Chapter 6
threshold only 41.2% of the patients regarded as at risk, were truly at risk. Increasing the threshold resulted in missed patients at risk (false negatives) and therefore at present we consider the automatic EDS unsuitable for perioperative solid emboli detection. Previous research has shown that the presence of MES predicts both stroke and the combined endpoint of stroke/TIA in patients with symptomatic (resp. OR 9.57, 95%CI 1.54-59.3, p=0.02 and OR 6.36, 95%CI 2.90-13.96) and asymptomatic carotid stenosis (resp. OR 7.46, 95%CI 2.24-24.89, p<0.001 and OR 12.00, 95%CI 2.43-59.34). 9,23 During all stages of CEA MES have been detected. However, only a high frequency of MES during dissection (OR 14.97, 95%CI: 5.15-42.47; p<0.00001) or immediately after CEA does (OR 24.54, 95%CI: 7.88-76.43; p<0.00001) predicts an increased postoperative risk of stroke.9 Repeated measurements in individual patients with symptomatic carotid stenosis showed stability of recordings over time, in contrast to asymptomatic patients with carotid stenosis. This may be relevant for detection of ‘’high risk’’ asymptomatic patients who might benefit from CEA, suggesting that repeated TCD measurements are mandatory in this patient category. 24 Nowadays stronger platelet inhibitors are prescribed for patients after stroke or TIA. Most patients undergoing CEA are on combination aspirin/ dipyridamole or monotherapy clopidogrel. Using these strong platelet inhibitors, one can expect that less solid emboli occur during and after CEA. Multiple studies have shown the potential efficacy of clopidogrel to reduce (a)symptomatic embolization in patients with symptomatic carotid artery stenosis before and during CEA.25,26 A previous study from 1997 reported ≥ 10 perioperative solid emboli in 24% of the patients treated with monotherapy aspirin. 27 Our study shows 28% of the patients displaying ≥ 10 perioperative solid emboli, despite stronger platelet inhibitors. This lack of major reduction indicates that perioperative TCD monitoring is still essential to minimize the risk of complications. An earlier study with the Versatile EDS, evaluating all signals ≥3 dB in patients post CEA, showed an overall agreement of EDS and HE of 96%. 16 Missed solid emboli were characterised by short duration, low intensity (≤ 4dB) and intermediate ZCI value. Equally, our study also shows a large number of solid emboli ≤ 4 dB pointed out by both the EDS as HE1 (Figure 2). However, no difference in intensity between the missed and registered solid emboli was found. Misclassification by the EDS can thus not be explained by the intensity of the signals. Further data on the clinical significance of low intensity- compared to high intensity solid emboli needs to be obtained. Moreover, improvement of this AEDS could be realised by an improved rejection of these low intensity artefacts. MES occurring after arterial opening and before vessel closure may contribute to either gaseous or solid emboli. After arterial opening, small air bubbles can be introduced, resulting in high intensity MES, a receiver overload and potential degree of aliasing. 28 The reflection of ultrasound is dependent of the acoustic impedance: air has an acoustic impedance of 1/4000th of whole blood, resulting in an extremely large reflection. The acoustic impedance of solid emboli is more similar to whole blood and therefore results in much weaker reflection.
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