|Microembolus detection by transcranial Doppler sonography: review of the literature.|
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|PMID: 22195291 Owner: NLM Status: In-Data-Review|
|Transcranial Doppler can detect microembolic signals which are characterized by unidirectional high intensity increase, short duration, random occurrence, and a "whistling" sound. Microembolic signals have been detected in a number of clinical settings: carotid artery stenosis, aortic arch plaques, atrial fibrillation, myocardial infarction, prosthetic heart valves, patent foramen ovale, valvular stenosis, during invasive procedures (angiography, percutaneous transluminal angioplasty), surgery (carotid, cardiopulmonary bypass, orthopedic), and in certain systemic diseases. Microembolic signals are frequent in large artery disease, less commonly detected in cardioembolic stroke, and infrequent in lacunar stroke. This article provides an overview about the current state of technical and clinical aspects of microembolus detection.|
|Type: Journal Article Date: 2011-11-30|
|Title: Stroke research and treatment Volume: 2012 ISSN: 2042-0056 ISO Abbreviation: Stroke Res Treat Publication Date: 2012|
|Created Date: 2011-12-23 Completed Date: - Revised Date: -|
Medline Journal Info:
|Nlm Unique ID: 101529024 Medline TA: Stroke Res Treat Country: United States|
|Languages: eng Pagination: 382361 Citation Subset: -|
|Department of Neurology, University Hospital Center "Sestre milosrdnice," 10000, Zagreb, Croatia.|
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Journal ID (nlm-ta): Stroke Res Treat
Journal ID (publisher-id): SRT
Publisher: Hindawi Publishing Corporation
Copyright © 2012 Vlasta Vuković-Cvetković.
Received Day: 1 Month: 8 Year: 2011
Accepted Day: 17 Month: 10 Year: 2011
Print publication date: Year: 2012
Electronic publication date: Day: 30 Month: 11 Year: 2011
Volume: 2012E-location ID: 382361
PubMed Id: 22195291
|Microembolus Detection by Transcranial Doppler Sonography: Review of the Literature|
|Department of Neurology, University Hospital Center “Sestre milosrdnice,” 10000, Zagreb, Croatia
|Correspondence: *Vlasta Vuković-Cvetković: firstname.lastname@example.org
[other] Academic Editor: Arijana Lovrencic-Huzjan
Acute stroke is one of the leading cause of morbidity and mortality worldwide. In developed countries, stroke ranks as either second or third most common cause of death and embolization is the cause of ischemic stroke in 40%–80% of cases . TCD is a sensitive technique for real-time detection of microembolic signals (MESs). In the last 20 years, a substantial number of studies dealing with emboli detection have been carried out, showing that MES are proven to represent emboli passing within cerebral circulation. MES have been detected in a number of clinical conditions: carotid artery stenosis, aortic arch plaques, atrial fibrillation, myocardial infarction, prosthetic heart valves, patent foramen ovale, valvular stenosis, during carotid surgery, surgery on open heart, stent implantation, percutaneous transluminal angioplasty and angiography, and in patients with migraine and patent foramen ovale (PFO). Patients who have detectable MES, especially in larger number, should be considered as high-risk patients for stroke. MES detection may help in localization of embolic source, identification of patients with high stroke risk, monitoring during invasive procedures and surgery, and monitoring of the effectiveness of therapy.
Consensus on MES detection by TCD has been established ; MES can be identified as short lasting (<0.01–0.03 s), unidirectional intensity increase, and intensity increase (>3 dB) within the Doppler frequency spectrum; intensity increase is focused around 1 frequency. MESs appear randomly within the cardiac cycle and produce a “whistle,” “chirping,” or “clicking” sound when passing through the sample volume.
TCD is a very convenient tool to monitor intracranial circulation, however, the thick temporal bone window is an obstacle in certain patients. A new transcranial modality, power M-mode Doppler (PMD), has been developed to overcome the difficulties in location and insonation through transcranial ultrasound windows. PMD has 33 sample gates placed with 2 mm spacing for display of Doppler signal power, colored red and blue for directionality, in an M-mode format. The spectrogram from a user-selected depth is displayed simultaneously. PMD facilities window location and alignment of the ultrasound beam to view blood flow from multiple vessels simultaneously, without sound or spectral clues. MES appear as characteristic sloping high-power tracks in the PMD image [3, 4].
The optimal time of monitoring depends on the clinical entity. In patients with implanted artificial heart valves in whom MES can be detected in large proportion, monitoring during 30 minutes will be sufficient. In patients with carotid artery stenosis, atrial fibrillation, or other cardiac disease, frequency of MES is usually low, 1-2 MES over 60 minutes. Extended monitoring up to 8 hours, or repetitive monitoring over a couple of days in succession, is in relation with the percentage of MES positive patients [5, 6]. The embolic activity is highest in the first couple of hours after stroke; however, MES may be detectable days and weeks after cerebrovascular incidents which means that those patients are under higher risk for stroke [7–11].
Although technological improvement in the area of MES detection has recently developed, it is still impossible to reliably distinguish the composition of emboli (particles of fat, platelet aggregates, or particles of atheroma). Differentiation between solid and gaseous microemboli is based on the principle that solid emboli reflect more ultrasound at higher frequency, whereas the opposite is the case for gaseous emboli. This principle is used in multifrequency TCD instrumentation where the vessels are insonated simultaneously with 2.5 and 2.0 MHz and can be used for the differentiation between gaseous and solid emboli . A recent study has shown that there is a significant relationship between low- and high-intensity MES, indicating that many MESs routinely rejected because of their low intensity are real and may predict future occurrence of high-intensity MES .
Carotid artery stenosis is a well-known source of cerebral MES [7, 8, 14–19]. Systematic review of the literature showed that MES can be detected in 43% of patients with symptomatic and in 10% with asymptomatic carotid stenosis; presence of one MES indicated an increased risk of future events (OR 7.5, 95% confidence interval (CI): 3.6–15.4, P < 0.0001 for symptomatic and OR 13.4, 95% CI: 6.5–27.4, P < 0.0001 for asymptomatic disease) . A meta-analysis of the literature revealed that MESs are most frequent in large artery disease, less frequent in cardioembolic stroke, and infrequent in lacunar stroke. For symptomatic carotid stenosis, ES predicted stroke alone (OR, 9.57; P = 0.02) and stroke/TIA (OR, 6.36; P < 0.00001). For asymptomatic carotid stenosis, ES predicted stroke alone (OR, 7.46; P = 0.001) and stroke/TIA (OR, 12.00; P = 0.002) but with heterogeneity (P = 0.004). In acute stroke, ES predicted stroke alone (OR, 2.44; P = 0.02) and stroke/TIA (OR, 3.71; P = 0.002). A high frequency of ES immediately after carotid endarterectomy predicted stroke alone (OR, 24.54; P < 0.00001) and stroke/TIA (OR, 32.04; P < 0.00001). The meta-analysis suggests that MES predict stroke risk in acute stroke, symptomatic carotid stenosis, and postoperatively after carotid endarterectomy; however, in asymptomatic carotid stenosis, the predictive value of MES is less clear .
In the asymptomatic carotid emboli study (ACES), a prospective observational study, patients with asymptomatic carotid stenosis of at least 70% were monitored by TCD; the results showed that the hazard ratio for the risk of ipsilateral stroke and transient ischaemic attack from baseline to 2 years in patients with MES compared with those without was 2.54 (95% CI 1.20–5.36; P = 0.015). For ipsilateral stroke alone, the hazard ratio was 5.57 (1.61–19.32; P = 0.007). The absolute annual risk of ipsilateral stroke or transient ischaemic attack between baseline and 2 years was 7.13% in patients with MES and 3.04% in those without, and for ipsilateral stroke was 3.62% in patients with MES and 0.70% in those without .
Studies have shown that intraluminal thrombosis, irregular plaque surface, and ulceration are in relation with emboli frequency [23–25]. Carotid plaque inflammation is associated with cerebral microembolism in patients with recent transient ischemic attack or stroke .
Despite optimum standard antiplatelet therapy, cerebral microembolisation occurs in 30% of patients with symptomatic carotid artery disease . Patients with symptomatic high-grade ICA stenosis and who were on antiplatelet treatment underwent bilateral MES monitoring for 30 minutes. The study has shown that the presence of MES is independent of intrastenotic blood flow disturbances and gray-scale ultrasound plaque characteristics. The authors concluded that the presence of MES is an indicator of an unstable plaque .
Carotid plaques in patients with severe unilateral carotid restenosis at least one year after surgery are similar to patients with primary severe stenosis in their embolic potential and ultrasonic characteristics .
Dissection of carotid arteries is an embolic source and MES in those patients can be detected in a high proportion . Among patients with cervical artery dissection presenting with TIA or stroke, 50% had MES compared with 13% of patients with local symptoms (P = 0.006) .
Aortic arch atheroma has long been underestimated as an embolic source. Studies have shown that severe atheroma of the aortic arch has now been established as an important and independent risk factor for stroke. The prevalence of severe arch atheroma among patients presenting with acute ischaemic stroke is approximately 20%.
The odds ratio for stroke or peripheral embolism in patients with severe arch atheroma (>4 mm) is greater than four, and for mobile atheroma it is greater than twelve, particularly in patients with other stroke risk factors. Patients found to have severe atheroma are at high risk of recurrent events (14.2% per year) and may, therefore, need an aggressive secondary prevention strategy [19, 20].
Intracranial stenosis is a significant source of cerebral emboli, although in most studies not appreciated as important as carotid stenosis. A recent study has shown that MESs were reported in 25% of 220 patients with symptomatic versus 0% of 86 patients with asymptomatic intracranial stenosis (P < 0.0001) .
Thrombolysis is a well-established therapy in acute stroke. TCD has proven to serve as an enhancement tool in clot dissolution. MES detected by TCD at the site of arterial obstruction can indicate clot dissolution and recanalization of intracranial arteries, and therefore serve as a predictor for outcome .
After carotid endarterectomy, MESs disappear or the frequency is significantly lower [31, 32]. However, patients with clinically significant postoperative microembolism have an approximately 15 times higher risk of ipsilateral stroke or TIA . Efficacy of CEA largely depends on postoperative results, that is, perisurgical complications. Intraoperative monitoring of hemodynamic changes and detection of MES may significantly influence postsurgical outcome . Different antiplatelet regimens (combination of dipyridamole, aspirin and clopidogrel) following CEA does not show a significant influence on postoperative TCD embolization . However, administration of dual antiplatelet therapy (clopidogrel 75 mg plus aspirin 75 mg) prior to CEA reduces postoperative embolisation and thromboembolic events .
Meta-analysis of trials to date shows that symptomatic and asymptomatic CAS patients had significantly higher 30-day postprocedure incidence of death/stroke/MI when compared with CEA patients [37, 38].
Experimental studies have shown that during PTA, the majority of MESs are gaseous in origin, while MESs detected during balloon inflation are probably attributable to solid particles .
The use of cerebral protection devices appears to reduce thromboembolic complications during PTA and stenting. The combined stroke and death rate within 30 days in patients treated with cerebral protection devices was 1.8% compared with 5,5% in patients without .
MESs detected during angiography are attributable to gas bubbles, contrast injection, clot formation in catheter, and disrupted atheromatous material [41, 42]. Magnetic resonance studies have shown increased number of brain parenchymal lesions after angiography, although the majority of patients had nor neurological deficit . However, angiography of the aortic arch is associated with 1% risk for stroke with permanent deficit, and in 3% mild-to-moderate stroke or TIA [41, 42]. In a study with 24 patients undergoing angiography, all had detectable MES, approximately 51 per patient. The majority of MES had the characteristics of gas bubbles. The number of detected MESs correlated with the volume of injected contrast and all patients except one who had stroke were asymptomatic .
Approximately 15–30% of strokes are caused by cardiac diseases . Prospective studies have shown that recurrent stroke or systemic embolization in that group of patients is high, approximately 20% [7, 45].
Atrial fibrillation (AF) is present in 1,7% of population aged 60–64 years, and in 6% of population older than 75 years . Incidence of stroke in patients with AF is 4,5% per year . In cases when AF is associated with mitral valve stenosis, risk of stroke is 17 times higher . Majority of strokes in patients with AF are embolic in origin; MES can be detected in 15–30% [49, 50].
The prevalence of patent foramen ovale (PFO) in common population is 22–34.4% [51, 52]. In patients with cryptogenic stroke, especially younger patients, a high prevalence of PFO has been found [53, 54]. The rate of recurrent stroke or TIA is 9.9% . A multicentric study has shown that stroke risk over 4 years is 5,6% in patients with isolated PFO and 19,2% in patients with PFO and atrial septal aneurysm (ASA) . However, a prospective population-based study has established that PFO is not an independent risk factor for stroke when age and comorbiditiy are considered .
A connection between migraine (especially migraine with aura), stroke, and PFO has been established [58–63]. Studies have shown that the prevalence of PFO in patients with migraine is about 2.5 times greater in comparison with patients who do not suffer from migraine [64, 65]. Patients with migraine with aura have twice as high risk for stroke. Patients with probable migraine are 1, 5 times higher risk. If female patients with migraine smoke and take oral contraceptives, the risk increases up to seven times compared to those who do not have migraine [66–68].
According to one of the proposed hypothesis, paradoxal embolization causes segmental hypoperfusion and vasodilatation, that is, PFO enables vasoactive substances (hypotheticaly serotonin) and microemboli from venous circulation to pass the pulmonal filter (normally they would be stopped in lungs), and entering the brain they can induce cortical spreading depression which characterizes migrainous attack . This hypothesis could explain the decrease of migraine prevalence and intensity after PFO closure (in most studies). In favor of microembolization as a provoking factor speaks the MRI study in which a 13.7 times higher incidence of white matter lesions has been found in patients with migraine with aura compared to brains of controls [70–72]. Furthermore, most TCD studies have shown that most paradoxical MES can be detected in posterior brain circulation , which is interesting because in these patients PFO and migraine are more frequently present. However, up to now, there is no definite evidence for proposed theories regarding migraine onset caused by circulating microemboli.
Thromboembolism is a significant complication in patients with prosthetic heart valves (PHV). MES can be detectable in cerebral circulation ranging from 50 to 90% [73–75]. The majority of HITS in patients with PHV correspond to gaseous, for example, due to cavitations at mechanical heart valves .
Approximately 2.5% of patients with acute myocardial infarction (MI) will have stroke within 2–4 months . In a prospective study in patients with anterior wall MI, MES could be detected in 21% .
The prevalence of stroke in patients with infective myocarditis is 15–20% . The size of vegetations has a predictive value: risk for embolization is higher in patients with vegetations larger than 10 mm, in patients with endocarditis of the mitral valve and mobile vegetations .
Prevalence of mitral valve prolapse (MVP) in common population is 1–15% . Isolated MVP is not considered as a significant risk factor for stroke in older patients, but in younger patients myxomatous change of mitral valves is considered to be in relationship with cerebrovascular incidents .
Although rare, atrial myxoma is the most frequent primary cardiac tumor, usually present in the left atrium. Due to its fragile nature, myxoma has a high potential for embolization to the brain as well as to other organs .
MESs in cerebral circulation are detectable in primary antiphospholipid syndrome, Sneddon's syndrome, systemic lupus, Behcet's disease, and Takayasu's arteritis and are in temporal relation with cerebrovascular incidents in those patients [82–85].
Monitoring of therapeutic effect has shown that after CEA, MESs disappear or decrease in frequency, this finding is consistent through studies [31, 32]. Studies that investigated the efficacy of anticoagulant and antiaggregation therapy and frequency of MES have shown various results. Although some studies have shown decrease in MES frequency after aspirin or heparin administration, consistent correlation has not been found .
The first multicenter, randomized, double-blind trial that used MES detection as an endpoint to evaluate antiplatelet therapy, the Clopidogrel (CARESS and Aspirin for Reduction of Emboli in Symptomatic Carotid Stenosis) trial, has shown that clopidogrel plus aspirin is superior to aspirin alone in reducing the frequency of MES in patients with recent symptomatic carotid stenosis . Glycoprotein IIb/IIIa receptor antagonist tirofiban is a highly selective platelet aggregation inhibitor. Administration of tirofiban resulted in microembolic rate drop down to zero in patients with severe carotid artery stenosis in two studies. However, the inhibitory effect of tirofiban is reversible [92, 93].
It is important to emphasize that the vast majority of MESs do not produce immediate symptoms. MESs in cerebral circulation indicate asymptomatic patients with increased stroke risk. Nevertheless, correlation of cerebral microemboli with clinical symptoms (stroke or TIA ipsilateral to carotid stenosis, higher incidence of stroke in patients with cardiac diseases, neurological complications after angiography, postoperative neurological complications after CEA, in patients after CABG) in a number of studies has been shown. In symptomatic patients, the etiology of neurological deficit may be elucidated and adequate therapy may be introduced.
Patients with cerebral microembolism have higher cognitive deficits; cumulative effect of embolism is thought to be the cause. Even minor neuropsychological impairment should not be underestimated, the presence of an embolic source should be regarded as the possible cause for cognitive decline. Imaging techniques (CT scan, MRI, DWI-MRI) can show “silent” areas of cerebral ischemia. These small and multiple areas of acute or subacute brain infarction may occasionally present with clinical features atypical for brain embolism or will not produce any apparent symptoms .
Despite disputable clinical significance in certain conditions, the potential benefit of TCD detection of MES remains substantial.
|1.||Bogousslavsky J,Cachin C,Regli F,Despland PA,Van Melle G,Kappenberger L. Cardiac sources of embolism and cerebral infarction—clinical consequences and vascular concomitants: the Lausanne Stroke RegistryNeurologyYear: 19914168558592046930|
|2.||Ringelstein RB,Droste DW,Babikian VI,et al. Consensus on microembolus detection by TCD: international consensus group on microembolus detectionStrokeYear: 19982937257299506619|
|3.||Moehring MA,Spencer MP. Power M-mode Doppler (PMD) for observing cerebral blood flow and tracking emboliUltrasound in Medicine and BiologyYear: 2002281495711879952|
|4.||Choi Y,Saqqur M,Asil T,et al. A combined power M-mode and single gate transcranial doppler ultrasound microemboli signal criteria for improving emboli detection and reliabilityJournal of NeuroimagingYear: 201020435936719912481|
|5.||Droste DW,Ritter M,Kemeny V,Schulte-Altedorneburg G,Ringelstein BE. Microembolus detections at follow-up in 19 patients with acute stroke. Correlation with stroke etiology and antithrombotic treatmentCerebrovascular DiseasesYear: 200010427227710878431|
|6.||Molloy J,Khan N,Markus HS. Temporal variability of asymptomatic embolization in carotid artery stenosis and optimal recording protocolsStrokeYear: 1998296112911329626283|
|7.||Sliwka U,Lingnau A,Stohlmann WD,et al. Prevalence and time course of microembolic signals in patients with acute strokeStrokeYear: 19972823583639040690|
|8.||Forteza AM,Babikian VL,Hyde C,Winter M,Pochay V. Effect of time and cerebrovascular symptoms on the prevalence of microembolic signals in patients with cervical carotid stenosisStrokeYear: 19962746876908614931|
|9.||Demarin V,Rundek T,Vuković V. Klingerhoefer JPrevalence of cerebral emboli in patients with carotid artery diseaseNew Trends in Cerebral Hemodynamics and NeurosonologyYear: 1997Elsevier Science B.V.420444|
|10.||Marcus HS,Thompson N,Droste DW,et al. Cerebral embolic signals in carotid artery stenosis and their temporal variabilityCerebrovascular DiseasesYear: 19944, article 22|
|11.||van Zuilen EV,Mauser HW,van Gijn J,et al. The relationship between cerebral microemboli and symptomatic cerebral ischaemia: a study of transcranial Doppler monitoringCerebrovascular DiseasesYear: 19944, article 20|
|12.||Russell D,Brucher R. Embolus detection and differentiation using multifrequency transcranial DopplerStrokeYear: 200536, article 706|
|13.||Telman G,Sprecher E,Kouperberg E. Potential relevance of low-intensity microembolic signals by TCD monitoringNeurological SciencesYear: 20113210711120953814|
|14.||Ries S,Schminke U,Daffertshofer M,Schinlmayr C,Hennerici M. High intensity transient signals and carotid artery diseaseCerebrovascular DiseasesYear: 19955124127|
|15.||Eicke BM,von Lorentz J,Paulus W. Embolus detection in different degrees of carotid diseaseNeurological ResearchYear: 19951731811847643973|
|16.||Hutchinson S,Riding G,Coull S,McCollum CN. Are spontaneous cerebral microemboli consistent in carotid disease?StrokeYear: 200233368568811872888|
|17.||Molloy J,Markus HS. Asymptomatic embolization predicts stroke and TIA risk in patients with carotid artery stenosisStrokeYear: 19993071440144310390320|
|18.||Vassileva E,Schnorf H,Personeni O,Floch-Rohr J. Microembolic signals and early recurrent cerebral ischemia in carotid artery diseaseStrokeYear: 19993014901493|
|19.||Viguier A,Pavy le Traon A,Massabuau P,Valton L,Larrue V. Asymptomatic cerebral embolic signals in patients with acute cerebral ischaemia and severe aortic arch atherosclerosis.Journal of NeurologyYear: 2001248976877111596781|
|20.||Ritter MA,Dittrich R,Thoenissen N,Ringelstein EB,Nabavi DG. Prevalence and prognostic impact of microembolic signals in arterial sources of embolism: a systematic review of the literatureJournal of NeurologyYear: 2008255795396118458865|
|21.||King A,Markus HS. Doppler embolic signals in cerebrovascular disease and prediction of stroke risk: a systematic review and meta-analysisStrokeYear: 200940123711371719850894|
|22.||Markus HS,King A,Shipley M,et al. Asymptomatic embolisation for prediction of stroke in the Asymptomatic Carotid Emboli Study (ACES): a prospective observational studyThe Lancet NeurologyYear: 201097663671|
|23.||Sitzer M,Muller W,Siebler M,et al. Plaque ulceration and lumen thrombus are the main sources of cerebral microemboli in high-grade internal carotid artery stenosisStrokeYear: 1995267123112337604420|
|24.||Siebler M,Kleinschmidt A,Sitzer M,Steinmetz H,Freund HJ. Cerebral microembolism in symptomatic and asymptomatic high-grade internal carotid artery stenosisNeurologyYear: 19944446156187909360|
|25.||Zhang C,Qu S,Li H,et al. Microembolic signals and carotid plaque characteristics in patients with asymptomatic carotid stenosisScandinavian Cardiovascular JournalYear: 200943534535119863395|
|26.||Moustafa RR,Izquierdo-Garcia D,Fryer TD,et al. Carotid plaque inflammation is associated with cerebral microembolism in patients with recent transient ischemic attack or stroke: a pilot studyCirculationYear: 20103553654120639303|
|27.||Zuromskis T,Wetterholm R,Lindqvist JF,et al. Prevalence of micro-emboli in symptomatic high grade carotid artery disease: a transcranial Doppler studyEuropean Journal of Vascular and Endovascular SurgeryYear: 200835553454018291690|
|28.||Telman G,Kouperberg E,Hlebtovsky A,et al. Embolic potential and ultrasonic characteristics of plaques in patients with severe unilateral carotid restenosis more than one year after surgeryJournal of the Neurological SciencesYear: 20092851-2858719501842|
|29.||Molina CA,Alvarez-Sabín J,Schonewille W,et al. Cerebral microembolism in acute spontaneous internal carotid artery dissectionNeurologyYear: 200055111738174011113235|
|30.||Alexandrov AV,Demchuk AM,Felberg RA,Grotta JC,Krieger DW. Intracranial clot dissolution is associated with embolic signals on transcranial DopplerJournal of NeuroimagingYear: 2000101273210666979|
|31.||Siebler M,Sitzer M,Rose G,Bendfeldt D,Steinmetz H. Silent cerebral embolism caused by neurologically symptomatic high-grade carotid stenosis. Event rates before and after carotid endarterectomyBrainYear: 19931165100510158221045|
|32.||van Zuilen EV,Moll FL,Vermeulen FEE,Mauser HW,van Gijn J,Ackerstaff RGA. Detection of cerebral microemboli by means of transcranial Doppler monitoring before and after carotid endarterectomyStrokeYear: 19952622102137831689|
|33.||Abbott AL,Levi CR,Stork JL,Donnan GA,Chambers BR. Timing of clinically significant microembolism after carotid endarterectomyCerebrovascular DiseasesYear: 2007235-636236717268167|
|34.||Lennard N,Smith J,Dumville J,et al. Prevention of postoperative thrombotic stroke after carotid endarterectomy: the role of transcranial Doppler ultrasoundJournal of Vascular SurgeryYear: 19972645795849357457|
|35.||de Borst GJ,Hilgevoord AAJ,de Vries JPPM,et al. Influence of antiplatelet therapy on cerebral micro-emboli after carotid endarterectomy using postoperative transcranial Doppler monitoringEuropean Journal of Vascular and Endovascular SurgeryYear: 200734213514217521930|
|36.||Sharpe RY,Dennis MJS,Nasim A,et al. Dual antiplatelet therapy prior to carotid endarterectomy reduces post-operative embolisation and thromboembolic events: post-operative transcranial doppler monitoring is now unnecessaryEuropean Journal of Vascular and Endovascular SurgeryYear: 201040216216720451426|
|37.||Sidawy AN,Zwolak RM,White RA,Siami FS,Schermerhorn ML,Sicard GA. Risk-adjusted 30-day outcomes of carotid stenting and endarterectomy: results from the SVS Vascular RegistryJournal of Vascular SurgeryYear: 2009491717919028045|
|38.||Brahmanandam S,Ding EL,Conte MS,Belkin M,Nguyen LL. Clinical results of carotid artery stenting compared with carotid endarterectomyJournal of Vascular SurgeryYear: 200847234334918241758|
|39.||Markus HS,Brown MM. Differentiation between different pathological cerebral embolic materials using transcranial Doppler in an in vitro modelStrokeYear: 1993241158418529|
|40.||Kastrup A,Gröschel K,Krapf H,Brehm BR,Dichgans J,Schulz JB. Early outcome of carotid angioplasty and stenting with and without cerebral protection devices: a systematic review of the literatureStrokeYear: 200334381381912624315|
|41.||Gerraty RP,Bowser DN,Infeld B,Mitchell PJ,Davis SM. Microemboli during carotid angiography: association with stroke risk factors or subsequent magnetic resonance imaging changes?StrokeYear: 1996279154315478784127|
|42.||Bendszus M,Koltzenburg M,Burger R,Warmuth-Metz M,Hofmann E,Solymosi L. Silent embolism in diagnostic cerebral angiography and neurointerventional procedures: a prospective studyThe LancetYear: 1999354919015941597|
|43.||Gerraty RP,Bowser DN,Infeld B,Mitchell PJ,Davis SM. Microemboli during carotid angiography: association with stroke risk factors or subsequent magnetic resonance imaging changes?StrokeYear: 1996279154315478784127|
|44.||Sliwka U,Job F-P,Wissuwa D,et al. Occurrence of transcranial Doppler high-intensity transient signals in patients with potential cardiac sources of embolism: a prospective studyStrokeYear: 19952611206720707482651|
|45.||Yasaka M,Yamaguchi T,Oita J,Sawada T,Shichiri M,Omae T. Clinical features of recurrent embolization in acute cardioembolic strokeStrokeYear: 19932411168116858236343|
|46.||Lake FR,Cullen KJ,De Klerk NH,McCall MG,Rosman DL. Atrial fibrillation and mortality in an elderly populationAustralian and New Zealand Journal of MedicineYear: 19891943213262789508|
|47.||Wolf PA,Abbott RD,Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham studyStrokeYear: 19912289839881866765|
|48.||Lin HJ,Wolf PA,Kelly-Hayes M,et al. Stroke severity in atrial fibrillation: the Framingham studyStrokeYear: 19962710176017648841325|
|49.||Cullinane M,Wainwright R,Brown A,Monaghan M,Markus HS. Asymptomatic embolization in subjects with atrial fibrillation not taking anticoagulants: a prospective studyStrokeYear: 1998299181018159731600|
|50.||Rundek T,Demarin V,Vuković V,Podobnik-Šarkanji S,Starčević B. Klingerhoefer JTCD detection of cerebral emboli in patients with nonvalvular atrial fibrillation: a 1 year follow-up surveyNew Trends in Cerebral Hemodynamics and NeurosonologyYear: 1997Elsevier Science B.V.435440|
|51.||Konstadt SN,Louie EK,Black S,Rao TLK,Scanlon P. Intraoperative detection of patent foramen ovale by transesophageal echocardiographyAnesthesiologyYear: 19917422122161990894|
|52.||Hagen PT,Scholz DG,Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal heartsMayo Clinic ProceedingsYear: 198459117206694427|
|53.||Lechat P,Mas JL,Lascault G,et al. Prevalence of patent foramen ovale in patients with strokeThe New England Journal of MedicineYear: 198831818114811523362165|
|54.||Jeanrenaud X,Bogousslavsky J,Payot M,Regli F,Kappenberger L. Patent foramen ovale and cerebral infarct in young patientsSchweiz Med WochenschrYear: 19901208238292360007|
|55.||Nedeltchev K,Arnold M,Wahl A,et al. Outcome of patients with cryptogenic stroke and patent foramen ovaleJournal of Neurology Neurosurgery and PsychiatryYear: 2002723347350|
|56.||Mas J-L,Zuber M. Recurrent cerebrovascular events in patients with patent foramen ovale, atrial septal aneurysm, or both and cryptogenic stroke or transient ischemic attack. French Study Group on Patent Foramen Ovale and Atrial Septal AneurysmAmerican Heart JournalYear: 19951305108310887484740|
|57.||Stratton JR,Resnick AD. Increased embolic risk in patients with left ventricular thrombiCirculationYear: 1987755100410113568301|
|58.||Piechowski-Jozwiak B,Devuyst G,Bogousslavsky J. Migraine and patent foramen ovale: a residual coincidence or a pathophysiological intrigue?Cerebrovascular DiseasesYear: 2006222-39110016685120|
|59.||Schwedt TJ,Dodick DW. Patent foramen ovale and migraine - Bringing closure to the subjectHeadacheYear: 200646466367116643562|
|60.||Spies C,Kavinsky CJ,Schräder R. Patent foramen ovale in patients with migraine headache. Should it be closed?Minerva MedicaYear: 2007981253617372579|
|61.||Wammes-van der Heijden EA,Tijssen CC,Egberts ACG. Right-to-left shunt and migraine: the strength of the relationshipCephalalgiaYear: 200626220821316426277|
|62.||Carolei A,Marini C,De Matteis G,the Italian National Reasearch Council Study Group on Stroke in the Young. History of migraine and risk of cerebral ischaemia in young adults The LancetYear: 1996347901415031506|
|63.||Ries S,Steinke W,Neff W,Schindlmayr C,Meairs S,Hennerici M. Ischemia-induced migraine from paradoxical cardioembolic strokeEuropean NeurologyYear: 199636276788654489|
|64.||Del Sette M,Angeli S,Leandri M,et al. Migraine with aura and right-to-left shunt on transcranial Doppler: a case-control studyCerebrovascular DiseasesYear: 1998863273309774749|
|65.||Anzola GP,Magoni M,Guindani M,Rozzini L,Volta GD. Potential source of cerebral embolism in migraine with aura: a transcranial Doppler studyNeurologyYear: 19995281622162510331688|
|66.||Wingerchuk DM,Spencer B,Dodick DW,Demaerschalk BM. Migraine with aura is a risk factor for cardiovascular and cerebrovascular disease: a critically appraised topicNeurologistYear: 200713423123317622918|
|67.||Becker C,Brobert GP,Almqvist PM,Johansson S,Jick SS,Meier CR. Migraine and the risk of stroke, TIA, or deathin the UK (CME)HeadacheYear: 200747101374138418052947|
|68.||MacClellan LR,Giles W,Cole J,et al. Probable migraine with visual aura and risk of ischemic stroke: the stroke prevention in young women studyStrokeYear: 20073892438244517690308|
|69.||Wilmshurst PT,Nightingale S,Walsh KP,Morrison WL. Effect on migraine of closure of cardiac right-to-left shunts to prevent recurrence of decompression illness or stroke or for haemodynamic reasonsThe LancetYear: 2000356924216481651|
|70.||Venketasubramanian N,Sacco RL,Di Tullio M,Sherman D,Homma S,Mohr JP. Vascular distribution of paradoxical emboli by transcranial DopplerNeurologyYear: 1993438153315358351007|
|71.||Kruit MC,van Buchem MA,Hofman PAM,et al. Migraine as a risk factor for subclinical brain lesionsJAMAYear: 2004291442743414747499|
|72.||Rocca MA,Colombo B,Inglese M,Codella M,Comi G,Filippi M. A diffusion tensor magnetic resonance imaging study of brain tissue from patients with migraineJournal of Neurology Neurosurgery and PsychiatryYear: 2003744501503|
|73.||Müller HR,Burckhardt D,Casty M,Pfisterer ME,Buser MW. High intensity transcranial Doppler signals (HITS) after prosthetic valve implantationJournal of Heart Valve DiseaseYear: 1994366026068000601|
|74.||Markus HS,Droste DW,Brown MM. Detection of asymptomatic cerebral embolic signals with doppler ultrasoundThe LancetYear: 1994343890410111012|
|75.||Braeken SK,Russell D,Brucher R,et al. Cerebral emboli in prosthetic heart valve patientsStrokeYear: 199425, article 739|
|76.||Droste DW,Hansberg T,Kemény V,et al. Oxygen inhalation can differentiate gaseous from nongaseous microemboli detected by transcranial Doppler ultrasoundStrokeYear: 19972812245324569412631|
|77.||Manning WJ. Role of transesophageal echocardiography in the management of thromboembolic strokeAmerican Journal of CardiologyYear: 1997804, supplement 319D28D|
|78.||Cerebral Embolism Task ForceCardiogenic brain embolism. The second report of the Cerebral Embolism Task ForceArchives of NeurologyYear: 19894677277432662950|
|79.||Freedberg RS,Goodkin GM,Perez JL,Tunick PA,Kronzon I. Valve strands are strongly associated with systemic embolization: a transesophageal echocardiographic studyJournal of the American College of CardiologyYear: 1995267170917127594107|
|80.||Orencia AJ,Petty GW,Khandheria BK,et al. Risk of stroke with mitral valve prolapse in population-based cohort studyStrokeYear: 19952617137839400|
|81.||Cerebral Embolism Task ForceCardiogenic brain embolism. The second report of the Cerebral Embolism Task ForceArchives of NeurologyYear: 19894677277432662950|
|82.||Kumral E,Evyapan D,Aksu K,Keser G,Kabasakal Y,Balkir K. Microembolus detection in patients with Takayasu’s arteritisStrokeYear: 200233371271611872893|
|83.||Sitzer M,Sohngen D,Siebler M,et al. Cerebral microembolism in patients with Sneddon’s syndromeArchives of NeurologyYear: 19955232712757872880|
|84.||Specker C,Rademacher J,Söhngen D,et al. Cerebral microemboli in patients with antiphospholipid syndromeLupusYear: 1997686386449364422|
|85.||Kumral E,Evyapan D,Oksel F,Keser G,Bereketoğlu MA,Balkir K. Transcranial doppler detection of microembolic signals in patients with Behcet’s diseaseJournal of NeurologyYear: 1999246759259510463362|
|86.||Vuković V. Korelacija transkranijskog doplera s kliničkim statusom i parametrima koagulacije u otkrivanju moždanih embolusaMagistarski RadYear: 1997Zagreb, CroatiaMedicinski Fakultet, Sveučilište u Zagrebu|
|87.||Resch KL,Ernst E,Matrai A,Paulsen HF. Fibrinogen and viscosity as risk factors for subsequent cardiovascular events in stroke survivorsAnnals of Internal MedicineYear: 199211753713751503327|
|88.||Heppell RM,Berkin KE,McLenachan JM,Davies JA. Haemostatic and haemodynamic abnormalities associated with left atrial thrombosis in non-rheumatic atrial fibrillationHeartYear: 19977754074119196408|
|89.||Coull BM,Beamer N,de Garmo P,et al. Chronic blood hyperviscosity in subjects with acute stroke, transient ischemic attack, and risk factors for strokeStrokeYear: 19912221621682003279|
|90.||Goertler M,Baeumer M,Kross R,et al. Rapid decline of cerebral microemboli of arterial origin after intravenous acetylsalicylic acidStrokeYear: 199930166699880390|
|91.||Markus HS,Droste DW,Kaps M,et al. Dual antiplatelet therapy with clopidogrel and aspirin in symptomatic carotid stenosis evaluated using doppler embolic signal detection: the clopidogrel and aspirin for reduction of emboli in symptomatic carotid stenosis (CARESS) trialCirculationYear: 2005111172233224015851601|
|92.||Junghans U,Siebler M. Cerebral microembolism is blocked by tirofiban, a selective nonpeptide platelet glycoprotein IIb/IIIa receptor antagonistCirculationYear: 2003107212717272112742983|
|93.||van Dellen D,Tiivas CAS,Jarvi K,Marshall C,Higman DJ,Imray CHE. Transcranial Doppler ultrasonography-directed intravenous glycoprotein IIb/IIIa receptor antagonist therapy to control transient cerebral microemboli before and after carotid endarterectomyBritish Journal of SurgeryYear: 200895670971318425794|
|94.||Aly A,Babikian VL,Barest G,Artinian M,Forteza A,Kase CS. Brain microembolismJournal of NeuroimagingYear: 200313214014612722496|
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