Leukocyte count predicts microembolic Doppler signals during carotid stenting: A link between inflammation and embolization

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Conclusion: Microembolic signals during carotid stenting are increased with increased preprocedure leukocyte counts.

Summary: Microembolization detected by transcranial Doppler imaging inevitably accompanies carotid artery stenting. The authors chose to study the relationship between microembolization during carotid artery stenting and preprocedure leukocyte count. Forty-three patients underwent simultaneous transcranial Doppler monitoring of the middle cerebral artery during carotid artery stenting. Microembolic signals detected by transcranial Doppler were used to quantify microembolization. Preprocedure leukocyte counts were then related to microembolic signals detected by transcranial Doppler.

The preprocedure leukocyte count in an unadjusted analysis was correlated positively with total procedure microembolic signals (R² = 0.16; P = .008). With adjustments for age, comorbidities, gender, medical therapies, and use of embolic protection devices, increasing leukocyte count (β = 35 for each 1000/μL increment; P = .018) remained an independent and significant predictor of microembolization (model-adjusted R² = 0.365; P = .0005). The relationship with increased leukocyte count was most marked in the third tertile of the leukocyte count, with a median number of microembolic signals being 259 in the first tertile, 276 in the second tertile, and 350 in the third tertile leukocyte count.

Embolic protection devices were used in 16% of the population. Overall, 12% of the patients died, had a myocardial infarction, or had a stroke. For every 1000/μL increase in leukocyte count, transcranial Doppler detected 35 additional microembolic signals.

Comment: The association of increased leukocyte count with microembolic signals during carotid stenting is interesting. However, the patients reported in this series are unlikely representative of current practice in that only 16% underwent carotid stenting with cerebral protection devices. The 12% major procedural complication rate also seems high. Finally, the only marker of inflammation used in this retrospective study was leukocyte count. Further data using modern techniques and additional markers of inflammation such as C-reactive protein are required before a link can be established between inflammation and microembolization during carotid artery stenting.