(Stroke. 1999;30:2631.)
© 1999 American Heart Association, Inc.
Original Contributions |
From the Departments of Neurology (A.D.), Hospital Universitari Doctor Josep Trueta, Girona; Hospital Universitario Xeral de Galicia (J.C.), Santiago de Compostela, Spain; Departments of Neurological Sciences (D.T.) and Neuroradiology (S.B.), University La Sapienza, Rome, Italy; and the Biostatistical Centre for Clinical Trials (F.I., E.L.), Leuven, Belgium.
Background and PurposeThe present study was undertaken to identify potential predictors of and factors associated with early and late progression in acute stroke. We performed secondary analysis of the clinical, biochemical, and radiological data recorded in the acute phase of stroke patients enrolled in the European Cooperative Acute Stroke Study (ECASS) I.
MethodsEarly progressing stroke (EPS) was diagnosed when there
was a decrease of
2 points in consciousness or motor power or a
decrease of
3 points in speech scores in the Scandinavian
Neurological Stroke Scale from baseline to the 24-hour evaluation, and
late progressing stroke (LPS) was diagnosed when 1 of these decreases
occurred between the 24-hour evaluation and the evaluation at day 7.
Using logistic regression analyses, we looked for baseline
variables that predicted EPS and LPS and for factors measured after
the early or late acute phase and associated with the 2 clinical
courses.
ResultsOf the 615 patients studied, 231 (37.5%) worsened during the first 24 hours after inclusion. The overall incidence of EPS was 37% in the placebo group and 38% in the recombinant tissue plasminogen activator group (P=0.68, Fishers Exact Test). Focal hypodensity (odds ratio [OR], 1.9; 95% confidence interval [CI], 1.3 to 2.9) and hyperdensity of the middle cerebral artery sign (OR, 1.8; 95% CI, 1.1 to 3.1) on baseline computed tomography, longer delay until treatment (OR, 1.2; 95% CI, 1.1 to 1.4) and history of coronary heart disease (OR, 1.7; 95% CI, 1.1 to 2.8) and diabetes (OR, 1.8; 95% CI, 1.0 to 3.1) were independent prognostic factors for EPS. Extent of hypodensity >33% in the middle cerebral artery territory (OR, 2.5; 95% CI, 1.6 to 4.0) and brain swelling (OR, 1.8; 95% CI, 1.1 to 3.2) on CT at 24 hours but not hemorrhagic transformation of cerebral infarct nor decrease in systolic blood pressure within the first 24 hours after treatment were associated with EPS in multivariate analyses. LPS was observed in 20.3% of patients. Older age, a low neurological score, and brain swelling at admission independently predicted late worsening.
ConclusionsIn the setting of a multicenter trial, EPS and LPS are mainly related to computed tomographic signs of cerebral edema. Treatment with recombinant tissue plasminogen activator, hemorrhagic transformation, and moderate changes in systolic blood pressure did not influence the early clinical course.
Key Words: brain edema stroke outcome stroke, acute thrombolytic therapy tomography, x-ray computed
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