MD; Erwin Stark, MD;
RolandAtrial
Veltkamp,Fibrillation
MD; Darius Nabavi,
Markus Horn,
MD; Christian
MD;
Improved Detection of Silent
byMD;
72-Hour
Holter
ECG Weimar,3361
Martin Köhrmann, MD; Rolf Wachter, MD; Ludger Rosin, MD; Paulus Kirchhof, MD, FESC
ed
AF Detected
(n=49)
6
76.04±9.181
27
6
0.12±0.484
7
27.177±3.771
14 (28)
29 (59)
9 (18)
5 (55)
7 (78)
155.86±22.1
cumulative rate of detected AF [%]
ory and Clinical
Background and Purpose—Adequate diagnosis of atrial fibrillation (AF), including paroxysmal AF, is an important part
of stroke workup. Prolonged ECG monitoring may improve the detection of paroxysmal, previously undiagnosed AF
(unknown AF). Therefore, we evaluated systematic 72-hour Holter ECG monitoring to detect unknown AF for the workup
6
of patients with stroke.
Methods—Unselected survivors of a stroke or transient ischemic attack (TIA) without known AF were enrolled in a
5
prospective, multicenter cohort study of 72-hour Holter ECG monitoring in 9 German secondary and tertiary stroke
centers between May 2010 and January 2011. In addition to standardized workup of stroke pathogenesis according to the
4
underwent 72-hour Holter ECG monitoring directly after admission. All ECGs
P Value German Stroke Unit protocol, all patients
were centrally analyzed by 2 independent observers. We determined the proportion of unknown AF and compared the
3
<0.0001 detection rates of 72- and 24-hour monitoring.
Results—A total of 1135 patients were enrolled (mean age, 67 years [SD, 13.1 years], 45% women, 29% TIA). Unknown
0.1868 AF was detected in 49 out of 1135 2patients (4.3%, [95% confidence interval, 3.4–5.2%]) by 72-hour ECG monitoring.
Unknown AF was diagnosed in 29 patients
(2.6%) within the first 24 hours of ECG monitoring, and in 20 more patients
1
0.038 only by 72 hours of ECG monitoring.
The number needed to screen by 72-hour ECG was 55 patients (95% confidence
interval [35–123]) for each additional
0 AF diagnosis. Patients with unknown AF were significantly older and had more
often a history of previous stroke. Patients
0 with unknown
24 AF were equally
48 distributed72within categories of pathogenesis
according
to
Trial
of
Org
10172
in
Acute
Stroke
Treatment
(TOAST)
classification. 626
ns
1091
944
Conclusions—In unselected survivors of stroke or TIA, 72-hour ECG monitoring is feasible and improves the detection rate
monitoring time [hours]
0.1766 of silent paroxysmal AF. (Stroke. 2013;44:3357-3364.)
patients at risk [n]
Key Words: anticoagulation ◼ atrial fibrillation ◼ Holter ECG ◼ new oral anticoagulants ◼ secondary prevention
◼ stroke ◼ vitamin K antagonists
Figure 2. Kaplan–Meier survival data analysis of cumulative monitoring time for each patient on the x axis, and risk of
trial fibrillation
is an independent
factorstudy
for
ECG monitoring,
theretime
is an unknown
atrial(AF)
fibrillation
(AF) risk
in the
cohort
at this
point proportion
given of patients
stroke. Survivors of a stroke with AF have a high risk
with stroke in whom the diagnosis of AF is missed (silent,
0.1088
is in percentage on the y axis. Gray
lines indicate the 95%
for recurrent stroke. Oral anticoagulation using vitamin K
undiagnosed paroxysmal AF). Observations from clinical triinterval.
antagonists orconfidence
novel oral anticoagulants
is highly effective for
als in patients with recurrent AF, analyses of atrial rhythm
0.0099
<0.001
A
1
4–6
prevention of stroke in these patients.2
AF is often transient or paroxysmal in nature, and the
0.308correct
diagnosis of AF can be challenging in patients with
paroxysmal AF. Guidelines for the management of stroke
ns patients3 therefore recommend ≥24 hours of ECG monitoring
after stroke to detect paroxysmal AF. Even after 24 hours of
in patients with pacemakers or defibrillators,7,8 and several
single-center studies (Table 1) suggest that AF can be better
detected by prolonged ECG recording using different recording methods such as continuous inpatient cardiac telemetry
(CICT), external loop recorders (ELR), internal loop recorders (ILR), and mobile cardiac outpatient telemetry (MCOT).
evaluation) yielded a correct diagnosis of AF in >90% of
patients, and our detection rates are in line with published
rates (Table 1).
Detection of Atrial Fibrillation With Concurrent Holter
Monitoring and Continuous Cardiac Telemetry Following
Ischemic Stroke and Transient Ischemic Attack
Marc A. Lazzaro, MD,* Kousik Krishnan, MD,† and Shyam Prabhakaran, MD, MS*
ATRIAL FIBRILLATION ON HOLTER MONITORING IN STROKE AND TIA
91
Table 1. Baseline characteristics of the cohort (n 5 133)
Age, years
Atrial fibrillation (AF) is a major risk factor for recurrent ischemic stroke. We aimed to
Mean (SD)
63.1 (13.5)
compare the detection rate of AF using continuous cardiac telemetry (CCT) versus
Median
64.0
Holter monitoring in hospitalized patients with ischemic stroke or transient ischemic
Male, n (%)
66 (49.6)
attack (TIA). Between June 2007 and December 2008, 133 patients were admitted to an
Race, n (%)
academic institution for ischemic stroke or TIA and underwent concurrent inpatient
White
42 (31.6)
CCT and Holter monitoring. Rates of AF detection by CCT and Holter monitoring
Black
76 (57.1)
were compared using the McNemar paired proportion test. Among the 133 patients,
Hispanic
13 (9.8)
8 (6.0%) were diagnosed with new-onset AF. On average, Holter monitoring was perOther
2 (1.5)
formed for 29.8 hours, and CCT was performed for 73.6 hours. The overall rate of AF
Hypertension, n (%)
93 (69.9)
detection was higher for Holter monitoring compared with CCT (6.0%; 95% confiDiabetes, n (%)
39 (29.3)
dence interval [CI], 2.9-11.6 vs 0; 95% CI, 0-3.4; P 5 .008). Holter detection of AF was
Coronary artery disease, n (%)
25 (18.8)
even higher in specific subgroups (those with an embolic infarct pattern, those age
92 n (%)
M.A. LAZZARO ET AL.
Figure 2. Durations and overlap of Holter monitoring and CCT.
Antiplatelet medication use,
55 (41.4)
.65 years, and those with coronary artery disease). Holter monitoring detected AF
Warfarin use, n (%)
in 6% of
ischemic
stroke and
TIA patients,
higherrates
proportions in
Table
2. hospitalized
Comparison
of abnormal
cardiac
rhythm with
detection
Recurrent cryptogenic stroke
3 (2.3)
high-risk subgroups. Compared with CCT, Holter monitoring is significantly more
analyses
(Table
2),
the
rate
of
AF
detection
on
Holter
Deep venous thrombosis
2 (1.5)
likely to detect arrhythmias. Key Words:
Cardiac
monitoring—cardioembolicCCT,
stroke.
monitoring,
monitoring
was
9.3%Association
(95% CI,Holter
4.3-18.3)
in patients with
Mechanical heart valve
1 (0.8)
! 2012
by National
Stroke
n (%) (n
[95%
CI]and 11.5% n (%) [95% CI]
P value
embolic topography ischemic stroke
5 75)
Cardiomyopathy
1 (0.8)
None
127 (93.2)
(95% CI 5.4-22.1) in those age .65 years (n 5 38). The
Cerebrovascular diagnosis, nAF
(%)
rate of NSVT detection was 8.3% (95% CI, 4.5%-14.3%)
Ischemic stroke
and
TIA (n 5 133)
8 (95%
(6.0%)CI,[2.9-11.6]
0 [0-3.4]
.008
Ischemic stroke
101fibrillation
(75.9)
Holter
5.0%
byin
CCT
40% 3.8-8.7)
reduction
the risk of recurrent stroke in patients
Atrial
(AF)by
has
been monitoring
considered and
the most
Ischemic stroke32only
(n 5 101) 5 .180). All patients in whom
7 (6.9%)was
[3.2-13.9]
0 [0-4.4]
.016
TIA
(24.1)
4-6
detected
were diagnostic
AF.
important single cause of(Pischemic
stroke in elderly per- AFwith
Standard
evaluation of patients
Initial stroke subtype, n (%)* Embolic topography (n 5 75)* treated with warfarin for prevention
7
(9.3%)
[4.3-18.3]
0
[0-5.8]
of recurrent
stroke. stroke or transient ischemic .016
sons and is responsible for about 10% of all ischemic
admitted
for ischemic
attack
Lacunar
14
Cryptogenic
stroke
(n
5
53)
5
(9.4%)
[3.6-20.3]
0 [0-7.9]
.063
1 (13.9)
strokes. The prevalence of AF in the general population
(TIA) commonly does not reveal an etiology, however,
Large-artery atherosclerosis Age .65 years14(n(13.9)
5
61)nearly doubling every decade after age
7 (11.5%)
[5.4-22.1]
0 [0-7.1]
.016as
with
up to 40% of ischemic
strokes classified
varies with
age,
Discussion
Cardiac embolism
12disease
(11.9)
7
Coronary
artery
(n
5
25)
4
(16.0%)
[5.8-35.3]
0
[0-15.8]
.125
cryptogenic. Paroxysmal AF is difficult to diagnose
50, from
0.5% at age 50-59 years to 8.8%
and
Cryptogenic
53approximately
(52.5)
Embolicattopography
or
age2 .65
(n
5associated
86)
8 (9.3%)
[4.6-17.5]
0patients
[0-5.1] with cryptogenic
.008
This
is
the
first
study
to
compare
concurrent
Holter
age
80-89
years,
may
be
underdiagnosed
in
with
an
annual
stroke
Other determined
8 (7.9)
3
Embolicrisk
topography
and age
.65
(n 5 38) groups.
(15.8%)
[7.1-30.1]
[0-10.1]
.031
monitoring
and CCT
in the 6same
cohort.
Our
findings
stroke.
Recent
studies found 0that
up to 23% of patients
of up to 18.2%
in the
highest-risk
Compared
Infarct topography, n (%)y
Embolic
topography
and
age
.65
or
CAD
(n
5
38)
7 (18.4%)
[8.9-33.7]
[0-10.9] AF with.016
suggest
that
Holter
provides
a significantly
with
cryptogenic
stroke had 0paroxysmal
longwith antiplatelet
additional
Small deep
19 (17.1) therapy, warfarin provides an monitoring
NSVT
higher rate of AF detection compared
with
CCT during
term
outpatient
cardiac monitoring.8,9 Given the impact
Large deep
15 (13.5)
Ischemic stroke43and
TIA (n 5 133)
11 (8.3%)
7 (5.3%)
[3.8-8.7]
inpatient evaluation after ischemic
stroke
or TIA. In in
paon [4.5-14.3]
management
patients
with
AF and ischemic .180
stroke
Cortical
(38.7)
Border zone
2 (1.8)
tients at high risk for a cardiac sourceorof embolism
based tests that achieve the highest
TIA, diagnostic
From the *Department of Neurological Sciences, Section of CerebroMultiple
(7.2) multiple,
*Includes those
with8cortical,
mixed topography,
cortical/subcortical
patterns.
diagnostic
yield
onorinfarct
age, and
cardiac
history,
the are
AF critical. We sought to compare the
vascular Disease and Neurological Critical Care; and †Department of
Mixed cortical/subcortical
24 (21.6)
of detection of AF by 2 commonly used modalities,
even higher
18.4%).
Internal Medicine, Division ofdetection
Cardiology,rate
Rushwas
University
Medical (up torates
Anticoagulation on discharge,
n (%)
Holter
monitoring
continuous
cardiacfor
telemetry
Holter
monitoring
being
better suited
detecting
unit vs
general
medical
clear,
however,
Center,
Chicago,floor)
Illinois.is not always
A recent
study
of 56 patientswith
with
cryptogenic
TIA/and
AF, n (%)
8 March
(6.0) 12, 2010; accepted May 21, 2010.
Received
(CCT),
patients with
stroke and TIA.
stroke detected
AF by 21-day subtle
outpatient
telemetry
in ischemic
or in
short-duration
supraventricular
arrhythmias
possibly contributing
to the variability
in reported
Cardiomyopathy with or
(4.5)
Address6 correspondence
to Marc A. Lazzaro, MD, Department
8
23% of the patients.
Another ofstudy using 30-day cardiac
detection rates.
CCT was
reported
AF in about
Neurological
Sciences,
Sectiontoofdetect
Cerebrovascular
Disease and and CCT better suited for detecting malignant, lifewithout cardiac thrombus
event
monitors
in
ischemic
stroke
and Methods
TIA patients
deCritical Care,
University Medical
Center, 1725
threatening
rhythms.
patients
admitted
to Rush
an ‘‘investigative
stroke
Mechanical valve or 3% of strokeNeurological
4 (3.0)
tected
AF
in
20%
of
those
initially
considered
to
have
15
West
Harrison
Street,
Suite
1121,
Chicago,
IL
60612.
E-mail:
valvular thrombosis unit.’’ In another study, ambulatory 24- to 48-hour Holter
reviewed a prospective
stroke
registry of in
456patients
conThe We
cost-effectiveness
of Holter
monitoring
Detection of Atrial Fibrillation After Ischemic Stroke
or Transient Ischemic Attack
A Systematic Review and Meta-Analysis
Amit Kishore, MRCP; Andy Vail, MSc; Arshad Majid, MD; Jesse Dawson, MD;
Kennedy R. Lees, MD; Pippa J. Tyrrell, MD; Craig J. Smith, MD
Background and Purpose—Atrial fibrillation (AF) confers a high risk of recurrent stroke, although detection methods and
definitions of paroxysmal AF during screening vary. We therefore undertook a systematic review and meta-analysis to
determine the frequency of newly detected AF using noninvasive or invasive cardiac monitoring after ischemic stroke or
transient ischemic attack.
Methods—Prospective observational studies or randomized controlled trials of patients with ischemic stroke, transient ischemic
attack, or both, who underwent any cardiac monitoring for a minimum of 12 hours, were included after electronic searches
of multiple databases. The primary outcome was detection of any new AF during the monitoring period. We prespecified
subgroup analysis of selected (prescreened or cryptogenic) versus unselected patients and according to duration of monitoring.
Results—A total of 32 studies were analyzed. The overall detection rate of any AF was 11.5% (95% confidence interval, 8.9%–
14.3%), although the timing, duration, method of monitoring, and reporting of diagnostic criteria used for paroxysmal AF
varied. Detection rates were higher in selected (13.4%; 95% confidence interval, 9.0%–18.4%) than in unselected patients
(6.2%; 95% confidence interval, 4.4%–8.3%). There was substantial heterogeneity even within specified subgroups.
Conclusions—Detection of AF was highly variable, and the review was limited by small sample sizes and marked
heterogeneity. Further studies are required to inform patient selection, optimal timing, methods, and duration of monitoring
for detection of AF/paroxysmal AF. (Stroke. 2014;45:520-526.)
Key Words: atrial fibrillation ◼ ischemic attack, transient ◼ stroke
See related article, p 355.
C
ardioembolism accounts for 17% to 30% of all ischemic
strokes.1,2 Some data suggest that >50% of these are
because of atrial fibrillation (AF).3 Paroxysmal AF (PAF) is
often undetected because characteristics such as short duration, episodic, and frequently asymptomatic nature make it
challenging to diagnose at the bedside, leading to suboptimal
secondary prevention.4 It is likely that a proportion of strokes
labeled as cryptogenic are cardioembolic in origin because
of occult AF.5,6 Furthermore, ≥2 factors contributing to stroke
risk may coexist: even patients with an identified risk factor
for nonembolic stroke may have occult cardioembolism.
Detection rate of new AF from a standard 12-lead ECG after
ischemic stroke/transient ischemic attack (TIA) is ≈2% to 5%7,8
9–11
American Stroke Association13 recommend that 24-hour Holter
monitoring is used to detect occult AF/PAF when suspected,
and no other cause for stroke is found. However, the optimum
timing, duration, setting (outpatient or inpatient), and method
of monitoring to maximize the detection of PAF after stroke/
TIA are unclear. Furthermore, diagnostic criteria used for PAF
during monitoring may vary and have implications for risk of
recurrence. We therefore undertook a systematic review and
meta-analysis with the following objectives:
To determine the overall rate of detection of any new AF
with cardiac monitoring (invasive and noninvasive) after
ischemic stroke/TIA.
To evaluate detection rates of AF in selected versus
unselected patients with stroke/TIA.
Patients sélectionnés
new england
journal of medicine
The
june 26, 2014
established in 1812
vol. 370
no. 26
Atrial Fibrillation in Patients with Cryptogenic Stroke
David J. Gladstone, M.D., Ph.D., Melanie Spring, M.D., Paul Dorian, M.D., Val Panzov, M.D., Kevin E. Thorpe, M.Math.,
Judith Hall, M.Sc., Haris Vaid, B.Sc., Martin O’Donnell, M.B., Ph.D., Andreas Laupacis, M.D., Robert Côté, M.D.,
Mukul Sharma, M.D., John A. Blakely, M.D., Ashfaq Shuaib, M.D., Vladimir Hachinski, M.D., D.Sc.,
Shelagh B. Coutts, M.B., Ch.B., M.D., Demetrios J. Sahlas, M.D., Phil Teal, M.D., Samuel Yip, M.D., J. David Spence, M.D.,
Brian Buck, M.D., Steve Verreault, M.D., Leanne K. Casaubon, M.D., Andrew Penn, M.D., Daniel Selchen, M.D.,
Albert Jin, M.D., David Howse, M.D., Manu Mehdiratta, M.D., Karl Boyle, M.B., B.Ch., Richard Aviv, M.B., Ch.B.,
Moira K. Kapral, M.D., and Muhammad Mamdani, Pharm.D., M.P.H., for the EMBRACE Investigators and Coordinators*
Atrial Fibrillation in Cryptogenic Stroke
A BS T R AC T
DISCUSSION
Atrial fibrillation is a leading preventable cause of recurrent stroke for which
early detection and treatment are critical. However, paroxysmal atrial fibrillation
is often asymptomatic and likely to go undetected and untreated in the routine
care of patients with ischemic stroke or transient ischemic attack (TIA).
20
METHODS
We randomly assigned 572 patients 55 years of age or older, without known
atrial fibrillation, who had had a cryptogenic ischemic stroke or TIA within the
previous 6 months (cause undetermined after standard tests, including 24-hour
electrocardiography [ECG]), to undergo additional noninvasive ambulatory ECG
monitoring with either a 30-day event-triggered recorder (intervention group) or
a conventional 24-hour monitor (control group). The primary outcome was newly
detected atrial fibrillation lasting 30 seconds or longer within 90 days after randomization. Secondary outcomes included episodes of atrial fibrillation lasting
2.5 minutes or longer and anticoagulation status at 90 days.
Patients with Atrial Fibrillation
Detected (%)
and at 90 days, the proportion of patients treated
with anticoagulants was significantly higher in
the intervention group than in the control group:
18.6% (52 of 280 patients) versus 11.1% (31 of
279), for an absolute treatment difference of 7.5
percentage points (95% CI, 1.6 to 13.3; P = 0.01)
(Table 3). In the intervention group, 38 of 280
patients (13.6%) switched from antiplatelet to
anticoagulant therapy, as compared with 13 of
279 (4.7%) in the control group, a difference of 8.9
percentage points (95% CI, 4.2 to 13.6; P<0.001).
BACKGROUND
15
11.6
RESULTS
10
Atrial fibrillation lasting 30 seconds or longer was detected in 45 of 280 patients
(16.1%) in the intervention group, as compared with 9 of 277 (3.2%) in the control group (absolute difference, 12.9 percentage points; 95% confidence interval
[CI], 8.0 to 17.6; P<0.001; number needed to screen, 8). Atrial fibrillation lasting
2.5 minutes or longer was present in 28 of 284 patients (9.9%) in the intervention
group, as compared with 7 of 277 (2.5%) in the control group (absolute difference, 7.4 percentage points; 95% CI, 3.4 to 11.3; P<0.001). By 90 days, oral anticoagulant therapy had been prescribed for more patients in the intervention
group than in the control group (52 of 280 patients [18.6%] vs. 31 of 279 [11.1%];
absolute difference, 7.5 percentage points; 95% CI, 1.6 to 13.3; P = 0.01).
7.4
5
2.2
CONCLUSIONS
Among patients with a recent cryptogenic stroke or TIA who were 55 years of
age or older, paroxysmal atrial fibrillation was common. Noninvasive ambulatory ECG monitoring for a target of 30 days significantly improved the detection
of atrial fibrillation by a factor of more than five and nearly doubled the rate of
anticoagulant treatment, as compared with the standard practice of short-duration
ECG monitoring. (Funded by the Canadian Stroke Network and others; EMBRACE
ClinicalTrials.gov number, NCT00846924.)
0
24 Hr
1 Wk
2 Wk
From the Division of Neurology (D.J.G.), Department of Medicine (D.J.G., P.D., A.L., M.S.,
J.A.B., L.K.C., D.S., M. Mehdiratta, K.B.,
M.K.K.), and Dalla Lana School of Public
Health (K.E.T.), University of Toronto, the University of Toronto Stroke Program (D.J.G.),
Division of Neurology, Department of Medicine, and Brain Sciences Program, Sunnybrook Health Sciences Centre and Sunnybrook Research Institute (D.J.G., R.A.), the
Heart and Stroke Foundation Canadian Partnership for Stroke Recovery (D.J.G.), and the
Applied Health Research Centre, Li Ka Shing
Knowledge Institute of St. Michael’s Hospital
(V.P., K.E.T., J.H., H.V., A.L., M. Mamdani), Toronto, McMaster University, Hamilton, ON
(M.S., D.J.S.), McGill University, Montreal
(R.C.), University of Alberta, Edmonton (A.S.,
B.B.), Western University, London, ON (V.H.,
J.D.S.), Department of Clinical Neurosciences
and Radiology, Hotchkiss Brain Institute, University of Calgary, Calgary, AB (S.B.C.), University of British Columbia, Vancouver (P.T.,
S.Y.), Queen’s University, Kingston, ON (A.J.),
Thunder Bay Regional Health Sciences Centre,
Thunder Bay, ON (D.H.), Université Laval,
Quebec City (S.V.), and Vancouver Island
Health Research Centre, Victoria, BC (A.P.)
— all in Canada; and the National University
of Ireland, Galway (M.O.). Address reprint
requests to Dr. Gladstone at the Regional
Stroke Centre, Sunnybrook Health Sciences
Centre, A442-2075 Bayview Ave., Toronto, ON
M4N 3M5, Canada, or at david.gladstone@
sunnybrook.ca.
14.8
12.3
* A complete list of participating sites, investigators, and coordinators for the 30-Day Cardiac Event Monitor Belt for Recording Atrial
Fibrillation after a Cerebral Ischemic Event
(EMBRACE) trial is provided in the Supplementary Appendix, available at NEJM.org.
3 Wk
4 Wk
N Engl J Med 2014;370:2467-77.
DOI: 10.1056/NEJMoa1311376
Duration of ECG Monitoring
n engl j med 370;26
nejm.org
Copyright © 2014 Massachusetts Medical Society.
june 26, 2014
2467
Figure 2. Incremental Yield of Prolonged ECG Monitoring for the Detection
We found that ambulatory ECG monitoring for a
of Atrial Fibrillation in Patients with Cryptogenic Stroke or TIA.
target of 30 days was feasible to implement as
The proportion of patients in whom atrial fibrillation was detected increased
part of routine stroke care, detected atrial fibrilwith increasing duration of ECG monitoring. The data reflect the timing of
lation in one in six patients (which had not previthe first detected episode of atrial fibrillation; data for 2 patients are not
ously been detected by means of standard 24 to
shown because the exact date of the detection of atrial fibrillation was un48 hours of monitoring after stroke), was supeknown. Atrial fibrillation was detected in 6 of 277 patients who underwent
monitoring with a 24-hour Holter monitor (the control group). In the group
rior to an additional round of 24-hour ECG monof 284 patients who underwent 30-day monitoring, atrial fibrillation was
itoring and clinical follow-up (the detection rate
detected in 21 patients within the first week of monitoring, in 33 within the
with 30-day monitoring was increased by a factor
first 2 weeks of monitoring, in 35 within the first 3 weeks of monitoring, and
of five), and had an incremental yield over a pein 42 within 4 weeks of monitoring (including 1 patient with atrial fibrillation
riod of 30 days. Moreover, prolonged monitoring
that was first detected on day 34).
nearly doubled the proportion of patients who
subsequently received anticoagulant therapy for
secondary prevention of stroke — a finding we
interpret as a clinically meaningful change in
The finding of even brief atrial fibrillation in
treatment that has the potential to avert recur- this population is considered important, given
rent strokes. These findings, taken together with increasing evidence that brief subclinical atrial
The New England Journal of Medicine
Downloaded from nejm.org at UNIVERSITE DE SHERBROOKE on July 28, 2014. For personal use only. No other uses without permission.
Copyright © 2014 Massachusetts Medical Society. All rights reserved.
Plaque aortique et AVC…
EPIDEMIOLOGY, CLINICAL SIGNIFICANCE, AND MANAGEMENT OF AOR
TABLE I
Characteristics of Complex and Simple Atheromatous
Plaques
Complex Plaque:
Protruding atheroma >4-mm thickness
Presence of mobile components
Presence of > 2-mm surface ulceration
Simple Plaque:
Protruding atheroma <4-mm thickness
No mobile debris
No surface ulceration
Epidemiology
The prevalence of aortic atheromas on TEE
varies, depending on the population studied.
In a community-based TEE study from Olmsted County, Minnesota, aortic atheromas were
present in 51% of randomly selected residents
aged 45 years or older, with a greater prevalence in the descending aorta.11 In the same
study, complex atheromas were present in 7.6%
of Olmsted County residents, and the prevalence of both simple and complex atheromas increased with advancing age, smoking, and pulse
pressure. In patients with known significant
The presumed mechan
boembolism from unst
and large-sized intra
autopsy- and TEE-bas
ries7,16–19 and case-con
reported a strong ass
atheromas and stroke.
matous plaques invol
was consistently high
temic embolism (perip
bolism) compared with
and the association w
traditional atheroscler
age, hypertension, an
true cause-and-effect r
established because of
of the studies.
Subsequently, seve
up studies25–29 (summa
shown an association b
and stroke. In a prospe
volving 42 patients wi
of thoracic aorta on TE
vascular events in 33
complex plaques, as op
controls.25 On multiva
presence of protruding
Aortic Atherosclerotic Disease and Stroke
Itzhak Kronzon and Paul A. Tunick
Circulation. 2006;114:63-75
doi: 10.1161/CIRCULATIONAHA.105.593418
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2006 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539
Kronzon and Tunick
TABLE 2. Plaque Characteristics and Stroke Risk
The online version of this article, along with updated information and services, is located on the
World Wide Web at:
Thickness, mm
Risk, OR
!1
1–1.9
2–3.9
http://circ.ahajournals.org/content/114/1/63
1
3.3
4.1
!4
13.8
Findings associated with high stroke risk
Thrombus (mobile or not)
Ulceration
Large lipid core (hypoechoic)
Finding associated with lower stroke risk
Plaque calcification (hyperechoic)
Data derived from Amarenco et al.12
Pathological Correlations
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published
in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial
Office. Once the online version of the published article for which permission is being requested is located,
click Request Permissions in the middle column of the Web page under Services.
43Further information about
this process is available in the Permissions and Rights Question and Answer document.
In 1992, a landmark autopsy study evaluated 500 patients
with stroke and other neurological diseases. The authors
showed
that about
ulcerated
were
Reprints:
Information
reprints canplaques
be found online
at: present in the aortic arch
http://www.lww.com/reprints
in 26% of 239 patients with cerebrovascular disease but in
Subscriptions: Information about subscribing to Circulation is online at:
only 5% of 261 patients with other neurological diseases. In
http://circ.ahajournals.org//subscriptions/
Aortic Atheroscler
sized and larger arteries from
common is the “classic” syn
embolization, the atheroemb
latter entity, there is a diffu
from unstable aortic (or oth
may occur spontaneously or
plaques during trauma, inte
giography or cardiac cathe
tients with this syndrome su
failure, intestinal infarction,
diffuse, distal, and bilateral
rate. This syndrome is a
atherosclerosis than is the
Thromboembolism occurs i
aortic plaque on TEE in 1
was reported in 0.7% of pa
TEE.39
The thickest plaque was considered for classification. Atheroma
1 patient (1.1%).
were divided into lower risk (ie, !4 mm) and into higher risk (ie,
Stroke etiology could be classified by routine diagnostic
!4 mm), and presence of ulcerations or mobile components/thrombi
data (ie, without TEE data) in 276 (54.9%) patients (group 1)
was recorded. Aortic thrombus was defined as laminated deposition
along the intimal surface, with variable echogenicity, and which may
according to the TOAST classification (Figure 1). In the
be associated with mobile lesions.15,16
remainingby
227Transesophageal
(45.1%) patients, we found contraindications
Strategies
Afterac-Examination
Echocardiograms wereTherapeutic
stored on videotape
and categorized
against
OA
in
15:
severe cerebral small-vessel disease (n"7),
17,18
cording to a modified Hart classification.
Consequently,
echoEchocardiography
in 503
Patients
With
Ischemic
Stroke
severe
alcohol
abuse
or incompliance (n"2), ataxia with
cardiographic abnormalities were considered cardiac high and poAndreas
Matthias
Reinhard,
recurrent
fells
(n"2),MD;
uncontrollable hypertension (n"1), and
tential risk factors for embolism (Figure
2). Harloff, MD; Michael Handke, MD;
Annette Geibel, MD; Andreas Hetzel, MD
Background and Purpose—Transesophageal echocardiography (TEE) is the gold standard in detecting high-risk (ie, aortic
thrombi) and potential sources (ie, patent foramen ovale [PFO]) of cerebral embolism. We sought to evaluate the
additional information and therapeutic impact provided by TEE in stroke patients and to characterize patients in whom
TEE is indispensable.
Methods—We included 503 consecutive patients (mean age 62.2 years) with acute brain ischemia. Each patient received
TEE and the following routine diagnostics: ultrasound of brain supplying arteries, ECG or Holter-ECG, transthoracic
echocardiography, and brain imaging (computed tomography or MRI). Stroke etiology was classified according to the
Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria. High-risk sources in TEE were: aortic thrombi or
plaques !4 mm, thrombi in left atrial cavity/left atrial appendage, spontaneous echo contrast, and left atrial flow
velocity !30 cm/s. Potential sources in TEE were PFO, atrial septal aneurysm, and aortic plaques !4 mm.
Results—Stroke etiology was determined by routine diagnostics in 276 of 503 patients (54.9%). Of the remaining 227
patients (undetermined etiology), 212 (93.4%) were candidates for oral anticoagulation (OA). TEE revealed a high-risk
source, with indication for OA in 17 of them (8.0%). A potential source leading to OA was found in an additional 48
patients (22.6%). The remaining 147 patients (69.3%) were treated by platelet inhibitors or statins.
Conclusions—TEE strongly influenced secondary prevention and led to OA in one third of our patients with stroke of
undetermined etiology. TEE is indispensable in all patients being candidates for OA when routine diagnostics cannot
clarify stroke etiology. (Stroke. 2006;37:859-864.)
Key Words: echocardiography, transesophageal ! stroke, acute ! stroke management
T
ransesophageal echocardiography (TEE) is superior to
transthoracic echocardiography (TTE) in detecting highrisk sources and potential sources of cerebral embolism.1– 4
Complication rate in TEE is low,5 but the procedure is
semi-invasive, time consuming, and often not readily available everywhere. Therefore, it might be applied primarily to
patients with stroke of undetermined etiology (ie, patients
showing normal results in ECG, carotid ultrasound, and TTE,
who are candidates for oral anticoagulation [OA]).
However, recommendations of TEE in stroke patients are
controversial: in a systematic review, TEE was recommended
only for younger patients to exclude rare sources of cerebral
embolism such as atrial thrombi despite sinus rhythm.6 Leung
et al7 recommended TEE for patients with abnormal TTE and
for younger patients when finding of patent foramen ovale
(PFO) may contribute to patient management. Warner et al8
pointed out that routine TEE is not cost-effective; patients
with atrial fibrillation would receive OA anyway, and those
in sinus rhythm would usually have findings for which only
aspirin is indicated. However, others showed that TEE
changed secondary prevention toward OA in 10% of the
patients with stroke of undetermined etiology.9,10 In 441
unselected stroke patients, TEE revealed a cardiac abnormality leading to OA in 8% of the patients who were in sinus
rhythm and had no clinical evidence of a cardiac disease. TEE
was therefore recommended for all patients without contraindication against anticoagulation.3
Because of these conflicting data, our aim was to identify
the therapeutic impact of TEE in stroke patients and to
compile an algorithm of TEE indication based on our findings and the current treatment guidelines for different stroke
causes to characterize patients in whom TEE is indispensable.
Subjects and Methods
Study Population
A total of 596 consecutive patients admitted to our stroke unit
fulfilled the inclusion criteria (18 to 85 years of age and acute brain
ischemia). Twenty-four patients declined to undergo TEE examina-
Received June 8, 2005; final revision received November 22, 2005; accepted November 27, 2005.
From the Departments of Neurology and Clinical Neurophysiology (A.H., M.R., A.H.) and Angiology and Cardiology (M.H., A.G.), Albert-LudwigsUniversität Freiburg, Germany.
The first 2 authors contributed equally to this study.
Correspondence to Andreas Harloff, MD, Department of Neurology and Clinical Neurophysiology, Albert-Ludwigs-Universität Freiburg, Breisacher
Straße 64, D-79106 Freiburg, Germany. E-mail [email protected]
© 2006 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org
DOI: 10.1161/01.STR.0000202592.87021.b7
859
Figure 2. TEE-guided therapeutic management of patients with stroke of undetermined etiology. The finding of multiple high and
potential risk sources in some patients is the reason for the discrepancy between the number of TEE parameters and patients.
IRM cardiaque dans
l’investigation de
l’AVC ischémique…
On dirait qu’il n’y a pas
grand-chose dans la
littérature médicale làdessus!
CARDIAC SOURCES OF EMBOLIC STROKE
ast has been shown to be an
valuate the presence or abbus. An early study done usging sequences for revealing
imited by artifacts caused by
14
More recent studies with
MR (CE-MR) have shown
uracy for detecting mural
as for defining the presence
ardial scarring.15–17 A study
patients designed to assess
E-MR in detecting ventricuared with TTE revealed 12
ated in the LV apex or adptum as black, well-defined
nded by bright contrast enTE depicted thrombi in only
tion, CE-MR was normal in
spected apical thrombus on
s study suggests that CE-MR
n detecting thrombus in pac heart disease, its reliability
e lack of pathologic or clinical
.
R to clearly define LV thromin Figure 1. This is a CMR
tient with chronic coronary
o had an incomplete TTE
poor acoustic windows. MRI
neation of a large, bright-
Figure 2. Apical infarct with LV thrombus. This contrastenhanced two-chamber view was obtained from a patient
with atrial fibrillation. There is a region of decreased signal
in the apex that is due to LV thrombus (arrow). The region
of infarction is not seen in this view. Also shown in this view
is a LAA (arrowhead) with no thrombus.
appearing anterior and apical infarct with apical dyskinesis as well as an apical thrombus.
An example of a 69-year-old man with chronic
atrial fibrillation and history of coronary artery
bypass graft surgery who had a CMR to evaluate myocardial viability is shown in Figure 2.
Delayed contrast-enhanced images clearly
show an apical thrombus.
Et t’as vraiment tout
lu, incluant le très
célèbre Scandinavian
Journal of small and
medium size thrombi ?
CARDIAC SOURCES OF EMBOLIC STROKE
RUSTEMLI, BHATTI, AND WOLFF
intima-media was <5 mm; IV: plaque with a
cholesterol core, areas of ulceration, a total
large pectinate muscles can sometimes be miscontrast to the LA wall. Unfortunately there are
thickness
≥5on
mm
presence
of
taken for a thrombus on a TEE examination.intima–media
no published
studies yet
theor
accuracy
of this
29
calcification.
The accuracy of TEE may potentially be imtechnique. Studies using TEE as the goldfound
significantly
increased
proved by giving contrast. Intravenous contraststandard
Most
CMRaimages
are cardiac
gated andrisk
are
in patients
with
noncalcified
aortic
was used with TEE in a study of 41 patientsof stroke
an average
of several
heart-beats.
Optimal
im30
who had inconclusive initial TEE studies be-plaques
age >4
quality
on a regular
rhythm.
mmdepends
thickness.
The heart
hypoechoic,
cause of either dense SEC or artifacts. However,noncalcified
Therefore,
in patients
atrial fibrillation
the
plaques
arewith
lipid-laden
and are
incomplete filling of the LAA by intravenousconsidered
image quality
may beto
suboptimal.
However,
one
to be prone
rupture and
thromcontrast lead to further inconclusive result inboembolization.
should recognize
that atria do not contract in
31
13 patients.23
atrial fibrillation and are usually enlarged in
MRI
is
an
established
modality
to
size. Thus, image degradation
withofanchoice
irregular
CMR is an alternative method for assessing
the thoracic
atherosclerotic
disrhythm
may beaorta
less offor
a problem
when visualthe LAA. The accuracy in the detection of LAAassess
aneurysm,
The
MRI
evalof theand
atriadissection.
is concerned.
This
is demonthrombus by CMR was compared with TEE in aease, ization
of thein aortic
compares
strated
Figure atheromas
2, which shows
the LAA well
to be
cohort of 50 subjects with nonrheumatic chronicuation
24
free ofIn
thrombus
patient
whowith
was in
atrial
atrial fibrillation. The LAA was clearly visu-with TEE.
a studyin
ofa10
patients
known
during theby
CMR
exam.
alized by CMR in all patients. Black blood se-aorticfibrillation
plaque (identified
TEE),
T 1 -weighted
quences were used for CMR studies and clotproton density and T 2 -weighted images were
was identified as high intensity signal. In all 16obtained using MRI to assess the composition,
Other Cardiac Masses
patients where clot was demonstrated by TEE,
extent, and size of the plaque. Overall, there
high signal was seen in CMR. There were three
TTE is the conventional method used to decorrelationmasses.
(80% overall
agreement)
additional patients where high signal was seenwas strong
tect intracardiac
However,
its32 use is
MRI
and TEE
all criteria.
Preon CMR. It is unclear whether this signal wasbetween
limited
secondary
to for
difficulty
in discriminatliminary
research
studies
suggest
that,
in adfalse positive or whether it represented true
ing between certain masses due to lack
of
25,26
ditiontissue
to being
able to characterize
the plaque
clot.
characterization.
Additionally,
there
Bright blood sequences can also be used forburden,
are MRI
cardiac
that are
and more
canmasses
also study
thesmaller
characteristics
detecting LAA thrombus without the disadvan-of all posteriorly
located,
which 32,33
require a TEE for
atherosclerotic
plaques.
tage of having artifact from slow flowing blood. While
better
definition
of
their
anatomy.
CMR
is to
ofthere are a number of sequences
The image quality from the bright blood tech-evaluate
ten the
of choice aorta,
in evaluating
the patient
thetestthoracic
a T 1 -weighted
nique is excellent, as can be seen in Figure 3.
a cardiac mass. The goal of the study is
brightwith
blood
sequence with contrast is often
This is an example of a 70-year-old female with
to (1) confirm the presence or absence of the
best
at
assessing
plaque
Figure
is
chronic atrial fibrillation and LA appendage
mass, (2) establish
its thickness.
exact location
and its4 reof the to
thoracic
aortastructures,
using the (3)
bright
thrombus. The bright blood sequence providesan MRA
lationship
surrounding
contechnique
withare
gadolinium,
which
demonclear visualization of the thrombus borders inbloodfirm
that there
no additional
masses
that
strates
anhave
atherosclerotic
projecting into
may
been missedplaque
with echocardiography,
and (4)ofcharacterize
its descending
composition thoracic
based on
the lumen
the proximal
aorta.its signal characteristics.27,28 The role of CMR
for cardiac masses is discussed in greater detail
elsewhere in this issue.
IRM cardiaque: Qui?
!  Thrombus ventriculaire possible à l’ETO
!  CI à l’ETO
the patients who can benefit from transcatheter
or surgical closure of the PFO.
Traditionally, the method of choice to diagnose and describe the morphologic features of a
PFO is TEE.37,38 The sensitivity of TEE with
agitated saline injection to detect a right-toleft shunt through a PFO depends on the performance of an adequate Valsalva maneuver,
which can be limited secondary to the use of
sedation. If the only clinical question is to assess for the presence of a PFO, there are noninvasive techniques such as transcranial duplex sonography and TTE that have reasonable
sensitivities and specificities.39,40 It was shown
that, TTE with second harmonics in combination with agitated saline injection had a sensitivity of 90.5% and a specificity of 96.5% for
detection of right-to-left shunt when compared
with TEE as the gold standard.39
!  Masse cardiaque visualisée à l’ETO
Patent Foramen Ovale
Aortic Atheroma
Paradoxical embolization
through a PFO is
anotherAortic
important
cause
embolic
stroke,
esatheroma
is a of
potential
source
for em34
pecially
in patients
younger than
55 years.
A
bolization
of atheromatous
material
to the cerePFO is
defined
as a communication
between
bral
circulation.
The ascending aorta
and the
thoaorta
cannot
be that
fully assessed
TTE.
atria racic
at the
fossa
ovalis
typicallyusing
allows
a
Multiplanarhemodynamically
TEE performed and
interpreted
unidirectional,
insignificant
byIta is
highly
skilled
is the
method
of
shunt.
thought
tophysician
result from
the
lack of
forseptum
evaluation
of the and
thoracic
aorta.seA
fusionchoice
of the
primum
septum
study
evaluating
the
accuracy
of
TEE
in
de35
cundum.
tecting aortic atheromas with comparison to
Another
abnormality
the interatrial
seppathologic
correlates ofshowed
a sensitivity
of
tum is91%
theand
atrial
septal aneurysm
which
a specificity
of 90%.29(ASA),
The extent
of
is
defined
as
abnormal
bowing
of
the
atrial
sepaortic atherosclerosis was classified into four
Figure 3. LAA thrombus. This contrast-enhanced twoat least 15 mm.
The presence
of an thickASA
grades—Grade
I: normal;
II: mild intimal
chamber view shows a region of decreased signal in the LAAtum of
ening;
III:aplaque
with
an intact
cap and
due to thrombus (arrow). The thrombus is attached to thetogether
with
PFO is
reported
to fibrous
be associated
36
roof of the appendage.
a
fibrous
or
lipid
core,
where
the
thickness
of
with higher cerebral ischemic events. Thus,the
it
is important to rule out the presence of a PFO as
wellofasCVan
ASA in &
the
complete
evaluation
a
304
ECHOCARDIOGRAPHY: A Jrnl.
Ultrasound
Allied
Tech.
Vol. 24, No. 3,of
2007
patient with stroke. This is particularly important for further management and selection of
Vol. 24, No. 3, 2007
Figure 4. Aortic plaque. This contrast-enhanced image
shows atherosclerotic plaque projecting 9 mm into the lumen of the proximal descending thoracic aorta (arrow). In
addition, a thin layer of plaque can be seen extending proximally and distally along the arterial wall (arrowheads).
ECHOCARDIOGRAPHY: A Jrnl. of CV Ultrasound & Allied Tech.
305
Angio-MRI ou angio-CT pour
pathologies aortiques
!  Dissection aortique
!  Takayasu
!  Plaque aortique
Dans la « vraie vie »
!  Banque de données localeHCLM
Un autre névrosé
qui veut parler de
son expérience…
ETT
25%
75%
Fait
Non Fait
ETT - Fait
80%
70%
60%
50%
40%
30%
20%
10%
0%
Normal
Cardioembolique
Autres
Sources cardioemboliques à
l’ETT
!  FA 56%
!  Akinésie sévère 29%
!  FEVG <30% 19%
!  Foramen ovale 7%
!  Valve mécanique 3%
!  Thrombus 3%
!  Végétations 2%
!  Myxome de l'oreillette 0%
ETO
16%
84%
Fait
Non Fait
ETO - Fait
50%
40%
30%
20%
10%
0%
Normal
Cardioembolique
Autres
Sources cardioemboliques à
l’ETO
!  Foramen ovale 61%
!  Végétations 10%
!  FA 8%
!  Thrombus 7%
!  Akinésie sévère 6%
!  FEVG <30% 4%
!  Valve mécanique 3%
!  Myxome de l'oreillette 1%
ECG
7%
93%
Fait
Non Fait
ECG - Fait
70%
60%
50%
40%
30%
20%
10%
0%
Normal
FA ou flutter
Infactus aigu Infactus ancien
ou ischémie
aigue
Autres
Changement
significatif
dans les ECG
ultérieur
Population sans FA connue et
sans FA à l’ECG au baseline
Holter
28%
72%
Fait
Non Fait
Holter - Fait
100%
80%
60%
40%
20%
0%
Normal ou anomalie (s)
béningne(s)
FA ou flutter
Autre(s) anomalie(s)
Guidelines….
!  Les recommandations sont des suggestions…
!  Tout ne pas être « protocolé »
soit manifestement pas un candidat pour une revascularisation [niveau de preuve B]. Idéalement
iv.
devrait être effectuée aussitôt que possible afin de mieux comprendre la cause
de
et de mieux éclairer les décisions entourant la prise en charge du patient. Dans certains cas,
ultrasonographie duplex ou une angiographie par TDM ou IRM des vaisseaux extracrâniens et
certaines circonstances [niveau de preuve B].
3.3.3 : Investigations cardiovasculaires (Nouvelle section en 2010)
i.
ex., quotidiensI
devraient être effectués aucours des 72
fibrillation auriculaire GFAI et les autres arythmies aiguës [niveau de preuve B].
ii.
Les électrocardiogrammes en série durant les 72 premières heures combinées à un moniteur
la FA [niveau de preuve C].
215
iii.
pas de contre3.3.4 : Prise en charge de la tension artérielle en phase aiguë
ischémique
tension artérielle [niveau de preuve C].
i.
Si le patient
ischémique est admissible à un traitement thrombolytique, la tension
artérielle très élevée G>185/110 mm HgI devrait être traitée en même temps que le patient reçoit
une thérapie thrombolytique pour un AVC ischémique en phase aiguë, et ce, dans le but de
lre
ss
ron
es
ed
ed
le
ke
ct
seis
s.
ia
e3)
m
ed
m,
24
f),
d.
55
w-
avoids excessive resources, labor, and risk. It is reasonable
to follow the current American Diabetes Association recommendation to maintain the blood glucose in a range of 140
to 180 mg/dL in all hospitalized patients.457 There are multiple subcutaneous and intravenous insulin
protocols
AHA/ASA
Guidelinethat
use insulin to lower hyperglycemia during hospitalization,
Guidelineswith
for the
Early
Management
and these have not been compared
each
other
in acuteof Patients
With Acute Ischemic Stroke
stroke patients. The subcutaneous
insulin
protocols
canFrom
safely
A Guideline for Healthcare
Professionals
the American Heart
Association/American
Stroke
Association
lower and maintain blood glucose levels below 180 mg/dL
The American Academy of Neurology affirms the value of this guideline as an educational
in acute stroke patients without excessive tool
use
of healthcare
for neurologists.
the American Association of Neurological Surgeons and Congress
someby hospitals
may be prepared
resources.453,454,458 However, Endorsed
of Neurological Surgeons
to safely administer intravenous
insulin
toFAHA,
patients
with
acute
Edward C. Jauch,
MD, MS,
Chair; Jeffrey
L. Saver,
MD, FAHA, Vice Chair;
Harold P. Adams, Jr, MD, FAHA; Askiel Bruno, MD, MS; J.J. (Buddy) Connors, MD;
stroke and hyperglycemia andBartmaintain
glucose
levels
M. Demaerschalk,the
MD, MSc;
Pooja Khatri,
MD, MSc, FAHA;
Paul W. McMullan, Jr, MD, FAHA; Adnan I. Qureshi, MD, FAHA;
considerably below 200 mg/dL. Kenneth Rosenfield, MD, FAHA; Phillip A. Scott, MD, FAHA;
Recommendations
Debbie R. Summers, RN, MSN, FAHA; David Z. Wang, DO, FAHA;
Max Wintermark, MD; Howard Yonas, MD; on behalf of the American Heart Association Stroke
Council, Council on Cardiovascular Nursing, Council on Peripheral Vascular Disease,
and Council on Clinical Cardiology
Background and Purpose—The authors present an overview of the current evidence and management recommendations
1. Cardiac monitoring
isandrecommended
tostroke.screen
for are prehospital care providers,
for evaluation
treatment of adults with acute ischemic
The intended audiences
physicians, allied health professionals, and hospital administrators responsible for the care of acute ischemic stroke patients
within
the firstother
48 hours from stroke
onset. These guidelinesserious
supersede the prior car2007 guidelines and 2009 updates.
atrial fibrillation
and
potentially
Methods—Members of the writing committee were appointed by theAmerican StrokeAssociation Stroke Council’s Scientific Statement
Committee,
representingnecessitate
various areas of medical expertise.
Strict adherence to the American Heart Association conflict
diac arrhythmiasOversight
that
would
emergency
of interest policy was maintained throughout the consensus process. Panel members were assigned topics relevant to their areas of
expertise, reviewed the stroke literature with emphasis on publications since the prior guidelines, and drafted recommendations in
cardiac interventions.
Cardiac monitoring should be
accordance with the American Heart Association Stroke Council’s Level of Evidence grading algorithm.
Results—The goal of these guidelines is to limit the morbidity and mortality associated with stroke. The guidelines support
performed for at least
the
first
24
hours
Level
the overarching
concept
of stroke
systems
of care and(Class
detail aspects ofI;
stroke
care from patient recognition; emergency
medical services activation, transport, and triage; through the initial hours in the emergency
department and stroke unit.
13
The guideline discusses
early stroke
and general medical
care, as well as ischemic
of Evidence B). (Revised
from
theevaluation
previous
guideline
) stroke, specific interventions
such as reperfusion strategies, and general physiological optimization for cerebral resuscitation.
2. Patients who have elevated blood pressure and are
otherwise eligible for treatment with intravenous
rtPA should have their blood pressure carefully lowered (Table 9) so that their systolic blood pressure
is <185 mm Hg and their diastolic blood pressure is
<110 mm Hg (Class I; Level of Evidence B) before
The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship
or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete
and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.
This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on December 12, 2012. A copy of the
document is available at http://my.americanheart.org/statements by selecting either the “By Topic” link or the “By Publication Date” link. To purchase
additional reprints, call 843-216-2533 or e-mail [email protected].
The Executive Summary is available as an online-only Data Supplement with this article at http://stroke.ahajournals.org/lookup/suppl/
doi:10.1161/STR.0b013e318284056a/-/DC1.
The American Heart Association requests that this document be cited as follows: Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, Demaerschalk
BM, Khatri P, McMullan PW Jr, Qureshi AI, Rosenfield K, Scott PA, Summers DR, Wang DZ, Wintermark M, Yonas H; on behalf of the American Heart
Association Stroke Council, Council on Cardiovascular Nursing, Council on Peripheral Vascular Disease, and Council on Clinical Cardiology. Guidelines
for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American
Stroke Association. Stroke. 2013;44:870–947.
Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines
development, visit http://my.americanheart.org/statements and select the “Policies and Development” link.
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express
patients should be transitioned to another anticoagulant agent
without interruption of therapeutic effect.
Competing Causes
of Stroke or
TIA
AHA/ASA
Guideline
Approximately one fourth of patients who present with AF
Guidelines
for thestroke
Prevention
Stroke
in Patients
With
and an ischemic
will beoffound
to have
other potential
Stroke
and Transient
Attack452 For these
causes for
the stroke,
such as Ischemic
carotid stenosis.
A Guideline for Healthcare Professionals From the American Heart
patients, treatment
decisions should
focus on the presumed
Association/American
Stroke Association
most likely stroke cause. In most cases, it will be appropriate
The American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists.
to initiate anticoagulation because of the AF, as well as an
Endorsed by the American Association of Neurological Surgeons and Congress of Neurological Surgeons
additional therapy (such as CEA).
Walter N. Kernan, MD, Chair; Bruce Ovbiagele, MD, MSc, MAS, Vice Chair; Henry R. Black, MD;
Dawn M. Bravata, MD; Marc I. Chimowitz, MBChB, FAHA; Michael D. Ezekowitz, MBChB, PhD;
Margaret C. Fang, MD, MPH; Marc Fisher, MD, FAHA; Karen L. Furie, MD, MPH, FAHA;
Donald V. Heck, MD; S. Claiborne (Clay) Johnston, MD, PhD; Scott E. Kasner, MD, FAHA;
Steven J. Kittner, MD, MPH, FAHA; Pamela H. Mitchell, PhD, RN, FAHA; Michael W. Rich, MD;
DeJuran Richardson, PhD; Lee H. Schwamm, MD, FAHA; John A. Wilson, MD; on behalf of the
American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council
on Clinical Cardiology, and Council on Peripheral Vascular Disease
AF Recommendations
1. For patients who have experienced an acute ischemic stroke or TIA with no other apparent cause,
rhythm
monitoring
(≈30evidence-based
days) for
AF is
Abstract—The aim prolonged
of this updated guideline
is to provide
comprehensive and timely
recommendations
on the prevention of future stroke among survivors of ischemic stroke or transient ischemic attack. The guideline is
reasonable
6 months
theEvidence-based
index event
(Class
addressed to all clinicians
who managewithin
secondary prevention
for these of
patients.
recommendations
are
provided for control of risk factors, intervention for vascular obstruction, antithrombotic therapy for cardioembolism,
IIa; Level of Evidence C). (New recommendation)
and antiplatelet therapy for noncardioembolic stroke. Recommendations are also provided for the prevention of recurrent
stroke in2.
a variety
of specific
circumstances,(Class
including aortic
atherosclerosis,
arterial dissection,
foramen
VKA
therapy
I; arch
Level
of Evidence
A),patent
apixaovale, hyperhomocysteinemia, hypercoagulable states, antiphospholipid antibody syndrome, sickle cell disease, cerebral
venous sinus thrombosis,
pregnancy.I;
Special
sectionsof
address
use of antithrombotic
anticoagulation
therapy after
ban and
(Class
Level
Evidence
A), and
and
dabigatran
an intracranial hemorrhage and implementation of guidelines. (Stroke. 2014;45:2160-2236.)
(Class I; Level of Evidence B) are all indicated
Key Words: AHA Scientific Statements ◼ atrial fibrillation ◼ carotid stenosis ◼ hypertension ◼ ischemia
ischemic attack, transient
prevention ◼ stroke
for the ◼prevention
of ◼recurrent
stroke in patients
with nonvalvular AF, that
whether
paroxysmal or perach year in the United States, >690 000 adults experience
impairment, and the high risk for recurrence. An addiE
The enormous morbidity
ischemic
an ischemic stroke.
tional
of US adults, estimated at 240
000, will
manent.
The ofselection
oflarge
annumber
antithrombotic
agent
stroke is the result of interplay between the resulting neuroexperience a transient ischemic attack (TIA). Although a TIA
leaves noon
immediate
individualsfachave a
logical impairment, the
emotional andbe
socialindividualized
consequences of
should
theimpairment,
basisaffected
of risk
tors, cost, tolerability, patient preference, potential
The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship
or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete
for drug
andas other
and submit a Disclosure Questionnaire
showing allinteractions,
such relationships that might be perceived
real or potential clinical
conflicts of interest. charac1
2
This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on February 28, 2013. A copy of the
hemorr
tiation o
IIa; Lev
9. For pat
who req
coagula
equival
rin) is r
thromb
Evidenc
10. The use
age wit
ischemi
IIb; Lev
Acute MI an
Patients with la
fraction <40%
at increased ris
of stasis of bl
injury with as
acute reperfusi
antithrombotic
thrombus was
acute MI.453–456
of mural throm
27% in those w
<40%.457–459 In
Bottom line…
!  ECG = tous
!  Holter ou télémétrie 24h = minimum
!  ETT = utilité moins claire mais recommandation pour
l’ensemble des cas, peut-être sauf si:
!  AVC lacunaire prouvé à l’imagerie
!  Source carotidienne convaincante (encore là…)
ETO: Qui?
!  Endocardite
!  Lésion suspecte de thrombus à l’ETT
!  Lésions multiples au CT ou à l’IRM
!  AVC chez le jeune (moins de 60-65 ans) ou en absence de facteur de risque
classique
!  ATCD d’AVC chez un patient se présentant avec un nouvel AVC et sans explication
Monitoring cardiaque prolongé
si…
!  En absence de CI à l’ATC et sans cause définie
!  MCAS
!  ECG anormal (infarctus ancien, ischémie aigu, BBG, etc)
!  Troponines élevés
!  Valvulopathies (sténose mitrale++) ou dilatation de
l’oreillette gauche
!  Sx d’arythmie (ex: palpitations)
!  Source cardiaque fortement suspectée cliniquement ou
radiologiquement (ex:lésions de plus d’un territoire)
Le temps d’enregistrement
dépend surtout…
!  Des ressources locales et de l’aspect réaliste de la
chose…un pacemaker n’est pas souhaitable pour tous!!!
!  Monitoring externe = préférable
!  7j-30j me semble raisonnable…
!  Surtout
Merci de votre
attention !