Multiple logistic regression analysis showed that the risk of stroke in patients with KC increased independently by 0.8% (odds ratio [OR] 1.008; 95% confidence interval [CI] 1.002, 1.013; p=0.004) with a 1 ng/mL increase in D-dimer levels, by 1.2% (OR 1.012; 95% CI 1.007, 1.018; p=0.000) with a 1 U/mL increase in CA125, by 2.5% (OR 1.025; 95% CI 1.012, 1.038; p=0.000) with a 1 U/mL increase in CEA by 1.4% (OR 1.014; 95% CI 1.005, 1.024; p=0.004) with a 1 mg increase in urine protein in 24 hours.
For symptomatic and asymptomatic patient with high or intermediate risk of CEA complications, CAS with the use of EPDs has a very low rate of in-hospital stroke and death There is no statistically significant difference in ipsilateral stroke/TIA and any stroke/TIA between the different device platforms Further efforts to assess differences between EPD devices would likely need to involve a surrogate endpoint due to the very low rates of clinical events.
This paper will provide a comparison of classical endpoints like stroke and mortality versus biochemical (non-STEMI) myocardial infarction and DW-MRI new brain lesions and will discuss the importance of cranial nerve lesion in CEA.
Propensity-matched logistic regression revealed that symptomatic males vs females had lower odds of stroke after CEA (odds ratio [OR] 0.81; 95% CI 0.72 to 0.91) and CAS (OR 0.72; 95% CI 0.57 to 0.90).
The effect size of stroke and stroke/death of CEA performed <48h from symptoms was 7.4% (95% CI: 3.7-11.2) and 7.9% (95% CI: 4.0-11.8) respectively, and for CEA <2-week was 4.5% (95% CI: 2.8- 6.3) and 5.4% (95% CI: 3.4-7.4) respectively.
Multivariable logistic and Cox-regression analyses were used to compare risk-adjusted perioperative and 1-year outcomes (stroke, death, and high-grade restenosis [>70%]) between c-CEA (using direct closure or patch angioplasty) and e-CEA.