Potential relevance of low-intensity microembolic signals by TCD monitoring.
ABSTRACT The significance of low-intensity microembolic signals (MES), as well as their relationship with high-intensity MES, has not yet been studied. We monitored MES by TCD in 256 arteries of 229 patients with carotid stenosis. All microemboli were detected automatically without a preliminary set threshold. For those 110 patients who evidenced any emboli, the correlation between the number of high- and low-intensity MES was r = 0.50, p < 0.0001. A statistically significant relationship between both types of MES was found, with a degree of association of 0.42, as assessed by Cohen's kappa. Later occurrence of high-intensity MES based on early low-intensity MES was statistically significant, with a chi-square p = 0.0006 and a degree of association of 0.24, as assessed by Cohen's kappa. There is a significant relationship between low- and high-intensity MES, thereby indicating that many MES routinely rejected because of their low intensity are real.
- SourceAvailable from: stroke.ahajournals.org[show abstract] [hide abstract]
ABSTRACT: Protected stenting has emerged as a safe and effective alternative to endarterectomy for the treatment of carotid stenosis in patients at high operative risk. Distal microembolization occurs invariably during carotid stenting. Little is known about the relationship between systemic inflammation and embolization during carotid stenting. We examined 43 consecutive patients who underwent carotid stenting with simultaneous transcranial Doppler (TCD) monitoring of the ipsilateral middle cerebral artery. Embolization was quantified by measuring microembolic signals (MES) on TCD. Preprocedure leukocyte counts were related to MES. In unadjusted analyses, preprocedure leukocyte count was positively correlated with total procedural MES (r2= 0.16; P=0.008). After considering age, gender, comorbidities, concomitant medical therapies, and the use of emboli prevention devices, increasing leukocyte count (beta=35 for each 1000/microL increment; P=0.018) remained a significant and independent predictor of embolization (model-adjusted r2=0.365; P=0.0005). Increasing preprocedure leukocyte count independently predicted more frequent MES during carotid stenting. These data suggest that systemic inflammation may influence the degree of procedural embolization.Stroke 10/2005; 36(9):1910-4. · 6.16 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: The CARESS (Clopidogrel and Aspirin for Reduction of Emboli in Symptomatic carotid Stenosis) trial proved the effectiveness of the combination of clopidogrel and aspirin compared with aspirin alone in reducing presence and number of microembolic signals (MES) in patients with recently symptomatic carotid stenosis. The present study aimed at installing primary and secondary quality control measures in CARESS because MES evaluation relies on subjective judgment by human experts. As primary quality control, centers participating in CARESS evaluated a reference digital audio tape (DAT) before the study containing both MES and artifacts. Interobserver agreement of classifying signals as MES was expressed as proportions of specific agreement of positive ratings (ps+/-values). For all DATs included in CARESS (n=300), online number of MES and off-line number of MES read by the central reader were compared using correlation coefficients. As secondary control, a sample of 16 of 300 DATs was cross-validated by another independent reader (post-trial validator). For the reference tape, the cumulative ps+/-value was 0.894 based on 12 of 14 observers. Two observers with very different results improved after a training procedure. Agreement between post-trial validator and central reader was ps+=0.805, indicating very good agreement. Correlation between online evaluation and off-line evaluation of DATs was very good overall (cumulative rho=0.84; P<0.001). Multicenter studies using MES as outcome parameter are feasible. However, primary and secondary quality control procedures are important.Stroke 04/2006; 37(4):1065-9. · 6.16 Impact Factor