(Stroke. 2002;33:712.)
© 2002 American Heart Association, Inc.
Original Contributions |
From the Department of Neurology (E.K., D.E., K.B.) and the Department of Rheumatology (K.A., G.K., Y.K.), Ege University Faculty of Medicine, Izmir, Turkey.
Correspondence to Prof Emre Kumral, MD, Stroke Unit, Department of Neurology, Ege University Faculty of Medicine, Bornova, 35100 Izmir, Turkey. E-mail ekumral{at}med.ege.edu.tr
| Abstract |
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Methods Eighteen patients with TA according to the criteria for the classification of TA of the American College of Rheumatology and 100 age-matched healthy controls were studied. Both middle cerebral arteries were monitored by transcranial Doppler (TCD) ultrasound for at least 30 minutes. All patients with TA were followed up for a mean duration of 2.1 months, and recurrent strokes were registered.
Results Microembolic signals (MES) were present in 22% of the patients overall, and the intensity of the MES varied between 9 and 30 dB. Moreover, MES were found in 30% of the patients with higher erythrocyte sedimentation rate. Two (67%) of 3 patients who did not receive any treatment had MES, but only 2 (13%) of 15 patients who received immunosuppressive and anticoagulant therapy before the TCD ultrasonography monitoring had MES. During the follow-up period after MES recording, we did not observe any recurrent stroke.
Conclusions TCD ultrasonography monitoring can be used as an additional noninvasive procedure to detect microembolus in patients with TA during the acute and chronic phase of the disease. The monitoring of MES may also help in choosing better treatment for the long-term prophylaxis of the disease from acute ischemic stroke, but further large studies are required to justify the efficacy of immunosuppressive treatment in these patients.
Key Words: embolism Takayasus arteritis ultrasonography, Doppler, transcranial
| Introduction |
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| Subjects and Methods |
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3 of the 6 following criteria is consistent with a diagnosis of TA: onset age <40 years, claudication of an extremity, decreased brachial artery pulse, >10 mm Hg difference in systolic blood pressure between arms, a bruit over the subclavian arteries or the aorta, and arteriographic evidence of narrowing or occlusion of the entire aorta, its primary branches, or large arteries in the proximal upper and lower extremities. Clinical classification of TA was defined in 4 subgroups as proposed by Lupi-Herrera et al3 and modified by us: (1) type I was presumed in patients with involvement of the aortic arch and its branches; (2) type II was confined to the ascending and descending aorta without involvement of the celiac artery and aortic arch; (3) type III was characterized by involvement of the descending aorta (from the end of aortic arch to the femoral artery); and (4) type IV was presumed in patients with involvement of all the aorta, its branches, and pulmonary arteries. The following vascular risk factors were recorded: age, sex, hypertension, diabetes mellitus, hypercholesterolemia, cigarette smoking, ischemic heart disease, atrial fibrillation, and cardiac valve prosthesis. Noninvasive investigations including extracranial and TCD sonography as well as duplex sonography, 12-lead ECG, and transthoracic/transesophageal echocardiography were performed in all cases. Cerebral CT and MRI (T1-weighted, T2-weighted, and proton density-weighted images) were performed in patients with neurological involvement. Digital subtraction angiography by the Seldinger technique with the ascendant arch, descendant aorta, and subclavian and carotid arteries was performed in all patients. Spouses and psychiatric outpatients (100 subjects) in sinus rhythm without a history of vascular disease, claudication of extremities, decreased brachial artery pulse, or bruit over the aorta or carotid arteries were enrolled in the present study as a normal control group. All control subjects were evaluated by carotid duplex ultrasound to exclude a significant carotid stenosis (>50% diameter).
Embolic Signal Monitoring
Bilateral TCD ultrasonography monitoring was performed over the middle cerebral arteries (MCAs) by using 2-MHz probes of a pulsed Doppler machine (Multi-Dop X-4, DWL, with multirange embolus detection software TCD-8 for MDX, version 8.00K) for 30 minutes per patient and control subject. Both MCAs were simultaneously monitored through the temporal window at an insonation depth of 50 to 55 mm. In multigate Doppler ultrasonography evaluations, 2 different depths of the same vessel were monitored, and an intergate distance of 5 mm was used. The sweep time was
6 seconds, and a velocity scale between -100 and 150 cm/s was used. We used a 128-point fast Fourier transform resolution and set the high-pass filter at 100 Hz. Power was 160 mW/cm2, and the pulse repetition frequency was 6500 Hz. A detection threshold of
9 dB was used to identify the microembolic events. Two examiners were present throughout the study and evaluated the monitoring results of the MCA online. The determination and detection of microemboli were performed according to the criteria of the International Consensus Group on Microembolus Detection7: (1) characteristic acoustic properties, (2) short duration (<0.3 seconds), (3) random appearance in the cardiac cycle, (4) unidirectional signal, and (5) intensity increase at least 9 dB above the background. Differentiation of MES from artifacts was based on the criteria of consensus conference. Artifacts were assumed if signals were registered simultaneously on both sides or bidirectionally above and below the baseline. All data were stored on the hard disk for subsequent analysis. The examiners were blind to the status of all subjects, and they evaluated MES counts in the MCA independent from each other and were asked to note both the exact position of each MES on the recording and the total MES counts. The MES recordings were repeated twice to assess interobserver agreement at the same point in time by 2 observers. Only signals recognized by both observers in 2 successive recordings were accepted as embolic in nature. Embolic signals were considered on the basis of the intensity and mean number of 2 consecutive recordings.
Data Analysis
The data were evaluated by using SPSS for Windows, release 8.0 (SPSS, Inc). Descriptive statistics were computed for each of the variables included in the present study. For between-group comparisons of continuous variables, t tests were used. Significance was set at the P<0.05 level.
| Results |
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| Discussion |
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In patients with TA, the inflammation primarily affects the aorta and extends into the cluster of arterial branches adjacent to primary lesion. Most commonly, the proximal portion of a vessel is affected, with continuation of the pathological process into the more distal portion. During the acute phase, inflammatory infiltrates usually consist of lymphocytes, plasma cells, and giant cells and involve all layers of the arterial wall. Thrombi are frequently observed distal to the sites of inflammatory changes. At the chronic phase, fibrous tissue replaces the damaged intima, media, and adventitia. Stenotic lesions develop and may resemble arteriosclerotic plaques.1416 Our findings suggest that MES frequency was higher during the active phase of the disease, which was followed by ESR assessment, than during the silent chronic phase. The mechanism of the presence of MES in patients with type III arteritis could be explained by the generalized inflammatory changes through the aorta during the acute phase.
Angiography and ultrasonographic methods show luminal morphology but provide no information on the inflammatory status of the vessel wall in patients with TA.2,3,1719 Thus, the finding of a patent vessel does not exclude the presence of early inflammation and active disease. A review of 33 surgical specimens demonstrated active inflammation in 20% of TA patients, and chronic changes of uncertain significance in 20%.20 Active focal skip lesions are often interspersed by inactive healed lesions and may contribute to the development of an embolus in the cerebrum. In the present study, 1 patient with stroke who had normal ESR exhibited MES, suggesting that an active inflammatory process in TA could continue in spite of a normal ESR and cause cerebral ischemia by embolic materials.
In TA patients, MES were present in more than two thirds of the patients who did not receive immunosuppressive therapy, whereas only one fifth of those who received treatment had MES, suggesting positive anti-inflammatory effects of these drugs on the vasculature, especially in the active phase.2,21
In conclusion, cerebral microembolus detection can be used as an additional noninvasive procedure in patients with TA during the acute and chronic phase of the disease. The monitoring of MES seems useful for selecting better treatment for long-term prophylaxis of disease from acute and recurrent stroke, but further large studies are required to justify the efficacy of immunosuppressive treatment in these patients.
Received May 22, 2001; revision received September 28, 2001; accepted October 1, 2001.
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