Does pathologic sympathetic activation (norepinephrine > 300 pg/mL) predict adverse outcomes in patients with first brain infarction?
Pathologic sympathetic activation, indicated by elevated initial norepinephrine, is an independent predictor of poor functional outcome and increased cardiovascular/cerebrovascular events at 1 year after first brain infarction.
OBJECTIVE: To evaluate the prognostic impact of early pathologic sympathetic activation after stroke. METHODS: The authors examined 112 consecutive patients (mean age, 69 years; 60 men) with their first brain infarction. A pathologic sympathetic activation was presumed if the initial norepinephrine level exceeds 300 pg/mL. In addition, involvement of the insular cortex, nighttime blood pressure changes, and several cardiovascular risk factors were determined. One-year outcome measures were mortality rate, cardiovascular and cerebrovascular events, and activities of daily living (Barthel index and Rankin score). RESULTS: Norepinephrine levels greater than 300 pg/mL, nighttime blood pressure increases, and insular involvement were associated with a lower Barthel index (p < 0.005) at the 1-year follow-up. By stepwise logistic regression analysis, insular infarction, serum norepinephrine concentration, right-sided infarction, and nighttime blood pressure increase were significant and independent predictors of an unfavorable functional outcome. Cox regression analysis showed a higher rate of cardiovascular and cerebrovascular events (hazard ratio, 2.9; 95% CI, 1.07; 6.83; p < 0.04) in patients with initially increased norepinephrine concentrations. CONCLUSIONS: The involvement of the insular cortex, the occurrence of a pathologic nighttime blood pressure increase, and an initially increased serum norepinephrine concentration are independent predictors of poor long-term outcome.
Sander et al. (Tue,) studied this question.