Impaired baroreflex sensitivity predicts outcome of acute intracerebral hemorrhage

Objective. Impaired blood pressure regulation in the acute phase of stroke has been associated with less favorable outcome. Mechanisms and effects of blood pressure dysregulation in stroke are not well understood; however, central autonomic impairment with sympathetic overactivity and baroreflex involvement are discussed. Baroreflex sensitivity (BRS) in spontaneous intracerebral hemorrhage has not been investigated. We sought to examine BRS in patients with intracerebral hemorrhage and evaluate the relationship between BRS and short-term outcome measures. Design: An open, prospective study. Setting. Neurocritical care unit and stroke unit in a university hospital. Patients and Measurements: We studied 45 patients with acute intracerebral hemorrhage within 72 hrs from onset of symptoms and 38 control subjects. BRS was measured noninvasively using a hemodynamic monitoring device. Beat-to-beat blood pressure variability was derived. The effects of the BRS, hemorrhage volume, intraventricular blood, and admission scores on outcome at 10 days were studied using a multivariate regression model. Main Results: Compared with the control group, patients with intracerebral hemorrhage had significantly decreased BRS (p = 0.002) and significantly increased systolic, diastolic, and mean beat-to-beat blood pressure variability (p < 0.0001, p = 0.007, p = 0.015). After adjusting for age, National Institute of Heath Stroke Scale at admission, volume of intracerebral hemorrhage and presence of intraventricular blood in a multivariate regression model, BRS gain was an independent predictor of outcome at 10 days. Conclusions. We found that BRS was decreased in patients with acute intracerebral hemorrhage and correlated with increased beat-to-beat blood pressure variability. BRS independently predicted outcome at 10 days. Modulation of baroreceptor reflex sensitivity may represent a new therapeutic target in acute stroke and warrants future studies. (Crit Care Med 2008; 36: 3074-3079)