(Stroke. 2005;36:1110.)
© 2005 American Heart Association, Inc.
Letters to the Editor |
Department of Vascular Surgery, and Department of Academic Radiology
Department of Academic Radiology
Division of Rehabilitation and Ageing
Department of Vascular Surgery, University of Nottingham, Queens Medical Centre, Nottingham, UK
To the Editor:
We read with interest the recent article in Stroke by Wolf et al1 describing the relationship between transcranial detected microembolic signals (MES) and serial diffusion-weighted imaging (DWI) of the brain. The authors have studied 5 phases of the carotid endarterectomy (CEA) (dissection, clamping, shunting, de-clamping and wound closure). The authors observe microembolic signals detected during the dissection phase and de-clamping phase of CEA correlated significantly with the evolution of new DWI lesions and brain infarction on T1-weighted MRI. This study highlights the importance of good surgical technique especially in the dissection phase of the operation. However, MES detected in the dissection phase may be unavoidable because it also reflects the unstable carotid plaque,2 which even on minimal dissection may cause particulate embolization. It is of no surprise that no associations were found between DWI lesions and MES detected in de-clamping phase as microemboli in this phase of the operation tend to be gaseous in nature and therefore does not cause brain ischemia. In contrast, MES detected in the shunt phase tend to be a mix of particulate and gaseous microemboli and a nonsignificant correlation with DWI lesions in this study is consistent with previous studies.3
The wound closure phase of the operation tends to be short and gives us a glimpse of MES activity in the postoperative (or after restoration of blood flow) phase. MES detected in the postoperative and the recovery room period is particulate in nature and arises secondary to platelet aggregation and occasionally leads to thrombus formation on the denuded endarterectomized endothelium.4 Postoperative carotid thrombosis complicates 2% to 3% of CEAs and tends to occur within 4 to 6 hours of the operation. Patients who progress to this condition and subsequently brain ischemia have a 1- to 2-hour postoperative period of increased embolization.5 Approximately 12% of cases undergoing CEA are complicated by this postoperative MES and significant MES in this period is associated with ischemic changes on FLAIR brain images.6,7 Additionally, Payne et al8 have described that postoperative thromboembolism was significantly effected by a combination of antiplatelet agents acting on different pathways of coagulation.
Because Wolf et al1 only assessed MES in the short wound closure phase, the lack of association of MES with DWI lesions therefore does not allow to assess the contribution of the postoperative period to DWI evolution. It certainly would be of interest to elucidate the relationship of DWI lesion development and MES detected in longer postoperative periods, and to assess the efficacy of preoperative and postoperative pharmaceutical agents such as anticoagulants and dextran 40, respectively, in preventing subclinical and clinical brain ischemia detected by DWI.
References
Department of Vascular Surgery
Department of Neurology
Department of Radiology, Technical University of Munich, Germany
We appreciate the interest of Altaf et al in our work.4 As mentioned in our discussion, we confirm the statement of Altaf et al that microembolization during dissection is a function of plaque stability and good surgical technique with early clamping.
Because no reliable measurement of plaque stability exists up to now, other parameters like recent neurological symptoms were used as a kind of surrogate markers for stenosis activity and a significant correlation to the incidence of postoperative cerebral ischemia was found.5
We agree with the statement that microembolic signals (MES) during shunting are a mix of gaseous and particulate microemboli and that MES during de-clamping seem to be harmless gaseous emboli.
New advances in MES detection using multifrequency Doppler sonography may allow to discriminate the nature of microemboli during the different phases of the carotid endarterectomy in the future.1
We are aware of the results that evaluated microembolization in the early postoperative period.2,3
Screening only during the procedure and not the early postoperative period may underestimate the relationship between diffusion-weighted imaging lesions and MES. We decided not to analyze the early postoperative period because of the limited ability to differentiate real MES from artifacts during this phase.
Transcranial Doppler as a monitor procedure is only reliable when an exact positioning of the probes can be realized and maintained.
Even during CEA, when the patient is in optimal position and under general anesthesia, this can be really challenging.
During the early postoperative period when the patient recovers from anesthesia, it is difficult to get reliable MES data because continuous monitoring is often not possible because of movements of the patient.
If these difficulties can be resolved, the elucidation of the efficacy of postoperative pharmaceutical agents to prevent cerebral ischemia might be of great clinical value.
References
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