Regarding "high embolic rate early after carotid endarterectomy is associated with early cerebrovascular complications, especially in women".

Postoperative carotid thrombosis (POCT) complicates 2% to 3% of carotid endarterectomies (CEAs) and classically occurs 4 to 6 hours after restoration of flow. It was previously held that POCT was almost invariably associated with some underlying technical error and incurred a poor outcome unless thrombectomy was performed within 1 hour. Viewed traditionally as being unpreventable, it would clearly be preferable to identify patients at high risk early and so intervene (therapeutically or surgically) to prevent progression onto thrombosis and stroke. The paper by Laman et al, in this edition of the Journal, is now the latest of five around the world to suggest that many of the traditionally held views regarding POCT need revising and that transcranial Doppler (TCD)–directed embolus monitoring may be invaluable in identifying those at highest risk. The available evidence suggests that a policy of quality control assessment will virtually abolish intraoperative stroke (apparent on recovery from anesthesia) but that this will have surprisingly little effect on the rate of stroke as the result of POCT. Secondly, provided technical error has been excluded with some form of completion assessment (eg, angioscopy), patients who subsequently have a stroke because of POCT are unlikely to have underlying technical error at reexploration. Interestingly, most are found to have platelet-rich thrombus that is adherent to the endarterectomy zone rather than to the patch. It is now well accepted that platelets begin to adhere to the endarterectomy zone within minutes of flow restoration, but no one knows why it becomes excessive in certain patients. Thirdly, there are now five studies (including that of Laman et al) that suggest that patients destined to progress to stroke because of POCT have a 1-hour to 2-hour period of increasing embolization before any neurologic deficit becomes apparent. The prevailing view is that, as the platelet thrombus accumulates, small particles are increasingly shed into the carotid circulation and detected with the TCD. Overall, about 50% of patients with CEA will have one or more emboli detected in the postoperative period, but only about 5% will progress to high-grade sustained embolization. In Laman et al’s series, 30% of these patients with high embolization progressed to stroke, increasing to 50% in the Leicester series and 60% in Levi et al’s Australian study. Unfortunately, because of methodologic differences among the five studies (varying monitoring times [10 to 180 minutes], divergent antiplatelet and reexploration policies [especially in Laman et al’s study] and differing policies regarding intervention [Boston gave dextran to all patients with CEA, Leicester administered dextran 40 to all patients with high-rate embolization]), it is currently impossible to combine the data and present an overview of the principal findings. This problem may, however, be resolved in the future when a collaboration of interested researchers reanalyze all of the raw data from the various major studies. Laman et al’s study proposes that an embolus rate of 0.9/min represents a threshold for increased risk, and in Leicester, we would only intervene if the embolus count exceeded 25 in any 10-minute monitoring period (2.5 emboli/min) or where the embolus distorted the waveform suggesting that it was large. Our threshold of 25 in 10 minutes was based on Gaunt et al’s original work. To date, we have not observed any early embolic stroke in anyone with an embolus rate of between 0.9/min and 2.5/min, which is clearly at variance with Laman et al’s findings, although part of the discrepancy might be explained by our use of completion angioscopy and the substitution of aspirin with warfarin 1 week before surgery in the Dutch center. However, despite the methodologic problems, these five studies should now be the catalyst for studying the phenomenon of POCT in a more standardized manner, especially regarding antiplatelet regimes (see below). In From the Department of Surgery, Leicester Royal Infirmary. Competition of interest: nil. Reprint requests: A. Ross Naylor, MD, FRCS, Leicester Royal Infirmary, Robert Kilpatrick Building, PO Box 65, Leicester LE2 7LX, United Kingdom (e-mail: arnaylor@hotmail.com). J Vasc Surg 2002;36:408-9. Copyright © 2002 by The Society for Vascular Surgery and The American Association for Vascular Surgery. 0741-5214/2002/$35.00 0 24/9/125797 doi:10.1067/mva.2002.125797