Elevated Admission Blood Pressure and Stroke Severity in Acute Ischemic Stroke: The Bergen NORSTROKE Study

<b><i>Background:</i></b> Transient elevated blood pressure (BP) is frequent in patients presenting with acute ischemic stroke. The pathophysiology of this response is not clear and its effect on clinical outcome has shown contradictory results. Some studies have suggested that BP elevation may represent a protective response to enhance perfusion in ischemic brain tissue. In this study, we aimed to explore the association between elevated admission BP and stroke severity in the acute phase of ischemic stroke. If it is true that elevated BP represents a protective response in acute ischemia, we expected an inverse association between elevated BP and admission stroke severity, and a positive association between elevated BP and complete neurological recovery within 24 h and/or favorable short-term outcome. <b><i>Methods:</i></b> Patients with ischemic stroke with hospital admission <6 h after symptom onset were prospectively included in a stroke registry (Bergen NORSTROKE Registry). BP was measured immediately after admission in all patients. Elevated BP was defined as systolic BP ≥140 mm Hg or diastolic BP ≥90 mm Hg. The National Institutes of Health Stroke Scale (NIHSS) was used to assess stroke severity upon admission. Mild stroke was defined as NIHSS score <8, moderate stroke as NIHSS score 8-14, and severe stroke as NIHSS score ≥15. Complete neurological recovery (CNR) was defined as no persistent ischemic stroke symptoms at 24 h after admission. Favorable short-term outcome was defined as a modified Rankin Scale score of 0 or 1 at day 7. <b><i>Results:</i></b> A total of 749 patients with ischemic stroke were included, of which 621 patients (82.9%) presented with elevated BP. Elevated BP was independently associated with mild stroke (odds ratio, OR: 2.12; 95% CI: 1.39-3.24; p < 0.001), whereas lack of elevated BP was independently associated with severe stroke (OR: 0.41; 95% CI: 0.25-0.68; p < 0.001). There was a nonsignificant association between elevated BP and CNR (OR: 2.11; 95% CI: 0.96-4.68; p = 0.063), yet no association between elevated BP and favorable short-term outcome (OR: 0.97; 95% CI: 0.59-1.59; p = 0.906) when adjusted for confounders. <b><i>Conclusion:</i></b> Our study showed an inverse association between elevated BP and stroke severity on admission, where elevated BP was associated with mild stroke and lack of elevated BP was associated with severe stroke. This could be explained by a protective effect of elevated BP in the acute phase of ischemic stroke, although the absence of association between elevated BP and favorable outcome argues against this hypothesis.