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(Stroke. 1996;27:691-694.)
© 1996 American Heart Association, Inc.
Articles |
Transesophageal Echocardiography in Patients With Focal Cerebral Ischemia of Unknown Cause
From Medizinische Poliklinik, München, Germany.
Correspondence to Günter Rauh, Medizinische Poliklinik, Pettenkoferstr 8a, D-80336 München, Germany.
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Abstract |
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Background and Purpose Identification of cardioembolic stroke is often limited by the difficulties involved in the detection of thrombi or the risk factors for thrombus formation. Patients in sinus rhythm with nondiagnostic transthoracic echocardiogram (TTE) and without carotid artery stenosis represent a subset in whom diagnostic recommendations are lacking. The aim of this study was to determine the value of transesophageal echocardiography (TEE) for diagnosis and therapy in this population.
Methods Thirty patients with the characteristics described above were studied prospectively with the use of blood analysis, TTE, TEE, and Holter monitoring (in patients with atrial thrombus).
Results TTE was abnormal in 16 of 30 patients, but no embolic source was identified. TEE disclosed left atrial appendage thrombus in 3 of 30 patients, atrial septal aneurysm in 2 of 30 patients, patent foramen ovale in 7 of 30 patients, and aortic plaques in 19 of 30 patients. The TEE resulted in a change of therapy in 3 of the 30 patients studied.
Conclusions This study demonstrates that TEE is a helpful diagnostic tool in delineating the risk of cardioembolic stroke and demonstrates significant pathology even in a subset of patients deemed to be at low risk. This additional new information led to a substantial change in therapy in 3 of 30 patients.
Key Words: cardioembolic stroke • cerebral ischemia, focal • echocardiography, transesophageal
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In patients with stroke, diagnostic efforts are directed toward a clarification of the individual etiology as subsequent therapy is directed toward prevention of further events. Stroke registries suggest that 22% to 39% of strokes are caused by cardiogenic emboli.1 2 Cardiac abnormalities detected only by TEE, particularly atrial septal aneurysm, aortic plaques, and patent foramen ovale, were identified as risk factors (and not causes) for recurrent stroke.3 4 5 6 7 8 In patients with first stroke, the identification of atrial septal aneurysm, aortic plaques, and patent foramen ovale usually has no effect on therapy. In contrast, left atrial appendage thrombi and spontaneous atrial contrast appearance are considered definite causes for cardioembolic stroke requiring oral anticoagulation.
Previous reports have shown left atrial appendage thrombi and spontaneous atrial contrast in patients with normal sinus rhythm and nondiagnostic TTE.9 10 11 12 These data, however, can only be extracted from studies that were performed for other reasons. The purpose of the present study was to determine the diagnostic value of TEE in a subset of patients with stroke without well-established causes for cerebral ischemia, ie, in patients with sinus rhythm and normal TTE and without carotid artery stenosis.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Patients
Between January 1994 and June 1995, 30 consecutive patients were prospectively enrolled in this study (median age, 62 years [range, 28 to 83 years]; 15 men). The inclusion criteria were as follows: (1) completed (neurological deficit lasting >24 hours) ischemic stroke; (2) sinus rhythm; (3) exclusion of cardiac diseases linked to the occurrence of cardiogenic emboli by TTE (ventricular and atrial thrombi, ventricular aneurysm, aortic and mitral valve stenosis, and LV global wall motion abnormalities with ejection fraction <25%); (4) exclusion of carotid artery stenosis by carotid artery duplex scanning13 ; and (5) the patient's consent to undergo detailed etiologic investigation. All patients were recruited in one center from patients demonstrating focal cerebral ischemia who were referred for further evaluation of a cerebral ischemic event; 152 stroke patients were investigated to obtain the 30 patients included in this study. The 122 patients who did not enter the study were excluded on the basis of carotid stenosis >50% (94); atrial fibrillation (9); aortic and mitral valve stenoses determined in TTE (5); LV aneurysms, thrombi, or global hypokinesia with an ejection fraction <25% determined by TTE (13); or refusal to undergo TEE (1).
Patients enrolled in the study were investigated according to a standardized protocol including ECG, TTE and TEE with a contrast study, and laboratory study (complete blood cell count, erythrocyte sedimentation rate, protein electrophoresis, antinuclear antibodies, glucose, serum cholesterol, triglyceride levels, and prothrombin and activated partial thromboplastin time). A 24-hour ECG Holter monitoring was performed in 3 patients with left atrial appendage thrombi (patients 4, 8, and 22) to detect possible arrhythmias. The following conditions were considered atherosclerotic risk factors: cigarette smoking, diabetes mellitus (fasting blood glucose concentration >5.6 mmol/L), hypercholesterolemia (cholesterol concentration >6.5 mmol/L), hypertension (blood pressure >160/90 mm Hg), and oral contraceptive use.
Echocardiographic Studies
All patients were studied by TTE and TEE. The
transthoracic studies were performed by standard techniques
with a 2.5- or 3.5-MHz phased transducer (Interspec Apogee CX 200,
Acuson 128 XP/10). Views were obtained in the parasternal, apical, and
subcostal windows.
The transesophageal images were obtained with a 5-MHz monoplane transducer (Interspec Apogee CX) in 16 of 30 patients and with a biplane transducer (Acuson 128 XP/10) in 14 of 30 patients. The study was performed in awake patients with no premedication other than topical lidocaine spray. The probe was passed to 25 to 30 cm from incisors and then manipulated to provide adequate views of both atria, left atrial appendage, atrial septum, mitral valve apparatus, and thoracic aorta. All examinations were recorded on videotape for subsequent playback and analysis.
Atrial septal aneurysm was diagnosed when the atrial septum
appeared abnormally redundant and mobile and exhibited an excursion
into the left or right atrium or both of 
10 mm.3 7 The
distance between the plane of the atrial septum and the point of
maximal aneurysmal bulging was measured from the
stopped-frame image. For patent foramen ovale, the
echocardiographic detection of interatrial
right-to-left shunting was accomplished by administration of 5
mL agitated galactose IV (Echovist, Behring). Two to four contrast
injections were systematically performed in each patient, in the
resting state and during provocative maneuvers (Valsalva
and cough test) to transiently reverse the interatrial pressure
gradient. The echocardiographic diagnosis of patent
foramen ovale was based on the appearance of more than five
microcavitations, either spontaneously or after provocation maneuvers,
into the left atrium within three cardiac cycles.3 7
Spontaneous echo contrast was defined as "smokelike" echoes
swirling slowly in the left atrium. Mitral valve prolapse was defined
on TTE as mitral leaflet thickening and displacement beyond the plane
of the mitral annulus and into the left atrium in the parasternal
long-axis view during systole.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The ECG, TTE, and TEE findings of our patients are described in the Table
. ECG performed with a rhythm strip revealed
single premature atrial contractions in 3 patients. All patients with a
history of myocardial infarction (patients 2, 4, and 16) showed
ECG changes consistent with this diagnosis.
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Pathological findings of the TTE were observed in 16 patients. However, no patient displayed findings linked to the occurrence of cardiogenic emboli. LV hypertrophy was present in 11 patients, all of whom had arterial hypertension. Regional wall motion abnormalities were identified in 4 patients with a history of myocardial infarction. Valvular calcifications were present in 9 patients, aortic insufficiency in 2 patients, mitral regurgitation in 4 patients, and mitral valve prolapse in 1 patient.
TEE confirmed the results seen with TTE. Additionally, we identified
left atrial appendage thrombi as a definite cause for cardiogenic
emboli in 3 of 30 patients (patients 4, 8, and 22). Fig 1 demonstrates a short-axis view of a thrombus
confined to the left atrial appendage in patient 4. Atrial septal
aneurysm as a risk factor for cardiogenic embolization was
present in 2 of 30 patients (patients 15 and 28). Fig 2 shows a short-axis view of a large (>10 mm
excursion) atrial septal aneurysm bulging into the left atrium.
Patent foramen ovale as a risk factor for paradoxical emboli was
identified in 7 patients. Aortic plaques (all with a thickness <4 mm)
as a risk factor for aortoarterial embolization were
noted in 19 patients.
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In patients with left atrial appendage thrombi (patients 4, 8, and 22), further evaluations were performed. Holter ECG demonstrated single premature atrial and ventricular contractions; intermittent atrial fibrillation was not documented. LV systolic function as determined by LV diameter and ejection fraction was normal in all patients with left atrial appendage thrombi.14 15 The transmitral Doppler flow image demonstrated an abnormal LV relaxation pattern with decreased E wave (peak rapid filling velocity), prolonged deceleration time, and increased A wave (peak atrial filling velocity) in all patients with left atrial appendage thrombi. Possible causes of the abnormal LV relaxation include coronary artery disease with a history of myocardial infarction (patient 4); hypertensive heart disease based on a 15-year history of arterial hypertension (patient 8); and irradiation of the heart and the mediastinum in mediastinal lymphoma (patient 22). All patients with left atrial thrombi had well-defined emptying waves with visible contractions of the left atrial appendage wall.16
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The etiology of stroke is undoubtedly multifactorial. If cerebral ischemia is associated with atherosclerotic disease of the carotid artery and the absence of severe carotid stenosis, acetylsalicylic acid and ticlopidine are standard therapy at present.17 If cerebral ischemia is associated with cardiac thrombi, oral anticoagulation is usually the treatment of choice. Therefore, the recognition of cardiac thrombi is essential. TTE is widely used to identify atrial and ventricular thrombi, ventricular aneurysm, aortic and mitral valve stenoses, and LV wall motion abnormalities with a low ejection fraction.9 10 11 12 Although TEE frequently reveals additional findings that are considered embolic risk factors, such as atrial septal aneurysm, aortic plaques, and patent foramen ovale, only the identification of thrombi induces a change of therapy from aspirin or ticlopidine to oral anticoagulation.
In a selected group of patients displaying cerebral ischemia, sinus rhythm, and absence of carotid stenosis, in whom a TTE disclosed no cardiac risk factors for emboli, TEE was evaluated for therapeutic consequences.
In 3 of 30 patients, left atrial appendage thrombi as a definite cause of cardiogenic emboli could be demonstrated by TEE. All patients with left atrial appendage thrombi had normal LV systolic function as determined by LV diameter and ejection fraction. However, in patients with LV wall motion abnormality, a systolic dysfunction can be missed, because M-mode echocardiography may not be a reliable method. All patients with left atrial appendage thrombi had an abnormal LV relaxation pattern as determined by transmitral Doppler flow.15 Coronary artery disease, arterial hypertension, and cardiac irradiation are possible causes of abnormal LV relaxation in these patients.14
However, in all patients with left atrial appendage thrombus the performance of the TEE resulted in a change of treatment, with the addition of oral anticoagulation to the regimen.
Atrial septal aneurysm and patent foramen ovale were demonstrated at a frequency that can be expected from the literature. The lack of aortic plaques >4 mm is most likely associated with suboptimal imaging of the aortic arch due to the use of monoplane TEE.
Various hypotheses may explain the formation of left atrial appendage thrombi in patients with sinus rhythm: (1) intermittent atrial fibrillation can be present in these patients despite an unremarkable 24-hour ECG Holter monitoring, (2) abnormal LV function associated with increased left atrial pressure may be an independent risk factor for left atrial appendage thrombi, and (3) coagulation disturbances may be present in these patients that were not diagnosed in the coagulation and immunologic studies.
In summary, this study shows that TEE repeatedly detected significant cardiac pathology in stroke patients with sinus rhythm in whom TTE was unremarkable with respect to an embolic cause. This additional new information led to a substantial change in therapy, namely, the institution of oral anticoagulation, in 3 of 30 patients. We suggest that TEE should be recommended for stroke patients without an otherwise proven etiology. Further studies may delineate the underlying mechanism.
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Selected Abbreviations and Acronyms |
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Received October 20, 1995; revision received November 30, 1995; accepted December 15, 1995.
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References |
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