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In our group of patients, patients suffering from MS had significantly more IJV morphological changes and haemodynamic abnormalities when compared with healthy individuals not suffering from MS. These findings can be well demonstrated by non-invasive and cost-effective Doppler ultrasound.

To analyze the outcome of urgent carotid endarterectomy (CEA) performed within less than six hours in patients with crescendo transient ischemic attack (TIA) and stroke in progression. From January 1998 to December 2008, 58 urgent CEAs were done for acute neurological ischemic events--46 patients with crescendo TIA and 12 patients with stroke in progression. Brain computed tomography (CT) was done prior and after the surgery. Disability level was assessed prior to and after urgent CEA using modified Rankin scale. Median follow-up was 42.1 ± 16.6 months. In the early postoperative period stroke rate was 0% for the patients in crescendo TIA group while in patients with stroke in progression group 3 patients (25%) had positive postoperative brain CT, yet neurological status significantly improved. Mid-term stroke rate was 2.2% in crescendo TIA group and 8.3% in stroke in progression group. In the early postoperative period there were no lethal outcomes, mid-term mortality was 8.3% in stroke in progression while in crescendo TIA group lethal outcomes were not observed. In conclusion, based on our results urgent CEA is a safe and effective treatment option for patients with crescendo TIA and stroke in progression with acceptable rate of postoperative complications.

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The aim of this article is to review our experience in surgical treatment of carotid atherosclerosis using eversion carotid endarterectomy (ECEA) in 5,034 patients, with particular attention to temporal changes in patients' characteristics, diagnostic approach, surgical technique, medical therapy, and outcome in the early (group A, 1991-1997) versus late (group B 1998-2004) period of ECEA. From January 1991 to December 2004, 5,034 primary ECEAs were performed for high-grade carotid stenosis. Patients treated for restenosis after previous carotid surgery were excluded from the analysis. Group A consisted of 1,714 patients who underwent surgery between 1991 and 1997, and group B consisted of 3,320 patients who underwent surgery between 1998 and 2004. Follow-up included routine clinical evaluation and noninvasive surveillance, with duplex scanning at 1 month after surgery, after 6 months, and annually afterward. Only 3% of patients in group A and 0.6% in group B were asymptomatic, with 23% and 47% of them having preoperative stroke, respectively. In group A, angiography was used for the final diagnosis in 78% of patients. In group B, duplex scanning was performed in 82% of patients and angiography in only 18% (p < .001). Clamping time was shorter in the latter group (12.4 +/- 3.1 vs 14.5 +/- 4.1 min, p < .01). Introperative shunting and regional anesthesia were rarely performed in both groups (1.4% vs. 0.4%, p < .01, and 2% vs 0.3%, p < .001). Total and neurologic morbidity was significantly higher in group A than in group B (6.41% +/- 0.47% vs 4.81% +/- 0.53%, p < .001, and 2.14% +/- 0.31% vs 1.23% +/- 0.29%, p < .001, respectively). Total mortality was also higher in group A than in group B (1.92% +/- 0.24% vs 1.36% +/- 0.50%, p < .05), but although there was a trend toward lower neurologic mortality, it did not reach statistical significance (1.04% +/- 0.5% vs 0.57% +/- 0.25%, p = .074). There was a lower rate of nonsignificant restenosis (< 50%) in group B (2% vs 5%, p < .01), but the incidence of restenosis > or = 50% was identical between the groups (5.5% for both). Our data show that ECEA is a reliable surgical technique for the treatment of atherosclerotic carotid disease. Temporal trends in our patients demonstrated a decline in periopertive mortality and morbidity, despite a higher incidence of preoperative stroke.

Increased hs-CRP before CEA, increased fibrinogen 48 hours after CEA, and not taking aspirin were the main predictors of early CR. With the clinical implementation of the Fisher equation, it is possible to identify patients at high risk for early CR and to apply an aggressive therapeutic algorithm, finally leading to a decreased CR rate.

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