From the Department of Neurology (L.V, V.L., A.P.le T., G.G.) and the
Department of Cardiology (P.M.), Rangueil Hospital, University of Toulouse,
Toulouse, France.
Correspondence to Vincent Larrue, MD. Department of Neurology, Rangueil Hospital, 31403 Toulouse, Cedex 04, France. E-mail larrue.v{at}chu-toulouse.fr
Methods—We studied the incidence of EIR in 73 consecutive
patients with carotid stroke or TIA in whom TCD scanning of the
symptomatic middle cerebral artery was performed within 7
days from the onset of symptoms. Patients with a potential cardiac
source of embolism were excluded from the study.
Results—Eight patients had EIR during a mean±SD follow-up of
10±8 days. The incidence of EIR was 4.3 per 100 patient-days in
patients with MES and only 0.5 per 100 patient-days in patients without
MES. The presence of MES was a significant predictor of EIR after
adjustment for the presence of carotid stenosis or aortic arch
atheroma, antiplatelet therapy during follow-up, and
other potential confounding variables (relative risk, 8.7; 95%
confidence interval, 2 to 38.2; P=0.0015).
Conclusions—Microembolism is a significant independent predictor
of EIR in patients with stroke or TIA of presumed arterial
origin.
Asymptomatic microembolic signals (MES) can
be demonstrated in patients with carotid stenosis or AAA using
transcranial Doppler (TCD) ultrasonographic monitoring
of the middle cerebral artery (MCA).4 5 6 7 In
patients with carotid stenosis, microembolism has been related
to the degree of carotid narrowing8 and to the
ulcerated appearance of the plaque.9 10 However,
the clinical relevance of MES remains uncertain. In patients with
asymptomatic severe carotid stenosis, microembolism
has been associated with an increased risk of subsequent stroke or
transient ischemic attack (TIA).11 Early
microembolism after carotid endarterectomy has also
been related to postoperative cerebral
ischemia.12 A few studies have suggested
that microembolism may be a risk factor for early ischemic
recurrence (EIR).13 14 15 However, none of
their designs permitted them to control for the effect of potential
confounding variables, such as severe carotid stenosis or
thick AAA. The purpose of our study was to assess the independent
contribution of microembolism to the risk of EIR in patients with
cerebral ischemia of presumed arterial origin.
The mean±SD age of the 73 remaining patients (52 men and 21 women) was
65±13 years (range, 32 to 96 years). Twenty-three patients
presented with TIA and 50 with ischemic stroke. The
diagnosis of lacune was made in 10 patients with lacunar syndromes
(pure hemiparesis, pure sensory stroke, pure sensorimotor syndrome) and
an appropriate small and deep infarct on CT or brain MRI, or in the
absence of any demonstrable lesion despite a repeat study. The
diagnosis of large stroke was made in 11 patients with a severe deficit
(complete hemiplegia with conjugate eye deviations and decreased
consciousness) and a large infarct in the MCA territory demonstrated on
CT. Among the 29 other patients with ischemic stroke, 13 had a
cortical infarct, 10 had a subcortical infarct of >15 mm in
diameter, and 6 had no detectable lesion on CT or MRI.
All patients underwent carotid duplex and TCD scanning. Carotid
angiography was performed in 32 patients and MR angiography in 7.
Carotid stenoses were graded using the North American
Symptomatic Carotid Endarterectomy
Trial criteria16 in patients who underwent
angiography, and standard ultrasonographic criteria (peak and
telediastolic velocities and spectral broadening) in the
others. Intracranial carotid stenosis, proximal common carotid
stenosis, and carotid dissection were diagnosed by angiography
after duplex and TCD screening. Severe atherosclerosis
and dissection of the proximal aorta were diagnosed by
transesophageal echocardiography
(TEE), performed in 49 patients, using a biplane or multiplane 5-MHz
probe (Hewlett-Packard Sonos 1000). The diagnosis of aortic dissection
was confirmed by chest CT scan. A potential arterial source
of emboli was defined as carotid stenosis of
Unilateral TCD monitoring of the MCA was performed on the
symptomatic side for 20 minutes in all patients. TCD
monitoring was performed on both MCAs in 33 patients. A repeat
examination was performed on the symptomatic MCA during
follow-up in 26 patients. TCD studies were performed with a Pioneer
2020 (EME Nicolet). Briefly, after location of the artery, a 2-MHz
transducer was attached with an elastic head strap. The depth chosen
was from 45 to 50 mm to obtain maximum insonation of the MCA.
Then, gain and sample volume were reduced (to 10 mm for the sample
volume), and the time window overlap was increased to 72% to obtain
better detection of MES. The audible Doppler shift and the fast
Fourier–transformed spectra were continuously observed by an
experienced investigator, who noted all events that could be sources of
artifact. All monitorings were recorded on digital audiotapes and
were analyzed off-line by an independent observer who was
blinded to the clinical data. High-intensity transient signals of an
intensity of
Duration of follow-up was reduced to the time of hospitalization in our
Department of Neurology. This was done because 11 patients had early
carotid endarterectomy following their
ischemic event. Two other patients had prompt surgical repair
of aortic dissection. With this definition, mean±SD follow-up was
10±8 days. EIR was defined as either ischemic stroke or TIA
that occurred after the first TCD monitoring, and was diagnosed
during hospitalization in our department by the attending neurologist
before discharge, carotid endarterectomy, or aortic
surgery. In patients with previous stroke, recurrence was
defined as a sudden clinical deterioration with a decrease of at least
2 points on the Scandinavian Stroke Scale18
caused by either worsening of the initial deficit or a new focal
deficit. Hemorrhagic transformations and brain edema were excluded by
brain CT scan. Antithrombotic treatment at the time of EIR or at the
end of follow-up in patients without EIR consisted of an
antiplatelet agent in 67 patients (aspirin in 56 patients,
ticlopidine in 8 patients, and ticlopidine and aspirin in 3 patients)
associated in all but 2 with an anticoagulant (low dose in 40, full
dose in 25) and an anticoagulant alone in 6 patients (low dose in 4,
full dose in 2).
The interobserver agreement for the diagnosis of MES was calculated
with the
In the 33 patients who had a bilateral TCD scan, MES were more
frequently found on the symptomatic side (24%) than on the
asymptomatic one (3%, P=0.03). Among the 26
patients with repeat TCD scanning of the symptomatic MCA,
MES were found in 7 patients on the initial monitoring. The results of
the second monitoring were different from the first results in 4
patients: MES appeared in 1 patient, but were no longer present in
3 others. The time between both scans was 3±3 days.
EIR occurred in 8 patients. EIR comprised 2 strokes and 6 TIAs. All
occurred in the same carotid territory as the initial ischemic
event. Six patients had fully recovered from the initial
ischemic event when EIR occurred. One patient had an
ischemic recurrence in the left MCA territory after an
initial anterior cerebral artery stroke. The last patient had sudden
worsening of his initial deficit. Two patients had a second EIR during
follow-up.
Five EIRs occurred in 15 patients with MES (33%), and 3 EIRs occurred
in 58 patients without MES (5%, P=0.008). The incidence of
EIR per 100 patient-days was 4.3 in patients with MES and only 0.5 in
patients without MES. The Kaplan-Meier curves were significantly
different from each other (Figure
These results were obtained in a selected population of patients with
cerebral ischemia of presumed arterial origin. They
cannot be generalized to the patients with a potential cardiac source
of embolism, because the incidence and the clinical significance of MES
and the risk of EIR may be different in these
patients.15 19
Analysis of endarterectomy specimens
has demonstrated that microembolism before surgery is closely related
to ulceration of the carotid plaque.9 An
appearance of ulceration on carotid angiogram has also been associated
with microembolism, whatever the degree of carotid
narrowing.10 On the other hand, in a recent
study7 there was no relationship between
microembolism and morphological features of thick aortic plaques of
presumed emboligenic potential on TEE. However, only 19 patients were
included in that study. These results and our own findings suggest that
consideration of microembolism allows recognition of a subset of
patients with unstable arterial sources of embolism and at
high risk for EIR.
Antiplatelet therapy was a significant negative predictor of EIR in
our study. This finding is consistent with the results of
recent clinical randomized trials which suggest that aspirin modestly
but significantly reduces the risk of EIR in stroke
patients.20 21
We found MES in 22% of patients with recent cerebral ischemia.
The rate of MES in previous studies of similar patients has varied from
9% to 71%.13 14 22 23 24 25 26 27 Some methodological
reasons may account for these discrepancies. Distinction of MES from
artifacts or random fluctuations of background Doppler signal may
be difficult, especially when a low-intensity threshold for MES
detection is used.28 Besides, one cannot exclude
the possibility of an unintentional bias favoring the diagnosis of MES,
when the observer is aware of the presence of a potential source of
embolism. In our study, we chose an intensity threshold that should
reject most normal Doppler speckles, and all recordings
were reviewed by investigators blinded to clinical data. Using these
methods we obtained good interobserver agreement for the diagnosis of
MES. A recent study29 has demonstrated that such
methods, with an intensity threshold of
We used a short duration of testing because stroke patients are often
restless and uncooperative. Short durations of testing may be
inappropriate to allow diagnosis of random fluctuations of
microembolism.30 Moreover, repeated
recordings permit detection of more patients with
MES.6 25 26 In our study, analysis of a
second recording increased the proportion of patients with MES
from 7 of 26 to 8 of 26. Hence, although we probably missed some
patients with MES, we believe that this occurrence was rare.
In conclusion, our findings suggest that microembolism of the
symptomatic MCA in patients with recent carotid stroke or
TIA of presumed arterial origin is a significant and
independent predictor of EIR. This may have important implications for
the monitoring of the effect of secondary preventive therapies in this
setting.
Received March 9, 1998;
revision received June 29, 1998;
accepted June 29, 1998.
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North American Symptomatic Carotid
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Siebler M, Sitzer M, Rose D, Benefeldt D, Steinmetz H.
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symptomatic high-grade carotid stenosis.
Brain. 1993;116:1005–1015.
6.
Markus H, Thomson N, Brown M. Asymptomatic
cerebral embolic signals, in symptomatic and
asymptomatic carotid artery disease. Brain. 1995;118:1005–1011.
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Valton L, Larrue V, Pavy le Traon A, Géraud G,
Bès A. Microembolism in patients with recent cerebral
ischemia and aortic arch atheroma. In: J.
Klingelhöfer et al, eds. New Trends in Cerebral
Hemodynamics and Neurosonology. Amsterdam,
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8.
Eicke B, von Lorentz J, Paulus W. Embolus detection in
different degrees of carotid disease. Neurol Res. 1995;17:181–184.[Medline]
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Sitzer M, Müller W, Siebler M, Hort W, Kniemeyer
H, Jäncke L, Steinmetz H. Plaque ulceration and lumen thrombus
are the main sources of cerebral microemboli in high-grade internal
carotid artery stenosis. Stroke. 1995;26:1231–1233.
10.
Valton L, Larrue V, Arrué P, Géraud G,
Bès A. Asymptomatic cerebral embolic signals in
patients with carotid stenosis: correlation with appearance of
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Siebler M, Natchmann A, Sitzer M, Rose G, Kleinschmidt
A, Rademacher J, Steinmetz H. Cerebral microembolism and the risk of
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Levi C, O'Malley H, Fell G, Roberts A, Hoare M, Royle
J, Chan A, Beiles B, Chambers B, Bladin C, Donnan G.
Transcranial Doppler detected cerebral microembolism
following carotid endarterectomy: high
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Tegeler C, Burke G, Dalley G, Stump D. Carotid emboli
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Valton L, Larrue V, Pavy le Traon A, Géraud G.
Cerebral microembolism in patients with stroke or transient ischaemic
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© 1998 American Heart Association, Inc.
Original Contributions
Microembolic Signals and Risk of Early Recurrence in Patients With Stroke or Transient Ischemic Attack
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Background and
Purpose—Asymptomatic microembolic
signals (MES) can be demonstrated in patients with cerebral
ischemia using transcranial Doppler (TCD)
ultrasonographic monitoring of the middle cerebral artery. However, the
clinical relevance of MES remains uncertain. The purpose of this study
was to estimate the independent contribution of microembolism to the
risk of early ischemic recurrence (EIR) in patients
with stroke or transient ischemic attack (TIA) of presumed
arterial origin.
Key Words: cerebral embolism • risk factors • stroke, acute • ultrasonography
Introduction
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Patients with symptomatic tight carotid
stenosis or thick aortic arch atheroma (AAA) are at
risk for stroke recurrence.1 2 3 However,
not all the patients with such arterial lesions develop
recurrence. Methods that might help to select patients at
highest risk would be useful for therapeutic decisions.
Subjects and Methods
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
We followed up 73 patients with stroke or TIA in the anterior
circulation. All subjects were selected from a series of 102
consecutive patients who were monitored for MES detection within 7 days
from the onset of symptoms. The diagnosis of ischemic stroke or
TIA was based on each patient's clinical presentation and
was supported by extensive laboratory investigations including early
brain CT scan. Twenty-nine patients were excluded for the following
reasons: in 4 patients the symptoms of focal cerebral impairment were
not related to an acute cerebral ischemia; ischemia
involved the vertebrobasilar territory in 6 patients; 3 patients were
not followed up in the Department of Neurology; recordings of
the TCD scans were not available for technical reasons in 2 patients;
and finally, because we wanted to focus on the risk of
recurrence in patients with cerebral ischemia of
presumed arterial origin, we excluded 14 patients with a
potential cardiac source of emboli (atrial fibrillation, intracardiac
thrombus, recent myocardial infarction, valvular disease, or
prosthetic valves) as detected by medical history, ECG, and
echocardiography. 
70%
(extracranial in 22, intracranial in 1, and proximal common carotid in
1), carotid dissection (n=6), thick (5 mm) atheroma
in the ascending or horizontal aorta (n=11), or proximal aortic
dissection (n=2). Among the other patients, 15 had no detectable
arterial lesion and 17 had a carotid
stenosis of <70% (n=14) or an aortic plaque of <5 mm
(n=6). A prior recent stroke or TIA was defined as a stroke or a TIA
that occurred during the 6 months preceding the qualifying
ischemic event. 6 dB were selected first. Measurement of the peak
intensity of each signal was performed by visually
"thresholding" the intensity of the spectral display in 1-dB
increments using the instrument gain-setting adjustments. Intensities
were averaged for each signal over 3 replays of the tape. The diagnosis
of MES was made among these selected signals in agreement with
international recommendations: unidirectional, within the blood flow
velocity spectrum, short duration (<0.15 and <0.3 seconds for
systolic and diastolic signals, respectively)
signals accompanied by a characteristic sound, occurring randomly
within the cardiac cycle and without any simultaneous
detectable source of artifact.17 To assess the
interobserver agreement for the diagnosis of MES among transient
signals of an intensity of 6 dB, the recordings of 32
patients were analyzed by a second independent observer. The
patients received the following antithrombotic treatments when TCD
scanning was performed: 46 patients were treated with an
antiplatelet agent (250 mg aspirin in 43, 500 mg ticlopidine in 3).
Most of them also received an anticoagulant (low dose in 14 patients,
full dose in 30 patients); 17 patients received only an anticoagulant
(low dose in 8 patients and full dose in 9 patients). Ten patients
received no antithrombotic treatment. 
statistic. Univariate analysis was
performed using the 
2 test with continuity
correction and 2-tailed Fisher's exact test for categorical
variables and Student's t test for continuous
variables. Tests were bilateral. The probability of survival free
of EIR according to the presence of MES at entry was estimated with the
Kaplan-Meier method. Kaplan-Meier curves were compared with use of the
log-rank test. To calculate the adjusted relative risk of EIR in the
presence of MES, we used a Cox model that included carotid
stenosis or aortic arch atheroma, large stroke,
lacune, prior stroke or TIA, and antiplatelet therapy during
follow-up. A stepwise procedure allowed only significant variables
to be retained in the final model. Significance was set at
P<0.05. Data were analyzed with SAS software.
Results
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Characteristics of patients at entry are summarized in the
Table
. Fifteen patients had MES on the first TCD
scanning of the symptomatic MCA. The mean±SD time between
the qualifying ischemic event and the TCD scan was 2±2 days.
The index for the diagnosis of MES was good (=0.895). Eight
patients with MES (53%) and 14 without MES (24%) had a history of
prior recent stroke or TIA (P=0.055). Arterial
sources of emboli were more common in patients with MES (93%) than in
those without MES (47%, P=0.001). A carotid source of
emboli was found in 11 patients with MES (73%) and in 19 patients
without MES (33%, P=0.007). An aortic source of emboli was
found by TEE in 4 of 7 patients with MES (57%) and in 9 of 42 patients
without MES (21%, P=0.02). There were no significant
differences between the 2 groups for cerebral ischemia patterns
and antithrombotic treatments received when TCD monitoring was
performed.
View this table:
[in a new window]
Table 1. Characteristics of Patients at
Entry ). In the Cox model the
stepwise procedure selected the presence of MES (relative risk, 8.7;
95% confidence interval, 2 to 38.2; P=0.0015) and
antiplatelet therapy during follow-up (relative risk, 0.18; 95%
confidence interval, 0.03 to 0.94; P=0.0221) as significant
independent predictors of EIR.
View larger version (16K):
[in a new window]
Figure 1. Estimation of survival free of EIR according to the presence
of MES at entry (Kaplan-Meier method).
Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
In this study, patients with recent cerebral ischemia in
whom TCD monitoring of the symptomatic MCA demonstrated
microembolism were at high risk for subsequent EIR. Most patients with
MES had a potential arterial source of embolism. However,
the effect of microembolism on the risk of EIR was independent from
that of severe carotid stenosis or thick AAA and other
potential confounding variables. 6 dB, permit a good
probability of agreement (0.872) between observers from different
centers.
Acknowledgments
We thank Antoine de Falguerolles and Gérard Tap
(Laboratory of Statistics, Toulouse University) for statistical advice;
Chantal Antolin, Maïté Seguy, and Jean Michel Caumont for
their technical assistance; and Edith Sambres for her secretarial
help.
References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
1.
European Carotid Surgery Trialists' Collaborative
Group. MRC European Carotid Surgery Trial: interim results for
symptomatic patients with severe (70–99%) or with mild
(0–29%) carotid stenosis. Lancet. 1991;337:1235–1243.[Medline]
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J. L. Stork, K. Kimura, C. R. Levi, B. R. Chambers, A. L. Abbott, and G. A. Donnan Source of Microembolic Signals in Patients With High-Grade Carotid Stenosis Stroke, August 1, 2002; 33(8): 2014 - 2018. [Abstract] [Full Text] [PDF]
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G. Orlandi, S. Fanucchi, F. Sartucci, L. Murri, C. D. Liapis, J. D. Kakisis, and A. G. Kostakis Can Microembolic Signals Identify Unstable Plaques Affecting Symptomatology in Carotid Stenosis? * Response Stroke, July 1, 2002; 33 (7): 1744 - 1746. [Full Text] [PDF]
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G. H. Danton, R. Prado, B. D. Watson, and W. D. Dietrich Temporal Profile of Enhanced Vulnerability of the Postthrombotic Brain to Secondary Embolic Events Stroke, April 1, 2002; 33(4): 1113 - 1119. [Abstract] [Full Text] [PDF]
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M Goertler, T Blaser, S Krueger, K Hofmann, M Baeumer, and C-W Wallesch Cessation of embolic signals after antithrombotic prevention is related to reduced risk of recurrent arterioembolic transient ischaemic attack and stroke J. Neurol. Neurosurg. Psychiatry, March 1, 2002; 72(3): 338 - 342. [Abstract] [Full Text] [PDF]
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G. Devuyst, G.A. Darbellay, J.-M. Vesin, V. Kemeny, M. Ritter, D.W. Droste, C. Molina, J. Serena, R. Sztajzel, P. Ruchat, et al. Automatic Classification of HITS Into Artifacts or Solid or Gaseous Emboli by a Wavelet Representation Combined With Dual-Gate TCD Stroke, December 1, 2001; 32(12): 2803 - 2809. [Abstract] [Full Text] [PDF]
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J. F. Arenillas, C. A. Molina, J. Montaner, S. Abilleira, M. A. Gonzalez-Sanchez;, and J. Alvarez-Sabin Progression and Clinical Recurrence of Symptomatic Middle Cerebral Artery Stenosis: A Long-Term Follow-Up Transcranial Doppler Ultrasound Study Stroke, December 1, 2001; 32(12): 2898 - 2904. [Abstract] [Full Text] [PDF]
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 H. Markus and M. Cullinane Severely impaired cerebrovascular reactivity predicts stroke and TIA risk in patients with carotid artery stenosis and occlusion Brain, March 1, 2001; 124(3): 457 - 467. [Abstract] [Full Text] [PDF]
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 C. A. Molina, J. Alvarez-Sabin, W. Schonewille, J. Montaner, A. Rovira, S. Abilleira, and A. Codina Cerebral microembolism in acute spontaneous internal carotid artery dissection Neurology, December 12, 2000; 55(11): 1738 - 1741. [Abstract] [Full Text] [PDF]
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T. Rundek, M. R. Di Tullio, R. R. Sciacca, I. V. Titova, J. P. Mohr, S. Homma, and R. L. Sacco Association Between Large Aortic Arch Atheromas and High-Intensity Transient Signals in Elderly Stroke Patients Stroke, December 1, 1999; 30(12): 2683 - 2686. [Abstract] [Full Text] [PDF]
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E. Vassileva, H. Schnorf, O. Personeni, and J. Le Floch-Rohr Microembolic Signals and Early Recurrent Cerebral Ischemia in Carotid Artery Disease Stroke, July 1, 1999; 30 (7): 1490 - 1493. [Full Text] [PDF]
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R. T.F. Cheung, L. Valton, and V. Larrue Early Ischemic Recurrence and Microembolic Signals Detected by Transcranial Doppler • Response Stroke, June 1, 1999; 30(6): 1290 - 1290. [Full Text] [PDF]
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